222 results on '"COBALT TOXICITY"'
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2. Foliar spray of stress protective chemicals alleviates cobalt toxicity by improving root antioxidant defense in maize (Zea mays).
- Author
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Nazir A and Wahid A
- Subjects
- Ascorbic Acid pharmacology, Ascorbic Acid metabolism, Oxidative Stress, Seedlings metabolism, Antioxidants metabolism, Zea mays
- Abstract
Cobalt (Co
2+ ) is a beneficial microelement for plants but toxic to metabolism in higher amounts. This study determined the influence of sublethal Co2+ level (0.5 mM) on the growth of maize (Zea mays L.) hybrids; Hycorn 11 plus (Co2+ sensitive) and P-1429 (Co2+ tolerant) and its alleviation with foliar spray of pre-optimized levels of stress protective chemicals (SPCs), i.e., salicylic acid (SA, 0.5 mM), thiourea (TU, 1.0 mM), and ascorbic acid (AsA, 0.5 mM) applied at seedling, vegetative, and late vegetative stages. Plants were harvested at early vegetative, late vegetative, and silking stages. Co2+ stress caused a decrease in shoot and root length, dry weight, leaf area, and culm diameter, reduced the activities of enzymatic antioxidants and concentrations of AsA and soluble phenolics more in root than shoot, but P-1429 was more tolerant of Co2+ than Hycorn 11 plus. SPCs spray alleviated oxidative damage by enhancing the antioxidant activity, AsA and soluble phenolics, sulfate-S and nitrate-N contents, which were significantly increased in roots than in shoots; P-1429 displayed better response than Hycorn 11 plus. Principal component analysis and correlation matrix revealed the profound roles of SPCs spray in improving Co2+ resistance in root leading to robust growth of hybrids. AsA was highly promising in reducing Co2+ toxicity while vegetative and silking stages were more sensitive. Results revealed that after translocation to root, the foliar-applied SPCs had individualistic modes of action in mitigating Co2+ toxicity on roots. In crux, the metabolism and phloem transport of the SPCs from shoot to root are plausible mechanism for Co2+ tolerance in maize hybrids., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)- Published
- 2023
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3. Reply to "Efficacy of unithiol (2,3-dimercaptopropanesulfonate) and acetylcysteine in a patient with arthroplastic cobalt toxicity".
- Author
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Carnovale M, Lonati D, Schicchi A, Petrolini VM, and Locatelli CA
- Subjects
- Humans, Antidotes, Cobalt, Unithiol, Acetylcysteine therapeutic use
- Published
- 2023
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4. Exogenously applied melatonin enhanced the tolerance of Brassica napus against cobalt toxicity by modulating antioxidant defense, osmotic adjustment, and expression of stress response genes.
- Author
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Ali S, Gill RA, Ulhassan Z, Zhang N, Hussain S, Zhang K, Huang Q, Sagir M, Tahir MB, Gill MB, Mwamba TM, Ali B, and Zhou W
- Subjects
- Antioxidants pharmacology, Antioxidants metabolism, Reactive Oxygen Species metabolism, Hydrogen Peroxide metabolism, Melatonin pharmacology, Melatonin metabolism, Brassica napus genetics, Brassica napus metabolism
- Abstract
The excessive accumulation of cobalt (Co) in plant tissues severely impairs plant growth that ultimately reduces the yield. However, melatonin (MT) has been known to mediate the abiotic stress tolerance in plants. The present study aimed at investigating the protective mechanisms of exogenously applied MT (0, 50 and 100 μM) under Co (0, 100, 200 and 300 μM) stress by focusing on morpho-physiological, biochemical and cellular characterizations of Brassica napus plants. Cobalt (300 μM) alone treatment drastically inhibited the stomatal conductance, plant height (45%), leaf area (30%), free amino acid (139%), relative electrolyte leakage (109%), and total soluble sugars (71%), compared with the control. However, the exogenous supply of MT notably minimized the oxidative damage, lipid peroxidation and maintained the membrane integrity under Co-toxicity by restricting the overproduction of ROS (H
2 O2 and O2 • ), and MDA in leaves and roots. Melatonin significantly enhanced the activities of ROS-scavenging antioxidant enzymes, secondary metabolism-related phenylalanine ammonia lyase (PAL), polyphenol oxidase (PPO), stress-responsive genes (heat shock protein as HSP-90, methyl transferase as MT) and regulated the Co-transporters, especially in roots. These findings indicated that an exogenous supply of MT improve the plant morphology, photosynthetic apparatus, osmotic adjustments, and antioxidant defense systems by enhancing the Co-detoxification in B. napus plants., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2023
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5. Efficacy of unithiol (2,3-dimercaptopropanesulfonate) and acetylcysteine in a patient with arthroplastic cobalt toxicity.
- Author
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Pelclova D and Lach K
- Subjects
- Humans, Antidotes therapeutic use, Cobalt, Unithiol, Acetylcysteine therapeutic use
- Published
- 2023
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6. Assessing the Clinical Value of Objective and Patient-Reported Audiovestibular Outcome Measures in the Risk Estimation of Systemic Cobalt Toxicity for Patients With a Metal-on-Metal Hip Implant.
- Author
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Leyssens L, Vinck B, Van Der Straeten C, Dhooge I, Wuyts FL, Winnock de Grave P, Bataillie F, Van Melkebeek J, De Smet K, Van Hecke R, Danneels M, and Maes L
- Subjects
- Audiometry, Pure-Tone, Cobalt, Humans, Metals, Patient Reported Outcome Measures, Hip Prosthesis adverse effects, Metal-on-Metal Joint Prostheses adverse effects
- Abstract
Objectives: Based on limited evidence from case reports and small cohort studies of metal-on-metal (MoM) hip implant patients with presumed systemic cobalt (Co) toxicity, and a few animal studies on Co-induced damage to the otovestibular system, it was hypothesised that Co exhibits an ototoxic potential alongside other systemic manifestations. Preliminary investigations from our research group in MoM patients confirmed this assumption for the auditory system, whereas no signs of Co-induced vestibular impairment were detected, and a clear dose-response relationship between the auditory function and the blood Co levels was lacking. Therefore, the current study aimed to extend and validate these findings in a larger sample of MoM patients and control subjects, to explore the potential clinical value of audiovestibular outcome measures in the risk estimation of systemic Co toxicity in this patient population., Design: Fifty patients (32 to 68 years) with a primary unilateral/bilateral MoM hip implant were matched for age, gender, and noise exposure to 50 nonimplanted control subjects. Both groups underwent the same protocol, consisting of an objective auditory [i.e., conventional and high-frequency audiometry, transient-evoked and distortion (TEOAEs and DPOAEs), auditory brainstem responses] and vestibular (i.e., cervical and ocular vestibular evoked myogenic potentials, horizontal and vertical video head impulse tests) test battery, a questionnaire inquiring auditory, balance, and general neurological symptoms, and a blood sample collection to determine the plasma Co concentration., Results: The auditory test battery presented consistently higher audiometric thresholds in the MoM patient group, with group differences ranging from 2.1 to 5.7 dB in the lower frequencies (0.25 to 6.0 kHz) and from 4.6 to 9.3 dB in the high frequencies (8.0 to 14.0 kHz). Group differences at high frequencies were statistically significant ( p ≤ 0.001). Additionally, significantly lower TEOAE ( p = 0.009) and DPOAE ( p < 0.001) amplitudes were observed in the MoM patients when the better ear was included in the analysis, and more absent TEOAE and DPOAE responses were found between 1.0 and 4.0 kHz (0.008 ≤ p ≤ 0.039). Within the vestibular test battery, the MoM patients showed longer N1 and P1 ocular vestibular evoked myogenic potentials latencies for the left ear, and lower video head impulse test gains for the left anterior and right posterior semicircular canals (0.005 ≤ p ≤0.035). The patient-reported (questionnaire) outcome delivered no significant group differences ( p > 0.01). Six patients had elevated Co levels according to our local institutional threshold (>4 or 5 µg/l for unilateral or bilateral MoM hip implants, resp.), but their audiovestibular outcome measures did not differ significantly from those of the other patients., Conclusions: Corresponding to our preliminary investigations, the results indicate possibly Co-induced (predominantly high-frequency) auditory impairment, probably triggered by toxic damage to the cochlear structures. However, the low mean difference values, the lack of group differences for the patient-reported outcome measures, and the lack of any relationship with the blood Co levels strongly reduce the clinical relevance of these findings. Therefore, the risk of Co-induced ototoxic impairment is considered to be clinically negligible for the majority of MoM hip implant patients, and the use of auditory tests in the risk estimation of systemic Co toxicity should be decided on a case-by-case basis., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)
- Published
- 2022
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7. Ellagic Acid from Terminalia arjuna Fruits Protects Against Chromium and Cobalt Toxicity in Primary Human Lymphocytes.
- Author
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Bodiga VL, Vemuri PK, Kudle MR, and Bodiga S
- Subjects
- Chromium, Cobalt, Cytokines, Ellagic Acid pharmacology, Fruit, Humans, Ions, Lymphocytes, Terminalia
- Abstract
Increased accumulation of heavy metal ions such as Cr
6+ and Co2+ due to release from prostheses and metallic implants has been reported. These metal ions have been shown to affect both resting and activated lymphocytes. Natural remedies towards mitigating the cytotoxic effects of metal ions are clearly warranted. Polyphenolic compounds which are part of hydrolysable tannins from natural plant sources are considered effective in cheating heavy metal ions in a biological system. We have isolated and characterized a polyphenolic compound (ellagic acid) from Terminalia arjuna fruits that has been tested for its ability to attenuate the metal ion toxicity in primary human lymphocytes in culture. Cr6+ and Co2+ (100 μM) decreased lymphocyte viability and proliferation and increased apoptosis of resting as well as CD3 and/or CD28-stimulated lymphocytes. Metal ions markedly diminished the cytokine (interleukin-2 and interferon-γ) secretion from activated lymphocytes. Pretreatment with ellagic acid at 25, 50, and 100 μM concentrations effectively improved viability and proliferative responses of both resting and activated lymphocytes, while attenuating the apoptotic index. Ellagic acid also tended to normalize the cytokine secretion from the activated lymphocytes even in the presence of metal ions, suggesting broad effects on the adaptive immune system., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)- Published
- 2022
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8. Prosthetic hip-associated cobalt toxicity: a systematic review of case series and case reports.
- Author
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Crutsen JRW, Koper MC, Jelsma J, Heymans M, Heyligers IC, Grimm B, Mathijssen NMC, and Schotanus MGM
- Abstract
Prosthetic hip-associated cobalt toxicity (PHACT) is caused by elevated blood cobalt concentrations after hip arthroplasty. The aim of this study is to determine which symptoms are reported most frequently and in what type of bearing. We also try to determine the blood level of cobalt concentrations associated with toxicological symptoms. A systematic review was conducted on the 10th of July according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A methodological quality assessment (risk of bias (RoB)) was performed. Primary outcomes were the reported symptoms of cobalt toxicity and the level of cobalt concentrations in blood. These levels were associated with toxicological symptoms. A total of 7645 references were found of which 67 relevant reports describing 79 patients. The two most used bearings in which PHACT was described were metal-on-metal (MoM) bearings (38 cases) and revised (fractured) ceramic-on-ceramic (CoC) bearings where the former ceramic head was replaced by a metal head (32 cases). Of all reported symptoms, most were seen in the neurological system, of which 24% were in the sensory system and 19.3% were in central/peripheral system, followed by the cardiovascular (22.1%) system. The mean cobalt concentration for MoM-bearings was 123.7 ± 96.8 ppb and 1078.2 ± 1267.5 ppb for the revised fractured CoC-bearings. We recommend not to use a metal-based articulation in the revision of a fractured CoC bearing and suggest close follow-up with yearly blood cobalt concentration controls in patients with a MoM bearing or a revised fractured CoC bearing. Level of Evidence: Level V, systematic review.
- Published
- 2022
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9. Cobalt Toxicity
- Author
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Chen RJ and Lee VR
- Abstract
Cobalt (Co) metal is a gray, ductile, magnetic element with an atomic number of 27 and an atomic weight of 58.9 Da. In the environment, cobalt is a component of naturally occurring minerals and is found in combination with other elements such as copper, nickel, manganese, arsenic, sulfur, and oxygen. Due to its ferromagnetic properties, high melting point (1495.05 C), and high boiling point (2927 C), cobalt is widely used in industry to produce hard metals and superalloys. For example, the alloy Alnico is a blend of iron, aluminum, nickel, and cobalt used for its permanent magnetic properties. A common source of chronic cobalt exposure is in the production of tungsten carbide, which is used for its hardness, heat resistance, and strength. Historically, cobalt chloride (CoCl2) has been used in medicine as a treatment for anemia due to its ability to promote erythropoiesis. However, due to its adverse effects of thyroid dysfunction and the development of goiters, the use of cobalt in treating anemia has fallen out of favor. A biochemically important cobalt compound is cyanocobalamin (vitamin B12) which contains a Co3+-ion. Vitamin B12 is an essential nutrient naturally found in foods of animal origin, such as dairy, eggs, fish, poultry, and meat. Deficiencies in vitamin B12 may lead to pernicious anemia as well as peripheral neuropathy. The precursor hydroxocobalamin is used as an antidote for cyanide poisoning and may have a role in treating vasoplegic shock. Potential cobalt exposure can occur via oral, respiratory, and dermal routes., (Copyright © 2022, StatPearls Publishing LLC.)
- Published
- 2022
10. Exploiting Unique Alignment of Cobalt Ferrite Nanoparticles, Mild Hyperthermia, and Controlled Intrinsic Cobalt Toxicity for Cancer Therapy.
- Author
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Balakrishnan PB, Silvestri N, Fernandez-Cabada T, Marinaro F, Fernandes S, Fiorito S, Miscuglio M, Serantes D, Ruta S, Livesey K, Hovorka O, Chantrell R, and Pellegrino T
- Subjects
- Animals, Cell Line, Tumor, Cobalt adverse effects, Ferric Compounds adverse effects, Humans, Hyperthermia, Induced, Magnetic Fields, Mice, Survival Analysis, Xenograft Model Antitumor Assays, Cobalt chemistry, Cobalt therapeutic use, Ferric Compounds chemistry, Ferric Compounds therapeutic use, Nanoparticles chemistry
- Abstract
Nanoparticle-based magnetic hyperthermia is a well-known thermal therapy platform studied to treat solid tumors, but its use for monotherapy is limited due to incomplete tumor eradication at hyperthermia temperature (45 °C). It is often combined with chemotherapy for obtaining a more effective therapeutic outcome. Cubic-shaped cobalt ferrite nanoparticles (Co-Fe NCs) serve as magnetic hyperthermia agents and as a cytotoxic agent due to the known cobalt ion toxicity, allowing the achievement of both heat and cytotoxic effects from a single platform. In addition to this advantage, Co-Fe NCs have the unique ability to form growing chains under an alternating magnetic field (AMF). This unique chain formation, along with the mild hyperthermia and intrinsic cobalt toxicity, leads to complete tumor regression and improved overall survival in an in vivo murine xenograft model, all under clinically approved AMF conditions. Numerical calculations identify magnetic anisotropy as the main Co-Fe NCs' feature to generate such chain formations. This novel combination therapy can improve the effects of magnetic hyperthermia, inaugurating investigation of mechanical behaviors of nanoparticles under AMF, as a new avenue for cancer therapy., (© 2020 The Authors. Published by Wiley-VCH GmbH.)
- Published
- 2020
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11. Cobalt toxicity: a preventable and treatable cause for possibly life threatening cardiomyopathy.
- Author
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Giacon G and Boon K
- Subjects
- Arthroplasty, Replacement, Hip instrumentation, Cardiomyopathies diagnosis, Cobalt blood, Echocardiography, Fatal Outcome, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Prosthesis Failure adverse effects, Radiography, Thoracic, Arthroplasty, Replacement, Hip adverse effects, Cardiomyopathies chemically induced, Cobalt toxicity, Hip Prosthesis adverse effects
- Abstract
Mr BH was a 53-year-old gentleman who presented to hospital in November 2019 with decompensated heart failure, new-onset paroxysmal atrial tachycardia and increasing left hip pain. Imaging of his hip demonstrated radiographic evidence of bony changes, suggestive of an adverse reaction to metal debris (ARMD), along with a non-traumatic left peri-prosthetic neck-of-femur fracture. Clinically, he had concurrent decompensated cardiomyopathy requiring dopamine and furosemide infusions. His serum cobalt (sCo) levels were 5244nmol/L (normal<12nmol/L). He had previous bilateral total hip arthroplasties using the Birmingham Hip Resurfacing (right side 2006, left side 2012). As part of routine metal-on-metal arthroplasty follow-up, Mr BH had sCo level checks. In 2013, these levels rose to 1981nmol/L. Although there has been no direct correlation between sCo levels and toxicity, levels above 119nmol/L are concerning. Unfortunately, Mr BH moved to a different health district and was subsequently lost to follow-up. In 2015, Mr BH was diagnosed with dilated cardiomyopathy, presumed secondary to viral myocarditis. Despite successful chelating therapy and heart failure treatment, he passed away secondary to cobalt-toxicity induced cardiomyopathy (CTCM)., Competing Interests: Nil.
- Published
- 2021
12. Transcriptomic Analysis of Streptococcus suis in Response to Ferrous Iron and Cobalt Toxicity.
- Author
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Jia M, Wei M, Zhang Y, and Zheng C
- Subjects
- ATP-Binding Cassette Transporters genetics, Animals, Bacterial Proteins genetics, Down-Regulation genetics, Gene Expression Profiling methods, Gene Expression Regulation, Bacterial genetics, Hydrolases genetics, Operon genetics, Oxidative Stress genetics, Swine, Cobalt toxicity, Iron toxicity, Streptococcus suis genetics, Transcriptome genetics
- Abstract
Streptococcus suis is a zoonotic pathogen causing serious infections in swine and humans. Although metals are essential for life, excess amounts of metals are toxic to bacteria. Transcriptome-level data of the mechanisms for resistance to metal toxicity in S. suis are available for no metals other than zinc. Herein, we explored the transcriptome-level changes in S. suis in response to ferrous iron and cobalt toxicity by RNA sequencing. Many genes were differentially expressed in the presence of excess ferrous iron and cobalt. Most genes in response to cobalt toxicity showed the same expression trends as those in response to ferrous iron toxicity. qRT-PCR analysis of the selected genes confirmed the accuracy of RNA sequencing results. Bioinformatic analysis of the differentially expressed genes indicated that ferrous iron and cobalt have similar effects on the cellular processes of S. suis . Ferrous iron treatment resulted in down-regulation of several oxidative stress tolerance-related genes and up-regulation of the genes in an amino acid ABC transporter operon. Expression of several genes in the arginine deiminase system was down-regulated after ferrous iron and cobalt treatment. Collectively, our results suggested that S. suis alters the expression of multiple genes to respond to ferrous iron and cobalt toxicity.
- Published
- 2020
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13. Hydrogen sulfide (H 2 S) and nitric oxide (NO) alleviate cobalt toxicity in wheat (Triticum aestivum L.) by modulating photosynthesis, chloroplastic redox and antioxidant capacity.
- Author
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Ozfidan-Konakci C, Yildiztugay E, Elbasan F, Kucukoduk M, and Turkan I
- Subjects
- Chloroplasts drug effects, Chloroplasts metabolism, Gene Expression Regulation, Plant drug effects, Nitroprusside pharmacology, Oxidation-Reduction, Oxidative Stress drug effects, Photosynthesis drug effects, Plant Leaves drug effects, Plant Leaves growth & development, Plant Leaves metabolism, Sulfides pharmacology, Triticum growth & development, Triticum metabolism, Cobalt toxicity, Hydrogen Sulfide metabolism, Nitric Oxide metabolism, Triticum drug effects
- Abstract
The role of hydrogen sulfide (H
2 S)/nitric oxide (NO) in mitigating stress-induced damages has gained interest in the past few years. However, the protective mechanism H2 S and/or NO has towards the chloroplast system through the regulation of redox status and activation of antioxidant capacity in cobalt-treated wheat remain largely unanswered. Triticum aestivum L. cv. Ekiz was treated with alone/in combination of a H2 S donor (sodium hydrosulfide (NaHS,600μM)), a NO donor (sodium nitroprusside (SNP,100μM)) and a NO scavenger (rutin hydrate (RTN,50μM)) to assess how the donors affect growth, water relations, redox and antioxidant capacity in chloroplasts, under cobalt (Co) concentrations of 150-300 μM. Stress decreased a number of parameters (growth, water content (RWC), osmotic potential (ΨΠ ), carbon assimilation rate, stomatal conductance, intercellular CO2 concentrations, transpiration rate and the transcript levels of rubisco, which subsequently disrupt the photosynthetic capacity). However, SNP/NaHS counteracted the negative effects of stress on these aforementioned parameters and RTN application with stress/non-stress was reversed these effects. Hydrogen peroxide (H2 O2 ) and TBARS were induced under stress in spite of activated ascorbate peroxidase (APX). SNP/NaHS under stress increased activation of superoxide dismutase (SOD), peroxidase (POX), APX, glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), ascorbate (tAsA) and glutathione (GSH). In conclusion, NaHS/SNP are involved in the regulation and modification of growth, water content, rubisco activity and up-regulation of ascorbate-glutathione cycle (AsA-GSH) in chloroplast under stress., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)- Published
- 2020
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14. Genetic analysis of oxidative and endoplasmic reticulum stress responses induced by cobalt toxicity in budding yeast.
- Author
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Zhao YY, Cao CL, Liu YL, Wang J, Li SY, Li J, and Deng Y
- Subjects
- Endoplasmic Reticulum metabolism, Endoplasmic Reticulum Stress physiology, Gene Expression Profiling methods, Homeostasis physiology, Oxidative Stress genetics, Protein Serine-Threonine Kinases genetics, Reactive Oxygen Species metabolism, Saccharomyces cerevisiae genetics, Saccharomyces cerevisiae metabolism, Saccharomyces cerevisiae Proteins genetics, Saccharomyces cerevisiae Proteins metabolism, Signal Transduction physiology, Spectrophotometry, Atomic methods, Unfolded Protein Response, Cobalt metabolism, Cobalt toxicity, Oxidative Stress physiology
- Abstract
Background: Cobalt is an important metal cofactor of many living cells. However, excessive cobalt is toxic and can cause cell death and even several diseases in humans. Saccharomyces cerevisiae is a useful tool for studying metal homeostasis and many of the genes and pathways are highly conserved in higher eukaryotes including humans., Methods: The intracellular cobalt and reactive oxygen species (ROS) levels were measured by an atomic absorption spectrometer and DHE staining method, respectively. The expression of genes involved in scavenging oxidative stress was tested by qPCR method, while the expression of UPRE-lacZ report gene was analyzed via β-galactosidase activity assay., Results: Using a genome-scale genetic screen, 153 cobalt-sensitive and 37 cobalt-tolerant gene deletion mutants were identified from Saccharomyces cerevisiae. We showed that 101 of the cobalt-sensitive mutants accumulated higher intracellular cobalt compared to wild-type. The intracellular ROS levels in 112 of the mutants were induced by cobalt, which might be caused by the decreased expression of genes involved in scavenging oxidative stress in response to cobalt. Moreover, more than one-third of the cobalt-sensitive mutants were also sensitive to tunicamycin, and cobalt stress might induce the unfolded protein response (UPR) through serine/threonine kinase and endoribonuclease Ire1., Conclusions: This study reinforced the fact that cobalt toxicity might be due to the high intracellular cobalt and ROS levels, and the endoplasmic reticulum stress responses induced by cobalt., General Significance: Elucidating the toxicity mechanisms of cobalt stress response will help reveal new routes for the treatment of the diseases induced by cobalt., (Copyright © 2020. Published by Elsevier B.V.)
- Published
- 2020
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15. Heart transplant secondary to cobalt toxicity after hip arthroplasty revision.
- Author
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Sanz Pérez MI, Rico Villoras AM, Moreno Velasco A, Bartolomé García S, and Campo Loarte J
- Subjects
- Artificial Limbs, Ceramics, Chromium blood, Chromium Alloys, Female, Heavy Metal Poisoning, Hip Prosthesis adverse effects, Humans, Male, Middle Aged, Polyethylene, Prosthesis Failure, Reoperation, Arthroplasty, Replacement, Hip adverse effects, Cobalt adverse effects, Cobalt blood, Heart Transplantation
- Abstract
Introduction: Cobalt toxicity in patients with hip arthroplasty is a rare complication, but it should be considered in those patients who, after a ceramic fracture, were implanted with a metal-on-polyethylene prosthesis. The complete removal of ceramic particles during revision surgery can be complicated. If the bearing surface is replaced with a metal-on-polyethylene prosthesis, these residual ceramic particles may wear down the chrome-cobalt head, producing localised metallosis. This can trigger blood metal ion levels to rise, causing systemic toxicity. Visual and auditory alterations, cognitive deterioration, hypothyroidism, neuropathy, cardiomyopathy, anorexia, fatigue, diabetes, polycythemia, and respiratory and cutaneous symptoms are some of the clinical manifestations of prosthetic cobaltism., Case Description: A young patient presented with multiorgan failure secondary to cobalt toxicity after a ceramic fracture and revision with a metal-on-polyethylene prosthesis; his serum cobalt and chromium levels were 652 μg/L and 270 μg/L, respectively. The patient needed a heart transplant after presenting with cobalt-induced cardiogenic shock., Conclusions: In a patient with a ceramic fracture who is subjected to revision surgery with a metal-on-polyethylene bearing, it is necessary to rule out the possibility of cobalt intoxication. Serum cobalt levels > 20 μg/L are inadmissible; in these cases, surgical treatment should be considered in the short term. A wide synovectomy and replacement of components should be performed with hard friction options, preferably with a ceramic-on-ceramic prosthesis.
- Published
- 2019
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16. Copper alleviates cobalt toxicity in barley by antagonistic interaction of the two metals.
- Author
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Lwalaba JLW, Louis LT, Zvobgo G, Fu L, Mwamba TM, Mukobo Mundende RP, and Zhang G
- Subjects
- Antioxidants metabolism, Drug Interactions, Glutathione metabolism, Hordeum enzymology, Hordeum metabolism, Lipid Peroxidation, Oxidative Stress drug effects, Photosynthesis drug effects, Cobalt toxicity, Copper toxicity, Hordeum drug effects, Soil Pollutants toxicity
- Abstract
Cobalt (Co) commonly co-exists with copper (Cu) in natural soils, but the information about their combined effects on plants is poorly available. In this study, we hydroponically investigated the combined effects of Co and Cu on two barley genotypes differing in Co toxicity tolerance to reveal the interaction pattern of these two metals. The results showed that single treatment of Co or Cu at the dose of 100 μM led to a significant decrease of growth and photosynthetic rate, and a significant increase of lipid peroxidation, ROS radicals as well as anti-oxidative enzyme (SOD, CAT and GR) activities and glutathione content, with the extent of effect being less in Yan66 than Ea52. The combined treatment of Co and Cu alleviated the toxicity of both metals in comparison with each metal treatment alone, as reflected by improved growth and photosynthesis, and much slight oxidative stress. The alleviation of metal toxicity upon combined treatment is mainly attributed to a drastic reduction of Co uptake and its translocation from roots to shoots. It may be suggested that interaction of Co and Cu on their uptake and movement in plants is antagonistic., (Copyright © 2019 Elsevier Inc. All rights reserved.)
- Published
- 2019
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17. An Analysis of the FDA MAUDE Database and the Search for Cobalt Toxicity in Class 3 Johnson & Johnson/DePuy Metal-on-Metal Hip Implants.
- Author
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Kavanagh KT, Kraman SS, and Kavanagh SP
- Subjects
- Aged, Arthroplasty, Replacement, Hip methods, Databases, Factual, Female, Humans, Male, Middle Aged, United States, United States Food and Drug Administration, Arthroplasty, Replacement, Hip adverse effects, Cobalt toxicity, Hip Prosthesis adverse effects, Metal-on-Metal Joint Prostheses adverse effects
- Abstract
Introduction: This study was designed to determine whether systemic cobalt toxicity as an adverse event could be documented using the Food and Drug Administration's (FDA) Manufacturer and User Facility Device Experience (MAUDE) database for cobalt-chromium containing hip implant recipients. Class 3 Johnson & Johnson (J&J)/DePuy devices were chosen for analysis because of the large number of adverse event reports related to their Pinnacle and ASR XL Acetabular hip replacement systems. A secondary goal was to characterize the reporters who are populating the information in the MAUDE database and to evaluate the quality of the data and information submitted., Methods: Using FDA MAUDE downloadable data files, 83,528 adverse event medical device narrative reports were identified with the product code of KWA (Prosthesis, Hip, Semiconstrained [Metal Uncemented Acetabular Component]) for J&J/DePuy (KWA Text File). These are class 3 devices and devices with known high failure rates. The ASR XL Acetabular hip replacement Systems and Pinnacle fall into this category. This group of implants was chosen because implant failure is associated with elevated cobalt levels. Two additional subfiles were created from Free Text records in the narrative reports containing key words that indicated a chromium or cobalt (CrCo) device and another for key words indicating elevated levels of cobalt or toxicity. These files were then searched for symptoms of systemic cobalt toxicity with Microsoft Excel using key words pertaining to symptom categories of: cognitive/memory loss, tremor, neuropathy, depression, auditory symptoms, visual symptoms, cardiac, and thyroid disease. Reports are submitted to the FDA at the device component level. It was common for multiple reports to be submitted for a single device., Results: It was not possible to differentiate systemic versus local symptoms for adverse event reports in the neuropathy category. This category was not analyzed. The number of adverse event reports in the other categories ranged from 119 to 16 for the J&J/DePuy KWA Text File and 59 to 4 in the file of records having key words indicating potential elevation of CrCo or toxicity. Cardiac, visual, and auditory conditions were most frequently reported. With the possible exception of cardiomyopathy, the numbers of these reports are far below the prevalence expected in the general population of comparable age. The content of the MAUDE database records often contained little objective data. We found less than 4% of 14,714 records, which indicated cobalt elevation or toxicity contained units for quantitative measurement. There was also frequent use of nondescript, all-encompassing words and phrases such as "mental anguish," found in 321 KWA Text File records. Manufacturers submitted more than 99% of the reports and the most common reporter occupation was attorney, found in 42.24% of the 83,550 J&J/DePuy KWA Reporter File records. Physician was the reporter's occupation in 20.48% of reports but seldom reported directly to the FDA., Conclusions: We were not able find in the FDA MAUDE database meaningful warning signs to support the contention that chromium-cobalt-containing Class 3 J&J and DePuy hip implants caused systemic neurological or thyroid symptoms in patients. The incidence of reported cardiomyopathy was rare but frequent enough to be cause of concern. The redaction of most patient data along with the nonstructured nature of data entry would be expected to hinder the identification of warning signs. Even identification of the type of device could not be consistently carried out. In addition, the FDA needs to implement a methodology to identify and group all reports from a single device implanted into a patient, so duplication of event counting would not occur. Of 83,550 J&J/DePuy KWA Reporter File records, we found only two physician reports sent directly to the FDA. Almost all reports are submitted by manufacturers and are most commonly authored by attorneys. A standard of care needs to be set for physicians to report medical device adverse events to the FDA.
- Published
- 2018
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18. Cobalt toxicity in humans-A review of the potential sources and systemic health effects.
- Author
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Leyssens L, Vinck B, Van Der Straeten C, Wuyts F, and Maes L
- Subjects
- Cobalt blood, Dose-Response Relationship, Drug, Environmental Monitoring, Environmental Pollutants blood, Humans, Prosthesis Design, Risk Assessment, Toxicity Tests, Cobalt adverse effects, Diet adverse effects, Dietary Supplements adverse effects, Environmental Exposure adverse effects, Environmental Pollutants adverse effects, Hip Prosthesis adverse effects, Metal-on-Metal Joint Prostheses adverse effects, Occupational Exposure adverse effects
- Abstract
Cobalt (Co) and its compounds are widely distributed in nature and are part of numerous anthropogenic activities. Although cobalt has a biologically necessary role as metal constituent of vitamin B
12 , excessive exposure has been shown to induce various adverse health effects. This review provides an extended overview of the possible Co sources and related intake routes, the detection and quantification methods for Co intake and the interpretation thereof, and the reported health effects. The Co sources were allocated to four exposure settings: occupational, environmental, dietary and medical exposure. Oral intake of Co supplements and internal exposure through metal-on-metal (MoM) hip implants deliver the highest systemic Co concentrations. The systemic health effects are characterized by a complex clinical syndrome, mainly including neurological (e.g. hearing and visual impairment), cardiovascular and endocrine deficits. Recently, a biokinetic model has been proposed to characterize the dose-response relationship and effects of chronic exposure. According to the model, health effects are unlikely to occur at blood Co concentrations under 300μg/l (100μg/l respecting a safety factor of 3) in healthy individuals, hematological and endocrine dysfunctions are the primary health endpoints, and chronic exposure to acceptable doses is not expected to pose considerable health hazards. However, toxic reactions at lower doses have been described in several cases of malfunctioning MoM hip implants, which may be explained by certain underlying pathologies that increase the individual susceptibility for Co-induced systemic toxicity. This may be associated with a decrease in Co bound to serum proteins and an increase in free ionic Co2+ . As the latter is believed to be the primary toxic form, monitoring of the free fraction of Co2+ might be advisable for future risk assessment. Furthermore, future research should focus on longitudinal studies in the clinical setting of MoM hip implant patients to further elucidate the dose-response discrepancies., (Copyright © 2017 Elsevier B.V. All rights reserved.)- Published
- 2017
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19. Alleviating effects of calcium on cobalt toxicity in two barley genotypes differing in cobalt tolerance.
- Author
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Lwalaba JL, Zvobgo G, Fu L, Zhang X, Mwamba TM, Muhammad N, Mundende RP, and Zhang G
- Subjects
- Antioxidants metabolism, Drug Interactions, Genotype, Glutathione metabolism, Hordeum genetics, Hordeum metabolism, Malondialdehyde metabolism, Oxidative Stress drug effects, Photosynthesis drug effects, Reactive Oxygen Species metabolism, Calcium pharmacology, Cobalt toxicity, Hordeum drug effects, Soil Pollutants toxicity
- Abstract
Cobalt (Co) contamination in soils is becoming a severe issue in environment safety and crop production. Calcium (Ca)
, as a macro-nutrient element, shows the antagonism with many divalent heavy metals and the capacity of alleviating oxidative stress in plants. In this study, the protective role of Ca in alleviating Co stress was hydroponically investigated using two barley genotypes differing in Co toxicity tolerance. Barley seedlings exposed to 100µM Co showed the significant reduction in growth and photosynthetic rate, and the dramatic increase in the contents of reactive oxygen species (ROS), malondialdehyde (MDA), reduced glutathione (GSH) and oxidized glutathione (GSSG), and the activities of anti-oxidative enzymes, with Ea52 (Co-sensitive) being much more affected than Yan66 (Co-tolerant). Addition of Ca in growth medium alleviated Co toxicity by reducing Co uptake and enhancing the antioxidant capacity. The effect of Ca in alleviating Co toxicity was much greater in Yan66 than in Ea52. The results indicate that the alleviation of Co toxicity in barley plants by Ca is attributed to the reduced Co uptake and enhanced antioxidant capacity., (Copyright © 2017 Elsevier Inc. All rights reserved.)- Published
- 2017
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20. Cobalt toxicity after revision total hip replacement due to fracture of a ceramic head.
- Author
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Pelayo-de Tomás JM, Novoa-Parra C, and Gómez-Barbero P
- Subjects
- Aged, Ceramics, Heavy Metal Poisoning diagnosis, Humans, Male, Arthroplasty, Replacement, Hip instrumentation, Cobalt poisoning, Heavy Metal Poisoning etiology, Hip Prosthesis adverse effects, Prosthesis Failure adverse effects
- Abstract
Symptomatic cobalt toxicity from a failed total hip replacement is a rare, but devastating complication. Potential clinical findings include cardiomyopathy, hypothyroidism, skin rash, visual and hearing impairment, polycythaemia, weakness, fatigue, cognitive impairment, and neuropathy. The case is presented of a 74year-old man in whom, after a ceramic-ceramic replacement and two episodes of prosthetic dislocation, it was decided to replace it with a polyethylene-metal total hip arthroplasty (THA). At 6months after the revision he developed symptoms of cobalt toxicity, confirmed by analytical determination (serum cobalt level=651.2μg/L). After removal of the prosthesis, the levels of chromium and cobalt in blood and urine returned to normal, with the patient currently being asymptomatic. It is recommended to use a new ceramic on ceramic bearing at revision, in order to minimise the risk of wear-related cobalt toxicity following breakage of ceramic components., (Copyright © 2016 SECOT. Publicado por Elsevier España, S.L.U. All rights reserved.)
- Published
- 2017
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21. Fatal Cobalt Toxicity after a Non-Metal-on-Metal Total Hip Arthroplasty.
- Author
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Peters RM, Willemse P, Rijk PC, Hoogendoorn M, and Zijlstra WP
- Abstract
This case illustrates the potential for systemic cobalt toxicity in non-metal-on-metal bearings and its potentially devastating consequences. We present a 71-year-old male with grinding sensations in his right hip following ceramic-on-ceramic total hip arthroplasty (THA). After diagnosing a fractured ceramic liner, the hip prosthesis was revised into a metal-on-polyethylene bearing. At one year postoperatively, X-rays and MARS-MRI showed a fixed reversed hybrid THA, with periarticular densities, flattening of the femoral head component, and a pattern of periarticular metal wear debris and pseudotumor formation. Before revision could take place, the patient was admitted with the clinical picture of systemic cobalt toxicity, supported by excessively high serum cobalt and chromium levels, and ultimately died. At autopsy dilated cardiomyopathy as cause of death was hypothesized. A third body wear reaction between ceramic remnants and the metal femoral head very likely led to excessive metal wear, which contributed systemic cobalt toxicity leading to neurotoxicity and heart failure. This case emphasizes that fractured ceramic-on-ceramic bearings should be revised to ceramic-on-ceramic or ceramic-on-polyethylene bearings, but not to metal-on-polyethylene bearings. We aim to increase awareness among orthopedic surgeons for clinical clues for systemic cobalt intoxication, even when there is no metal-on-metal bearing surface.
- Published
- 2017
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22. Fatal cobalt toxicity after total hip arthroplasty revision for fractured ceramic components.
- Author
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Fox KA, Phillips TM, Yanta JH, and Abesamis MG
- Subjects
- Arthroplasty, Replacement, Hip instrumentation, Ceramics chemistry, Chromium Alloys chemistry, Fatal Outcome, Female, Humans, Middle Aged, Prosthesis Failure adverse effects, Reoperation, Arthroplasty, Replacement, Hip adverse effects, Chromium Alloys toxicity, Cobalt toxicity, Hip Prosthesis adverse effects
- Abstract
Context: Post-arthroplasty metallosis, which refers to metallic corrosion and deposition of metallic debris in the periprosthetic soft tissues of the body, is an uncommon complication. Systemic cobalt toxicity post-arthroplasty is extremely rare. The few known fatal cases of cobalt toxicity appear to be a result of replacing shattered ceramic heads with metal-on-metal or metal-on-polyethylene implants. Friction between residual shards of ceramic and cobalt-chromium implants allows release of cobalt into the synovial fluid and bloodstream, resulting in elevated whole blood cobalt levels and potential toxicity., Case Details: This is a single patient chart review of a 60-year-old woman with prior ceramic-on-ceramic right total hip arthroplasty complicated by fractured ceramic components and metallosis of the joint. She underwent synovectomy and revision to a metal-on-polyethylene articulation. Ten months post-revision, she presented to the emergency department (ED) with right hip pain, dyspnea, worsening hearing loss, metallic dysgeusia, and weight loss. Chest CTA revealed bilateral pulmonary emboli (PE), and echocardiogram revealed new cardiomyopathy with global left ventricular hypokinesis with an ejection fraction (EF) of 35-40% inconsistent with heart strain from PE. Whole blood cobalt level obtained two days into her admission was 424.3 mcg/L and 24-h urine cobalt level was 4830.5 mcg/L. Although the patient initially clinically improved with regard to her PE and was discharged to home on hospital day 5, she returned 10 days later with a right hip dislocation and underwent closed reduction of the hip. The patient subsequently decompensated, developing cardiogenic shock, and respiratory failure. She went into pulseless electrical activity (PEA) and expired. Autopsy revealed an extensive metallic effusion surrounding the right hip prosthesis that tested positive for cobalt (41,000 mcg/L). There was also cobalt in the heart muscle tissue (2.5 mcg/g). A whole blood cobalt level obtained two days before she expired was 641.6 mcg/L., Discussion: This is a case of fatal cobalt-induced cardiomyopathy in a patient whose ceramic components of a total hip arthroplasty fractured causing metallosis with worsening cobalt toxicity. We recommend that when a fractured device is revised with a prosthesis with cobalt-chromium components, whole blood and urine cobalt measurements should be obtained and periodically monitored to evaluate for rising concentrations. Providers should be aware of clinical signs and symptoms of cobalt toxicity in patients who have prostheses with cobalt-chromium components. If suspected, toxicology and orthopedics should be involved for possible chelation and removal of the prosthesis.
- Published
- 2016
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23. Extreme Cobalt Toxicity: Bearing the Brunt of a Failed Ceramic Liner: A Case Report.
- Author
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Griffiths J, Colvin A, Yates P, Meyerkort D, Kop A, and Prosser G
- Abstract
Case: We present a case of systemic cobalt toxicity secondary to third-body wear of a cobalt-chromium (CoCr) femoral head following revision of a fractured ceramic bearing. Removal of the CoCr head was followed by resolution of much of the systemic symptoms., Conclusion: This case supports previous reports of cobalt toxicity secondary to catastrophic third-body wear of a CoCr femoral head following a fractured ceramic bearing. It also demonstrates the potential reversibility of many systemic sequelae associated with cobalt toxicity. To our knowledge, this case represents the highest documented blood cobalt level (45,840 nmol/L).
- Published
- 2015
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24. Does therapeutic plasma exchange have a role in the treatment of prosthetic hip-associated cobalt toxicity? A case report and literature review.
- Author
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Grant ML, Karp JK, Palladino M, Le N, Hall N, and Herman JH
- Subjects
- Arthroplasty, Replacement, Hip adverse effects, Chelation Therapy, Female, Humans, Middle Aged, Cobalt toxicity, Hip Prosthesis adverse effects, Plasma Exchange methods
- Abstract
Background: Prosthetic hip-associated cobalt toxicity (PHACT) is an uncommon, but potentially devastating, complication for patients with metal-on-metal hip implants (MoMs). Clinical management of PHACT is poorly defined, with primary intervention being MoM explant followed by chelation therapy. Therapeutic plasma exchange (TPE) in cobalt toxicity has not been previously described. Given that cobalt is predominantly albumin bound, it should theoretically be removed by TPE. Here we report a case of PHACT and our experience using TPE to lower plasma cobalt levels., Case Report: A 61-year-old woman developed deafness, blindness, ambulatory dysfunction, and endocrinopathies after MoM implant. Cobalt levels on admission were greater than 1500 µg/L. In an attempt to rapidly lower cobalt levels before MoM explant, hemodialysis and TPE were performed. Hemodialysis removed negligible amounts of cobalt. One session of TPE temporarily removed approximately two-thirds of measurable cobalt, but levels rebounded to pre-TPE values after 8 hours. It was only after MoM removal that cobalt levels plateaued below 300 µg/L and clinical symptoms improved., Discussion: TPE removed cobalt from a PHACT patient, but a durable decrease in cobalt was only achieved after MoM explant. These findings are comparable to reports where chelation was employed in PHACT patients before MoM explant. The observed rebound phenomenon is likely from rapid equilibration between the immense extravascular tissue source (the MoM) and the intravascular compartment., Conclusion: TPE may serve as adjunctive therapy for PHACT patients whose cobalt levels remain high after explant, especially in patients with renal failure, in whom chelation is contraindicated., (© 2016 AABB.)
- Published
- 2016
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25. Evidence against implant-derived cobalt toxicity: case report and retrospective study of serum cobalt concentrations in an orthopedic implant population.
- Author
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Tolan NV, Sierra RJ, and Moyer TP
- Subjects
- Acetabulum diagnostic imaging, Adult, Aged, Erythrocyte Count, Female, Humans, Male, Middle Aged, Pelvis diagnostic imaging, Radiography, Retrospective Studies, Cobalt adverse effects, Cobalt blood, Hip Prosthesis adverse effects
- Abstract
Objectives: Cobalt (Co) exposure has been documented to result in increased erythropoiesis. To evaluate the potential for implant-derived Co toxicity, we examined the relationship between serum Co (sCo) and erythrocyte counts (ERY) in a metal-containing total-hip arthroplasty implant population., Methods: Retrospective review of sCo concentrations identified 77 patients with concomitant ERY. Statistical analysis was performed to determine if there was a significant difference in ERY for patients divided into clinically relevant sCo ranges. A single detailed case review of a patient with a loose mal-positioned acetabular component and significantly elevated sCo was also performed for symptoms thought to arise from Co toxicity., Results: Statistical difference in ERY was not observed between patients with significantly elevated (>10 ng/mL), elevated (4-10 ng/mL), modestly elevated (1.0-3.9 ng/mL), or normal (<1.0 ng/mL) sCo. While the detailed case report was unremarkable for any of the clinical symptoms previously reported to be associated with Co toxicity and no increase in ERY was observed, this patient's sCo was 84 ng/mL., Conclusions: Increased erythropoiesis was not observed in patients with implant-derived increased sCo. Even with a sCo 100 × the upper-limit of normal, the patient presented did not have increased ERY nor exhibit any symptoms ascribed with Co toxicity., (Copyright © 2014 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)
- Published
- 2015
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26. Systemic effects of cobalt toxicity after revision hip replacement can manifest in intermediate to long term follow-up.
- Author
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Vasukutty NL and Minhas TH
- Subjects
- Adult, Arthroplasty, Replacement, Hip adverse effects, Ceramics, Humans, Male, Osteonecrosis surgery, Prosthesis Design adverse effects, Reoperation, Time Factors, Arthroplasty, Replacement, Hip instrumentation, Cobalt poisoning, Hip Prosthesis adverse effects, Postoperative Complications etiology
- Abstract
Introduction: Metal toxicity from metal-on-metal hip replacements is now well documented and several large series have reported local reactions. Although less common, there are reports of similar reactions from failed ceramic liners. Systemic effects documented in literature have been grouped into cardiac, neuro-ocular and thyroid signs., Methods and Results: We report a case of a patient who had revision for fractured ceramic liner to metal on polyethylene. Third body effect of the ceramic particles led to wear through of the poly liner and the head directly articulating with metal shell. He developed cardiac and neurological features of cobalt toxicity in addition to extensive soft tissue destruction. Revision of the bearing surfaces and synovectomy led to clinical improvement and fall in metal ion levels., Conclusions: We recommend 2-stage revision in such situations and close monitoring of all these patients.
- Published
- 2016
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27. Systemic cobalt toxicity from total hip arthroplasties: review of a rare condition Part 2. measurement, risk factors, and step-wise approach to treatment.
- Author
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Zywiel MG, Cherian JJ, Banerjee S, Cheung AC, Wong F, Butany J, Gilbert C, Overgaard C, Syed K, Jacobs JJ, and Mont MA
- Subjects
- Aged, Animals, Chelating Agents therapeutic use, Cobalt analysis, Disease Models, Animal, Female, Humans, Ions adverse effects, Ions analysis, Kidney Failure, Chronic complications, Long-Term Care, Male, Malnutrition complications, Metal-on-Metal Joint Prostheses, Middle Aged, Postoperative Complications therapy, Prosthesis Design, Rats, Risk Factors, Arthroplasty, Replacement, Hip adverse effects, Cobalt adverse effects, Hip Prosthesis adverse effects
- Abstract
Unlabelled: As adverse events related to metal on metal hip arthroplasty have been better understood, there has been increased interest in toxicity related to the high circulating levels of cobalt ions. However, distinguishing true toxicity from benign elevations in cobalt levels can be challenging. The purpose of this review is to examine the use of cobalt alloys in total hip arthroplasty, to review the methods of measuring circulating cobalt levels, to define a level of cobalt which is considered pathological and to review the pathophysiology, risk factors and treatment of cobalt toxicity. To the best of our knowledge, there are 18 published cases where cobalt metal ion toxicity has been attributed to the use of cobalt-chromium alloys in hip arthroplasty. Of these cases, the great majority reported systemic toxic reactions at serum cobalt levels more than 100 μg/L. This review highlights some of the clinical features of cobalt toxicity, with the goal that early awareness may decrease the risk factors for the development of cobalt toxicity and/or reduce its severity., Take Home Message: Severe adverse events can arise from the release of cobalt from metal-on-metal arthroplasties, and as such, orthopaedic surgeons should not only be aware of the presenting problems, but also have the knowledge to treat appropriately., (©2016 The British Editorial Society of Bone & Joint Surgery.)
- Published
- 2016
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28. Systemic cobalt toxicity from total hip arthroplasties: review of a rare condition Part 1 - history, mechanism, measurements, and pathophysiology.
- Author
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Cheung AC, Banerjee S, Cherian JJ, Wong F, Butany J, Gilbert C, Overgaard C, Syed K, Zywiel MG, Jacobs JJ, and Mont MA
- Subjects
- Carcinogens, Cobalt pharmacokinetics, Heart Diseases etiology, Hematologic Diseases, Humans, Ions adverse effects, Ions pharmacokinetics, Liver Diseases etiology, Metal-on-Metal Joint Prostheses adverse effects, Neoplasms etiology, Nervous System Diseases etiology, Prosthesis Design, Prosthesis Failure, Thyroid Diseases etiology, Arthroplasty, Replacement, Hip adverse effects, Cobalt adverse effects, Hip Prosthesis adverse effects
- Abstract
Unlabelled: Recently, the use of metal-on-metal articulations in total hip arthroplasty (THA) has led to an increase in adverse events owing to local soft-tissue reactions from metal ions and wear debris. While the majority of these implants perform well, it has been increasingly recognised that a small proportion of patients may develop complications secondary to systemic cobalt toxicity when these implants fail. However, distinguishing true toxicity from benign elevations in cobalt ion levels can be challenging. The purpose of this two part series is to review the use of cobalt alloys in THA and to highlight the following related topics of interest: mechanisms of cobalt ion release and their measurement, definitions of pathological cobalt ion levels, and the pathophysiology, risk factors and treatment of cobalt toxicity. Historically, these metal-on-metal arthroplasties are composed of a chromium-cobalt articulation. The release of cobalt is due to the mechanical and oxidative stresses placed on the prosthetic joint. It exerts its pathological effects through direct cellular toxicity. This manuscript will highlight the pathophysiology of cobalt toxicity in patients with metal-on-metal hip arthroplasties., Take Home Message: Patients with new or evolving hip symptoms with a prior history of THA warrant orthopaedic surgical evaluation. Increased awareness of the range of systemic symptoms associated with cobalt toxicity, coupled with prompt orthopaedic intervention, may forestall the development of further complications., (©2016 The British Editorial Society of Bone & Joint Surgery.)
- Published
- 2016
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29. Cobalt toxicity after revision to a metal-on-polyethylene total hip arthroplasty for fracture of ceramic acetabular component.
- Author
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Harris A, Johnson J, Mansuripur PK, and Limbird R
- Abstract
Cobalt metallosis after revision metal-on-polyethylene total hip arthroplasty for catastrophic failure of ceramic components is uncommon but a potentially devastating complication. Common findings associated with heavy metal toxicity include cardiomyopathy, hypothyroidism, skin rashes, visual disturbances, hearing changes, polycythemia, weakness, fatigue, cognitive deterioration, and neuropathy. We report a case of a 57-year-old woman who presented with complaints of progressively worsening hip pain, fatigue, memory loss, lower extremity sensory loss, persistent tachycardia, and ocular changes 5 years after synovectomy and revision of a failed ceramic-on-ceramic total hip arthroplasty to metal-on-polyethylene components. A cobalt level of 788.1 ppb and chromium level of 140 ppb were found on presentation and subsequently decreased to 468.8 ppb and 105.9 ppb, respectively, 2 weeks after revision to a ceramic-on-polyethylene total hip arthroplasty. Improvement of symptoms accompanied this decrease in cobalt and chromium levels. Revision of failed ceramic arthroplasties with later-generation ceramics to avoid this potential complication is recommended.
- Published
- 2015
- Full Text
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30. Interaction between nickel and cobalt toxicity in Enchytraeus crypticus is due to competitive uptake.
- Author
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He E, Baas J, and Van Gestel CA
- Subjects
- Animals, Environmental Exposure analysis, Survival Analysis, Time Factors, Cobalt toxicity, Nickel toxicity, Oligochaeta drug effects, Oligochaeta metabolism, Toxicity Tests
- Abstract
Uptake and toxicity of Ni-Co mixtures in Enchytraeus crypticus were determined after 4 d, 7 d, 10 d, and 14 d exposure. Generally, body concentrations of Ni and Co increased with increasing exposure concentrations. Ni body concentration was significantly reduced in the presence of Co, whereas Ni only marginally affected Co uptake. When expressed as free ion activities, individual toxicity of Ni and Co increased with time, with median lethal concentrations (LC50) decreasing from 78.3 μM and 511 μM at 4 d to 40.4 μM and 393 μM at 14 d, respectively. When expressed as body concentrations, LC50BodyNi remained constant with time whereas LC50BodyCo increased during the first 7 d but remained stable afterwards. As identified by the MIXTOX model, interactions between Ni and Co were mainly antagonistic when based on free ion activities, however, no interaction was observed when based on body concentrations. A process-based model, incorporating exposure time to analyze the mechanisms underlying the dynamic mixture toxicity confirmed the differences in toxicokinetics of the 2 metals. The author's findings suggest that body concentrations, which incorporate bioaccumulation processes, are time-independent and can act as a more constant indicator of metal toxicity. The observed antagonism was mainly caused by competition between Co and Ni for binding sites and subsequent inhibition of Ni uptake. This competitive interaction occurred at the uptake level (toxicokinetics), but not at the target level (toxicodynamics)., (© 2014 SETAC.)
- Published
- 2015
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31. 'Snake eyes' MRI sign: possible role of cobalt toxicity?
- Author
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Briani C, Cacciavillani M, Nicolli A, Trevisan A, and Gasparotti R
- Subjects
- Adult, Humans, Magnetic Resonance Imaging, Male, Osteoarthritis, Hip surgery, Cobalt poisoning, Hip Prosthesis adverse effects, Motor Neuron Disease etiology, Motor Neuron Disease pathology, Spinal Cord pathology
- Published
- 2015
- Full Text
- View/download PDF
32. Systemic allergic dermatitis caused by cobalt and cobalt toxicity from a metal on a metal hip replacement.
- Author
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Wong CC and Nixon RL
- Subjects
- Aged, 80 and over, Chromium, Cobalt poisoning, Cognition Disorders chemically induced, Female, Humans, Prosthesis Design, Reoperation, Arthroplasty, Replacement, Hip instrumentation, Cobalt adverse effects, Dermatitis, Allergic Contact etiology, Hip Prosthesis adverse effects
- Published
- 2014
- Full Text
- View/download PDF
33. Yap1 mediates tolerance to cobalt toxicity in the yeast Saccharomyces cerevisiae.
- Author
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Pimentel C, Caetano SM, Menezes R, Figueira I, Santos CN, Ferreira RB, Santos MA, and Rodrigues-Pousada C
- Subjects
- Cation Transport Proteins physiology, Cobalt metabolism, Copper Transport Proteins, Iron-Binding Proteins physiology, Phosphates metabolism, Proton-Phosphate Symporters physiology, Saccharomyces cerevisiae metabolism, Superoxides metabolism, Cobalt toxicity, Saccharomyces cerevisiae drug effects, Saccharomyces cerevisiae Proteins physiology, Transcription Factors physiology
- Abstract
Background: Cobalt has a rare occurrence in nature, but may accumulate in cells to toxic levels. In the present study, we have investigated how the transcription factor Yap1 mediates tolerance to cobalt toxicity., Methods: Fluorescence microscopy was used to address how cobalt activates Yap1. Using microarray analysis, we compared the transcriptional profile of a strain lacking Yap1 to that of its parental strain. To evaluate the extent of the oxidative damage caused by cobalt, GSH was quantified by HPLC and protein carbonylation levels were assessed., Results: Cobalt activates Yap1 under aerobiosis and anaerobiosis growth conditions. This metal generates a severe oxidative damage in the absence of Yap1. However, when challenged with high concentrations of cobalt, yap1 mutant cells accumulate lower levels of this metal. Accordingly, microarray analysis revealed that the expression of the high affinity phosphate transporter, PHO84, a well-known cobalt transporter, is compromised in the yap1 mutant. Moreover, we show that Yap1 is a repressor of the low affinity iron transporter, FET4, which is also known to transport cobalt., Conclusions: Cobalt activates Yap1 that alleviates the oxidative damage caused by this metal. Yap1 partially controls cobalt cellular uptake via the regulation of PHO84. Although FET4 repression by Yap1 has no effect on cobalt uptake, it may be its first line of defense against other toxic metals., General Significance: Our results emphasize the important role of Yap1 in mediating cobalt-induced oxidative damages and reveal new routes for cell protection provided by this regulator., (Copyright © 2014 Elsevier B.V. All rights reserved.)
- Published
- 2014
- Full Text
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34. Chelation in suspected prosthetic hip-associated cobalt toxicity.
- Author
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Giampreti A, Lonati D, and Locatelli CA
- Subjects
- Humans, Male, Arthralgia chemically induced, Arthroplasty, Replacement, Hip, Cobalt adverse effects, Heart Failure chemically induced, Hip Joint, Osteoarthritis surgery
- Published
- 2014
- Full Text
- View/download PDF
35. Prosthetic hip-associated cobalt toxicity.
- Author
-
Pizon AF, Abesamis M, King AM, and Menke N
- Subjects
- Biomarkers metabolism, Chelating Agents therapeutic use, Chelation Therapy, Cobalt metabolism, Device Removal, Humans, Metals, Heavy metabolism, Poisoning etiology, Poisoning metabolism, Poisoning therapy, Predictive Value of Tests, Prosthesis Design, Risk Assessment, Risk Factors, Time Factors, Treatment Outcome, Arthroplasty, Replacement, Hip adverse effects, Arthroplasty, Replacement, Hip instrumentation, Cobalt poisoning, Heavy Metal Poisoning, Hip Prosthesis adverse effects, Metal-on-Metal Joint Prostheses adverse effects, Poisoning diagnosis
- Abstract
Prosthetic hip-associated cobalt toxicity (PHACT) is gaining recognition due to the use of metal-on-metal total hip replacements. Identifying true toxicity from merely elevated cobalt levels can be extremely difficult due to the lack of available data. An extensive review of the medical literature was undertaken to characterize cobalt toxicity from prosthetic hips. As an objective approach to making the diagnosis of PHACT, we suggest the following criteria: (1) elevated serum or whole blood cobalt levels due to a prosthetic hip, (2) at least two test-confirmed findings consistent with cobalt toxicity, and (3) exclusion of other etiologies. Adhering to objective diagnostic data for PHACT is a realistic and prudent method by which to eliminate the subjectivity of vague or difficult to identify complaints. These diagnostic criteria are not meant to evaluate prosthetic hardware failure, but as a means to identify systemic cobalt toxicity. Finally, assessment of cobalt toxicity from prosthetic hips should be done in conjunction with a medical toxicologist.
- Published
- 2013
- Full Text
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36. Clinical features, testing, and management of patients with suspected prosthetic hip-associated cobalt toxicity: a systematic review of cases.
- Author
-
Devlin JJ, Pomerleau AC, Brent J, Morgan BW, Deitchman S, and Schwartz M
- Subjects
- Biomarkers metabolism, Chelating Agents therapeutic use, Chelation Therapy, Cobalt metabolism, Device Removal, Humans, Metals, Heavy metabolism, Poisoning etiology, Poisoning metabolism, Predictive Value of Tests, Prosthesis Design, Risk Assessment, Risk Factors, Time Factors, Treatment Outcome, Arthroplasty, Replacement, Hip adverse effects, Arthroplasty, Replacement, Hip instrumentation, Cobalt poisoning, Heavy Metal Poisoning, Hip Prosthesis adverse effects, Poisoning diagnosis, Poisoning therapy
- Abstract
Safety concerns regarding cobalt-containing metal alloy hip prosthetics (Co-HP) have resulted in product recalls, a medical device alert, and issuance of guidance for clinicians. Recently, cases of suspected prosthetic hip-associated cobalt toxicity (PHACT) from Co-HP have been reported. Although little is known about suspected PHACT, these patients may be referred to medical toxicologists for evaluation and management recommendations. We searched MEDLINE, EMBASE, and unpublished abstracts from toxicology scientific meetings for references relevant to PHACT. Authors independently screened publications for inclusion criteria: publication in English, human study population, subject(s) are symptomatic (except for isolated hip pain), and cobalt values in any matrix (blood, serum, urine, CSF, synovial fluid) available for review. Data from 10 cases are reviewed. Patients with suspected PHACT had findings consistent with cobalt toxicity, including thyroid, cardiac, and neurologic dysfunction. Signs and symptoms appeared between 3 and 72 months after arthroplasty (median 19 months). Neurologic symptoms were most common. Ancillary testing varied considerably. All patients had elevated cobalt levels in one or more matrices. Enhanced elimination was attempted in 27 % of patients. At this time, the information currently available regarding patients with suspected PHACT is inadequate to guide clinical decision making. No consensus has been reached regarding the management of Co-HP patients with systemic symptoms. Indications for chelation have not been established and require further study. Improved case definitions, improved surveillance, and controlled studies are needed to elucidate the scope of this problem and guide future investigations.
- Published
- 2013
- Full Text
- View/download PDF
37. Chelation in suspected prosthetic hip-associated cobalt toxicity.
- Author
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Devlin JJ, Schwartz M, and Brent J
- Subjects
- Humans, Male, Arthralgia chemically induced, Arthroplasty, Replacement, Hip, Cobalt adverse effects, Heart Failure chemically induced, Hip Joint, Osteoarthritis surgery
- Published
- 2013
- Full Text
- View/download PDF
38. Hip-implant related chorio-retinal cobalt toxicity.
- Author
-
Ng SK, Ebneter A, and Gilhotra JS
- Subjects
- Adult, Central Serous Chorioretinopathy blood, Central Serous Chorioretinopathy diagnosis, Cobalt blood, Female, Fluorescein Angiography, Fundus Oculi, Humans, Retinal Pigment Epithelium drug effects, Tomography, Optical Coherence, Central Serous Chorioretinopathy chemically induced, Cobalt adverse effects, Hip Prosthesis adverse effects, Retinal Pigment Epithelium pathology
- Abstract
A 39-year-old female with elevated serum cobalt levels from her bilateral hip prostheses presented with a 3-week history of blurred vision in her left eye. Optical coherence tomography revealed patchy degeneration of the photoreceptor-retinal pigment epithelium (RPE) complex. The lesions were hypofluorescent on indocyanine green angiography. We postulate that this is a case of implant-related chorio-retinal cobalt toxicity.
- Published
- 2013
- Full Text
- View/download PDF
39. Cobalt toxicity--an emerging clinical problem in patients with metal-on-metal hip prostheses?
- Author
-
Mao X, Wong AA, and Crawford RW
- Subjects
- Aged, Female, Humans, Male, Middle Aged, Prosthesis Failure adverse effects, Cobalt toxicity, Hip Prosthesis adverse effects
- Abstract
We report two Australian patients with possible cobalt toxicity related to metal-on-metal total hip replacements. Both patients were treated for osteoarthritis with a DePuy ASR (articular surface replacement) XL Acetabular Hip System prosthesis, which contains cobalt and chromium, and which has recently been recalled from the market.
- Published
- 2011
- Full Text
- View/download PDF
40. Optic Neuropathy from Cobalt Toxicity in a Patient who Ingested Cattle Magnets.
- Author
-
Bhardwaj N, Perez J, and Peden M
- Abstract
Cobalt is a widely used in the industrial production of hard metals. Cobalt ingestion has been reported to cause widespread systemic toxicity, but its effects on vision have been sparsely reported. The authors report the case of a patient who ingested cattle magnets, which remained in his stomach for an unknown duration of time. These magnets largely consist of cobalt that gradually leached into his blood stream, resulting in protean systemic manifestations, which included optic atrophy.
- Published
- 2011
- Full Text
- View/download PDF
41. Cobalt toxicity after total hip replacement: a neglected adverse effect?
- Author
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Rizzetti MC, Catalani S, Apostoli P, and Padovani A
- Subjects
- Humans, Peripheral Nervous System Diseases pathology, Arthroplasty, Replacement, Hip adverse effects, Cobalt adverse effects, Hip Prosthesis adverse effects, Peripheral Nervous System Diseases chemically induced, Peripheral Nervous System Diseases physiopathology
- Published
- 2011
- Full Text
- View/download PDF
42. Cobalt toxicity: chemical and radiological combined effects on HaCaT keratinocyte cell line.
- Author
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Gault N, Sandre C, Poncy JL, Moulin C, Lefaix JL, and Bresson C
- Subjects
- Cell Line, Cell Survival drug effects, Cell Survival radiation effects, Clone Cells, Cobalt metabolism, Comet Assay, DNA Damage, Dose-Response Relationship, Drug, Dose-Response Relationship, Radiation, Gamma Rays, Humans, Keratinocytes metabolism, Reactive Oxygen Species metabolism, Reactive Oxygen Species radiation effects, Risk Assessment, Skin cytology, Skin drug effects, Skin radiation effects, Cobalt toxicity, Cobalt Radioisotopes toxicity, Keratinocytes drug effects, Keratinocytes radiation effects
- Abstract
Cobalt (Co) is an essential trace element well known as a constituent of vitamin B(12), but different compounds of Co are also described as highly toxic and/or radiotoxic for individuals or the environment. In nuclear power plants, (58)Co and (60)Co are radioactive isotopes of cobalt present as activation products of stable Co and Ni used in alloys. Skin exposure is a current occupational risk in the hard metal and nuclear industries. As biochemical and molecular cobalt-induced toxicological mechanisms are not fully identified, we investigated cobalt toxicity in a model human keratinocyte cell line, HaCaT. In this study, we propose a model to determine the in vitro chemical impact on cell viability of a soluble form of cobalt (CoCl(2)) with or without gamma-ray doses to mimic contamination by (60)Co, to elucidate the mechanisms of cobalt intracellular chemical and radiological toxicity. Intracellular cobalt concentration was determined after HaCaT cell contamination and chemical toxicity was evaluated in terms of cellular viability and clonogenic survival. We investigated damage to DNA in HaCaT cells by combined treatment with chemical cobalt and a moderate gamma-ray dose. Additive effects of cobalt and irradiation were demonstrated. The underlying mechanism of cobalt toxicity is not clearly established, but our results seem to indicate that the toxicity of Co(II) and of irradiation arises from production of reactive oxygen species.
- Published
- 2010
- Full Text
- View/download PDF
43. Cobalt toxicity in anaerobic granular sludge: influence of chemical speciation.
- Author
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Bartacek J, Fermoso FG, Baldó-Urrutia AM, van Hullebusch ED, and Lens PN
- Subjects
- Anaerobiosis, Bacteria chemistry, Bacteria metabolism, Bioreactors microbiology, Carbonates chemistry, Chelating Agents chemistry, Cobalt metabolism, Culture Media chemistry, Culture Media metabolism, Edetic Acid chemistry, Methanol metabolism, Phosphates chemistry, Cobalt chemistry, Sewage chemistry, Sewage microbiology
- Abstract
The influence of cobalt speciation on the toxicity of cobalt to methylotrophic methanogenesis in anaerobic granular sludge was investigated. The cobalt speciation was studied with three different media that contained varying concentrations of complexing ligands [carbonates, phosphates and ethylenediaminetetraacetic acid (EDTA)]. Three fractions (nominal added, dissolved and free) of cobalt were determined in the liquid media and were correlated with data from batch toxicity experiments. The average concentration of cobalt that was required for 50% inhibition of methanogenic activity (IC50) for free Co2+ in the three sets of measurements was 13 micromol/L with a standard deviation of 22% and a similarity of 72% between the data obtained in the three different media for the range of cobalt concentrations investigated. The standard deviation of the IC50 for the other two fractions was much higher, i.e. 85 and 144% for the added cobalt and dissolved cobalt, respectively, and the similarity was almost 0% for both fractions. Complexation (and precipitation) with EDTA, phosphates and carbonates was shown to decrease the toxicity of cobalt on methylotrophic methanogenesis. The free cobalt concentration is proposed to be the key parameter to correlate with cobalt toxicity. Thus, the toxicity of cobalt to granular sludge can be estimated based on the equilibrium-free cobalt concentration.
- Published
- 2008
- Full Text
- View/download PDF
44. Mechanism to combat cobalt toxicity in cobalt resistant mutants of Aspergillus nidulans.
- Author
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Tripathi P and Srivastava S
- Abstract
Characteristics of fungal species tolerant to high levels of metals in natural environment can be amplified by isolation and selection of resistant mutants. Step-by-step culturing led to identification of highly stable Co-resistant (Co(R)) mutants of A. nidulans. Based on two distinct morphological features, Co-resistant mutants were categorized as Co(R)I and Co(R)II. The two mutants varied in their growth behavior and colony morphology that were reflected in supplemented as well as unsupplemented growth media over the generations. As compared to the Co(R)I, Co(R)II mutant exhibited sparse mycelia and conidiation but secreted higher amount of melanin. Co(R) mutants could tolerate up to 2.5mM Co in the medium, however, required a threshold concentration of 0.25mM Co for optimal growth and germination. Absence of Co in the medium caused a stressful situation for the Co(R) mutants and led to the secretion of a white extracellular precipitate found to be a glycoprotein. In response to interactions with Co-ions, Co(R) mutants produced oxalic acid and bioprecipitated Co as Co-oxalate providing scope for metal reclamation as well as oxalic acid extraction. The mutants could help to recover the insoluble Co-oxalate salt from aqueous solutions by entrapping it in their growing mycelial meshwork.
- Published
- 2007
- Full Text
- View/download PDF
45. Hydroxocobalamin vs cobalt toxicity on rat cardiac and diaphragmatic muscles.
- Author
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Pery-Man N, Houeto P, Coirault C, Suard I, Perennec J, Riou B, and Lecarpentier Y
- Subjects
- Analysis of Variance, Animals, Antidotes administration & dosage, Cobalt administration & dosage, Cyanides poisoning, Diaphragm pathology, Diaphragm physiopathology, Dose-Response Relationship, Drug, Drug Evaluation, Preclinical, Heart physiopathology, Hydroxocobalamin administration & dosage, Myocardium pathology, Poisoning drug therapy, Rats, Rats, Wistar, Antidotes toxicity, Cobalt toxicity, Diaphragm drug effects, Heart drug effects, Hydroxocobalamin toxicity
- Abstract
Background: Hydroxocobalamin has been shown to be a rapid and powerful antidote in acute cyanide poisoning and to prevent cyanide poisoning during sodium nitroprusside administration. This cobalt-containing compound has been shown to be devoid of significant immediate side effects during acute administration. However, its potential delayed toxicity related to cobalt accumulation in tissue remains unknown. Therefore, we evaluated the toxicity of hydroxocobalamin as compared with that of cobalt salts on rat cardiac and diaphragmatic muscles., Methods: For a 21-day period, rats were treated intraperitoneally with either hydroxocobalamin (70 mg kg-1 per day, n = 14), cobalt chloride hexahydrate (12 mg kg-1 per day, n = 14) or saline (n = 10). Hydroxocobalamin and cobalt chloride groups received equimolar doses of cobalt. We studied: (1) the mechanical properties of isolated left ventricular papillary muscles and diaphragmatic strips, (2) the cardiac and diaphragmatic cobalt tissue concentrations, and (3) the myocardial histological aspect., Results: During the study period, no significant increase in body weight was noted in the cobalt-treated group (-4 +/- 1%), which was in contrast to the hydroxocobalamin-treated group (+21 +/- 2%) and the saline-treated group (22 +/- 2%). Compared with controls, the mechanical properties of cardiac and diaphragmatic muscles were unchanged after either hydroxocobalamin or cobalt salt treatments, and myocardial histological characteristics were similar in all groups. Conversely, large amounts of cobalt deposit were observed in the cobalt-treated group in both the diaphragm (41.90 +/- 16.30 vs 0.70 +/- 0.40 mu mol mu g-1 in the control group, P < 0.001) and the myocardium (16.90 +/- 6.40 vs 0.14 +/- 0.01 mu mol mu g-1 in the control group, P < 0.001). After hydroxocobalamin administration, cobalt concentrations were significantly lower in the diaphragm (25.10 +/- 16.50 mu mol mu g-1, P < 0.001 vs cobalt-treated group) and the myocardium (4.50 +/- 1.20 mu mol mu g, P < 0.001 vs cobalt-treated group)., Conclusion: These results indicate that repeated administration of hydroxocobalamin was devoid of significant diaphragmatic and cardiac muscle toxicity and therefore remains a safe antidote for acute cyanide poisoning.
- Published
- 1996
- Full Text
- View/download PDF
46. Antagonistic effect of nickel on the fermentative growth of Escherichia coli K-12 and comparison of nickel and cobalt toxicity on the aerobic and anaerobic growth.
- Author
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Wu LF, Navarro C, de Pina K, Quénard M, and Mandrand MA
- Subjects
- Aerobiosis drug effects, Anaerobiosis drug effects, Drug Resistance, Microbial, Escherichia coli genetics, Escherichia coli growth & development, Fermentation drug effects, Mutation, Cobalt toxicity, Escherichia coli drug effects, Nickel toxicity
- Abstract
The facultative anaerobic enterobacterium Escherichia coli requires the activity of nickel-containing hydrogenase for its anaerobic growth. Deficiency of the specific nickel transport system led to a hydrogenase-minus phenotype and slowed down the fermentative growth in the nik mutant. Addition of 300 microM nickel to the growth medium could restore the hydrogenase activity. This restoration resulted in the recovery of anaerobic growth. A further increase of nickel concentration inhibited growth. Thus nickel shows an antagonistic effect on the anaerobic growth of E. coli. To study the mechanism of nickel toxicity, two classes of nickel-resistant mutants were isolated. The nkr mutant was obtained by selecting colonies grown on nickel-containing minimal plate. It acquired simultaneously the resistance to cobalt. A nonspecific magnesium transport mutant corA was isolated on cobalt-containing plate. The corA mutant was also resistant to nickel. When analyzing the influence of nickel and cobalt on the bacterial growth, we obtained two interesting observations. First, anaerobic growth was less sensitive than aerobic growth to cobalt toxicity. In contrast, nickel toxicity did not vary from the growth conditions. Second, cobalt seems to abolish the growth, while nickel appears to slow down the growth rate under the condition used.
- Published
- 1994
- Full Text
- View/download PDF
47. [Pharmacodynamics of cobalt toxicity].
- Author
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CARBONCINI G
- Subjects
- Humans, Cobalt toxicity
- Published
- 1951
48. Cobalt toxicity in cattle.
- Author
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Dickson J and Bond MP
- Subjects
- Animals, Cattle, Female, Male, Cattle Diseases chemically induced, Cobalt poisoning
- Published
- 1974
- Full Text
- View/download PDF
49. The effect of methionine or cysteine on cobalt toxicity in the chick.
- Author
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Southern LL and Baker DH
- Subjects
- Animals, Body Weight drug effects, Cobalt antagonists & inhibitors, Female, Kidney analysis, Liver analysis, Male, Chickens metabolism, Cobalt toxicity, Cysteine pharmacology, Methionine pharmacology
- Abstract
Three experiments were conducted to investigate the interaction of cobalt with sulfur-containing amino acids in the chick. Fortified corn-soybean meal diets were fed and tissue concentrations of cobalt were assessed. In Experiment 1, three levels of cobalt (0, 250, and 500 microgram/g) were fed in the presence and absence of .50% supplemental DL-methionine. Dietary additions of cobalt depressed growth rate and caused cobalt accumulation in the liver and kidney. Supplemental methionine in excess of the requirement for maximal chick weight gains partially alleviated the depression in performance and decreased cobalt accumulation in the liver and kidney. Two levels of cobalt (0 and 500 microgram/g) were fed in the presence and absence of .59% supplemental L-cysteine.HCl.H2O (isosulfurous to .50% DL-methionine) in Experiment 2. Again, cobalt depressed performance and accumulated in the liver and kidney. The surfeit of cysteine increased weight gain and decreased cobalt accumulation in the liver but not in the kidney. In Experiment 3, two levels of cobalt (0 and 250 microgram/g) were fed in the presence and absence of two levels of excess DL-methionine (.50 and 1.0%) or two levels of excess cysteine.HCl.H2O (.59 and 1.18%). Multiple linear regression analysis of gain on sulfur consumed from methionine or cysteine indicated that cysteine was almost 6 times more efficacious than methionine in alleviating cobalt toxicity. In fact, cysteine supplemented at a level of 1.18% completely alleviated the growth depression caused by 250 microgram/g cobalt. Both methionine and cysteine reduced cobalt accumulation in the liver and kidney, but the liver was affected to a greater extent than the kidney.
- Published
- 1981
- Full Text
- View/download PDF
50. Cobalt toxicity after McKee hip arthroplasty.
- Author
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Jones DA, Lucas HK, O'Driscoll M, Price CH, and Wibberley B
- Subjects
- Aged, Arthroplasty, Bone Resorption, Chromium Alloys, Cobalt urine, Female, Hip Dislocation etiology, Humans, Male, Middle Aged, Molybdenum, Radiography, Skin Tests, Spectrophotometry, Atomic, Time Factors, Cobalt adverse effects, Hip Joint diagnostic imaging, Hypersensitivity etiology, Joint Prosthesis
- Abstract
The significance of cobalt as a cause of symptoms after McKee hip arthroplasty is discussed. Seven patients are described in whom such arthroplasties. became unsatisfactory after periods varying from nine months to four years. Six of these patients were cobalt-positive but nickel- and chrome-negative on patch testing. Macroscopic and histological necrosis of bone, muscle and joint capsule around the prostheses was found in five patients whose hips were explored. The symptoms were progressive pain, a feeling of instability, and in two cases spontaneous dislocation. Radiological features included acetabular fracture, bone resorption, loosening and dislocation of the prosthesis. Increased cobalt concentrations (determined by atomic absorption spectrophotometry) in the urine of four patients and in a variety of tissues in one patient are presented. Patch testing is recommended in the investigation of patients with troublesome McKee hip arthroplasties
- Published
- 1975
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