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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. • The interaction of Co and Cu is antagonistic. • The combined treatment of Cu and Co alleviated Co toxicity relative to Co treatment alone. • The alleviation of Co toxicity by combined treatment is attributed to the uptake and transportation of Co in plants. [ABSTRACT FROM AUTHOR]

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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 100 µM 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. [ABSTRACT FROM AUTHOR]

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 O 2 and O 2 • ), 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. [Display omitted] • Cobalt stress drastically inhibited the plant growth and photosynthetic efficiency. • Exogenous supply of melatonin notably minimized Co-toxicity in plants. • Melatonin significantly enhanced the activities of antioxidant enzymes. • Application of MT significantly increased secondary metabolism-related enzymes. • Co-transporters regulated in B. napus roots with exogenously MT application. [ABSTRACT FROM AUTHOR]

More than 1 million arthroplasties are conducted annually worldwide, with 65% of patients aged 65 years and older. Complications include infection, dislocation, hypersensitivity reactions to metal implants, often requiring surgical re-intervention causing significant distress. Neuropsychiatric symptoms including dementia and depression secondary to chromium and cobalt toxicity with metal-on-metal implants have also been reported. These symptoms may persist even after removal of defective metal prostheses. Here we present a 51-year-old woman with delusional jealousy. She underwent bilateral hip arthroplasty following avascular necrosis X-12 years ago, with nine follow-up surgeries for complications. After getting lost in the orthopedist's office, and reporting memory lapses ultimately leading to a car accident in year X-2, she was diagnosed with neurocognitive disorder secondary to cobalt toxicity and depression by her orthopedist. Documented perioperative cobalt levels ranged from 5.6 to 14.9 µg/L (>1.0). She was treated with bilateral removal of the metal-on-metal implants. Ten months post-intervention, she attempted suicide by overdose on a lethal amount of pentazocine and naloxone. She claimed the overdose was secondary to stress caused by her husband's multiple romantic affairs. In the past 1-2 years, the patient had installed cameras in the house, accused her husband of hiding a girl under the table while washing dishes, repeatedly filed for divorce, and destroyed a motorcycle based on this claim. The patient was admitted to the psychiatric ward after medical clearance. Case report. No significant focal deficits on her neurological examination. No major findings on her brain imaging. Her Montreal Cognitive Assessment was positive for mild neurocognitive deficits. Patient was started on lurasidone 20mg by mouth at bedtime. She refused any psychotropic medication treatment at discharge. The final DSM-5 diagnosis was Delusional Disorder, Jealous type. Patient had metal-on-metal implant for 10 years with multiple complications prior to onset of neuropsychiatric symptoms. She had no prior psychiatric history other than mentioned above. The pathophysiology of delusional disorder may be associated to both organic and psychological stressors. Most commonly linked neurologic diseases are those affecting the basal ganglia and limbic systems. PET imaging studies in arthroprosthetic cobaltism have shown significant brain hypometabolism in these areas. Chronic, static damage by metallosis and multiple complications may have contributed to the delusional disorder. The dangerousness of delusional jealousy is also noteworthy. More research is necessary to understand the link between arthroplasty complications and delusional disorder. None. [ABSTRACT FROM AUTHOR]

The article discusses the cases of two osteoarthritic patients in Australia who were fitted with articular surface replacement (ASR) XL Acetbular Hip System prostheses that contains chromium and cobalt. It focuses on the revision surgeries performed on the patients despite the use of metal-on-metal bearings to reduce wear at the articulation interface. It explores the withdrawal of ASR implants because of the high failure rate and the increase of cobalt level in the body.

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. [ABSTRACT FROM AUTHOR]

The mechanisms underlying cobalt toxicity in aquatic species in general and cnidarians in particular remain poorly understood. Herein we investigated cobalt toxicity in a Hydra model from morphological, histological, developmental, and molecular biological perspectives. Hydra, exposed to cobalt (0-60 mg/L), were altered in morphology, histology, and regeneration. Exposure to standardized sublethal doses of cobalt impaired feeding by affecting nematocytes, which in turn affected reproduction. At the cellular level, excessive ROS generation, as the principal mechanism of action, primarily occurred in the lysosomes, which was accompanied by the upregulation of expression of the antioxidant genes SOD, GST, GPx, and G6PD. The number of Hsp70 and FoxO transcripts also increased. Interestingly, the upregulations were higher in the 24-h than in the 48-h time-point group, indicating that ROS overwhelmed the cellular defense mechanisms at the latter time-point. Comet assay revealed DNA damage. Cell cycle analysis indicated the induction of apoptosis accompanied or not by cell cycle arrest. Immunoblot analyses revealed that cobalt treatment triggered mitochondria-mediated apoptosis as inferred from the modulation of the key proteins Bax, Bcl-2, and caspase-3. From this data, we suggest the use of Hydra as a model organism for the risk assessment of heavy metal pollution in aquatic ecosystems. [ABSTRACT FROM AUTHOR]

Cobalt nanoparticles (NPs) when released into the air during industrial processes, can enter the lungs through inhalation, leading to potential toxicity and respiratory issues. The mechanism of cobalt toxicity is not well understood and needs further investigation. We, therefore, studied the effects of two kinds of cobalt-based nanoparticles (NPs) on lung cells. These NPs were Co NPs (i.e. Cobalt NPs) and Co-Fe NPs (i.e. CoFe 2 O 4 NPs) that were similar in size and shape but slightly differed for the surface iron composition. The average size of Co NPs was 28 ± 18 nm, and that of Co-Fe was 26 ± 13 nm. We exposed the cells to the NPs for 24 h and measured their viability by MTT assay and CalceinAM fluorescence imaging. Potential induction of reactive oxygen species (ROS) was detected by probes DHE specific for superoxide (O 2 •–) and DCFH-DA for hydrogen peroxide (H 2 O 2). Antioxidant glutathione (GSH) quantification was followed by measuring apoptotic/necrotic potential. Using Co NPs and Co-Fe NPs, we measured the IC50 for cell growth in A549 cells after 24 h of exposure. The values were 79 μg/mL and 163 μg/mL, respectively. We also observed that both NPs induced ROS and reduced the fluorescence of CalceinAM in the cells, but Co NPs had a stronger effect than Co-Fe NPs. This was correlated with the production of O 2 – by the NPs, which was higher for Co NPs than for Co-Fe NPs. On the other hand, H 2 O 2 production was higher for Co-Fe NPs than for Co NPs. Our study suggests that the main cause of differential O 2 – production is the differential release Co2+ ion due to surface modification resulting in differential quenching of green (CalceinAM) fluorescence by both NPs. Both NPs induced apoptosis mode of cell death. Our data from the use of naïve and surface-modified cobalt-based NPs, suggest that NAC can protect cells from cobalt-based NP toxicity by not only restoring cellular GSH levels but also by chelating released Co2+ ions from the NPs surfaces. Additionally, this study for the first time to our knowledge indicates that CalceinAM alone is not sufficient to assess the toxicity of cobalt-based NPs. Other methods should be used to confirm the cytotoxicity data of cobalt-based NPs. [ABSTRACT FROM AUTHOR]

Background: Cobalt toxicity has become a health concern in recent years, due to overexposure resulting in neurological impairments like dementia. With a growing interest in the therapeutic roles of herbs, in toxicity research, it's worth looking into the curative effects of aqueous Prosopis africana seed extract, a plant rich in flavonoids on cobalt‐induced dementia‐like and anxiogenic behaviour. Method: We treated rats with Cobalt (CoCl2) or CoCl2 in combination with aqueous Prosopis africana seed extract (PAE) orally for 14 days. Control rats received distilled water for the same period. Following treatments, behavioral experiments for cognition and anxiety, analysis for oxidative stress, inflammation, histological and immunohistochemical analysis were performed. Result: Results revealed that CoCl2 reduced the exploration time, recognition index in the novel object recognition test, percentage spontaneous alternation in the Y‐maze tests, and reduced open arm entry and duration in elevated plus‐maze. However, treatment with PAE improved these parameters to levels comparable with those of the control group. Furthermore, PAE therapy reduced CoCl2‐induced surge in hydrogen peroxide, malondialdehyde, TNF‐α and IL‐1β levels in brain homogenate, while also increasing superoxide dismutase and reduced reduced‐glutathione activities. CoCl2 exposure resulted in obvious features of neurodegeneration like nuclear disintegration, nuclear shrinkage, and cytoplasmic vacuolations of the cells of the hippocampus and amygdala, with an increased expression of GFAP. The hippocampal and amygdala histology improved after PAE administration, while exacerbated GFAP expressions were attenuated. Conclusion: These findings imply that PAE may be anxiolytic and can help reduce cognitive impairments and hippocampal damage caused by CoCl2 neurotoxicity, via mechanisms that involve attenuation of oxidative stress and neuroinflammation. [ABSTRACT FROM AUTHOR]

Background: Ocular cobalt toxicity is a rare phenomenon reported with increased frequency due to the rise of cobalt–chromium metal hip implants. We report the case of a 66-year-old previously healthy man who developed decreased vision due to cobalt–chromium toxicity from a metal-on-metal hip arthroplasty. Our objective was to determine whether the origin of his visual loss was due to toxicity of the optic nerve, of the retina, or of both. Methods: Ocular examination, 10-2 SITA-Standard Humphrey Visual Field (VF), standard full-field electroretinogram (ERG) as indicated by the International Society for Clinical Electrophysiology of Vision (ISCEV), multifocal electroretinogram (mfERG), multifocal visual evoked potentials (mfVEP), and optical coherence tomography (OCT) were conducted. Results: Ocular examination revealed decreased visual acuity, poor color vision, normal funduscopy, and cecocentral scotomas on VF testing. Because his right eye was amblyopic since childhood, test results from only the left eye are shown. Electrophysiology studies revealed an ISCEV standard full-field ERG with photopic and scotopic responses within normal limits, mfERG with amplitudes and latencies within normal limits, and mfVEP with latencies within normal limits, but with decreased central amplitudes. Peripapillary and macular OCT showed retinal nerve fiber layer and retinal ganglion cell–inner plexiform layer thickness within normal limits. Conclusion: Because decreased color vision and cecocentral scotoma on 10-2 VF are most consistent with toxic optic neuropathy, and decreased central amplitudes on mfVEP are suggestive of neural dysfunction, we hypothesize that our patient presented with an early stage of optic nerve toxicity that was not yet apparent as a structural abnormality on OCT. [ABSTRACT FROM AUTHOR]

Abstract: A Biotic Ligand Model was developed predicting the effect of cobalt on root growth of barley (Hordeum vulgare) in nutrient solutions. The extent to which Ca2+, Mg2+, Na+, K+ ions and pH independently affect cobalt toxicity to barley was studied. With increasing activities of Mg2+, and to a lesser extent also K+, the 4-d EC50Co2+ increased linearly, while Ca2+, Na+ and H+ activities did not affect Co2+ toxicity. Stability constants for the binding of Co2+, Mg2+ and K+ to the biotic ligand were obtained: log K CoBL =5.14, log K MgBL =3.86 and log K KBL =2.50. Limited validation of the model with one standard artificial soil and one standard field soil showed that the 4-d EC50Co2+ could only be predicted within a factor of four from the observed values, indicating further refinement of the BLM is needed. [Copyright &y& Elsevier]

Cobalt toxicity is a rare cause of infiltrative cardiomyopathy. We describe a case of cobalt-induced cardiomyopathy that progressed to end stage heart failure requiring orthotopic heart transplantation. A 67 year old woman with history of bilateral cobalt-chromium hip replacements presented with dyspnea of 3 weeks duration. She was tachycardic and hypotensive, with elevated NT- proBNP. Electrocardiogram demonstrated sinus tachycardia, low voltage and right bundle branch block. Transthoracic echocardiogram revealed left ventricular ejection fraction of 20-25% with global hypokinesis and a moderate circumferential pericardial effusion. Left and right heart catheterization showed normal coronaries, elevated filling pressures and low cardiac index. Dobutamine infusion was initiated for management of cardiogenic shock. Cardiac magnetic resonance imaging (MRI) illustrated diffuse late gadolinium enhancement concerning for infiltrative cardiomyopathy. Extensive non-ischemic and rheumatologic workup was negative. Cobalt and chromium levels were significantly elevated at 121 mcg/L (Nl <=1mcg/L) and 46 mcg/L (Nl <=5 mcg/L) respectively, concerning for cobalt-induced cardiomyopathy. MRI of the hips showed pseudotumor formation surrounding the left prosthesis. She underwent left hip arthroplasty with removal of the source, and was placed on oral chelation therapy. She was discharged home on inotropic support. Despite decline in serum cobalt and chromium levels, the patient was readmitted with cardiogenic shock requiring a second inotropic agent. She was stabilized and evaluated for heart transplant. She underwent successful cardiac transplantation and was discharged to a rehab facility. Pathology of the native heart with electron microscopy revealed cardiomyocytes with enlarged distorted mitochondria, large lipid droplets and elevated tissue cobalt level of 0.95 mcg/g (reporting limit <0.018 mcg/g) consistent with cobalt-induced cardiomyopathy. Cobalt-induced cardiomyopathy is a potentially reversible cause of infiltrative cardiomyopathy, with the diagnosis hinging on obtaining a thorough medical history. Treatment includes routine heart failure management and removal of the cobalt source with the role of chelation therapy remaining unclear. Once progressed to end stage heart failure, preferred treatment is cardiac transplantation. [ABSTRACT FROM AUTHOR]

Nickel and cobalt are essential elements that become toxic at high concentrations. Little is known about nickel and cobalt toxicity in aquatic animals. This study aimed to investigate acute and chronic toxicity of nickel and cobalt in Japanese flounder (Paralichthys olivaceous), with emphasis on oxidative stress reactions, histopathological changes, and differences in gene expression. The lethal concentration for 50% mortality (LC 50) in 3 and 8 cm Japanese flounder exposed to nickel for 96 h was found to be 86.2 ± 0.018 and 151.3 ± 0.039 mg/L; for cobalt exposure, LC 50 was 47.5 ± 0.015 and 180.4 ± 0.034 mg/L, respectively. Chronic nickel and cobalt exposure caused different degrees of oxidative enzyme activity changes in gill, liver, and muscle tissues. Erythrocyte deformations were detected after acute or chronic exposure to nickel and cobalt. the nickel and cobalt exposure also caused pathological changes such as spherical swelling over other gill patches, rod-like proliferations in the gill patch epithelial cell layer, and disorder in hepatocyte arrangement, cell swelling, and cytoplasm loosening. RNA-Seq indicated that there were 184 upregulated and 185 downregulated genes in the liver of Japanese flounder exposed to 15 mg/L nickel for 28 d. For cobalt, 920 upregulated and 457 downregulated genes were detected. Among these differentially expressed genes, 162 were shared by both nickel and cobalt exposure. In both nickel and cobalt, pathways including fatty acid elongation, steroid biosynthesis, unsaturated fatty acid biosynthesis, fatty acid metabolism, PPAR signaling, and ferroptosis were significantly enriched. Taken together, these results aided our understanding of the toxicity of nickel and cobalt in aquatic animals. Image 1 • Heterozygous clonal Japanese flounder with genetic similarity of 1.00 were used. • Lethal concentration for 50% mortality that exposed to nickel and cobalt were determined in Japanese flounder. • Chronic nickel and cobalt exposure changed oxidative enzyme activity in Japanese flounder. • Nickel and cobalt induced stress response signaling pathways were explored in Japanese flounder. Chronic nickel and cobalt exposure induced ferroptosis in the liver of Japanese flounder. [ABSTRACT FROM AUTHOR]

In a subset of high-altitude dwellers, the appropriate erythrocytotic response becomes excessive and can result in chronic mountain sickness. We studied men with (study group) and without excessive erythrocytosis (packed-cell volume >65%) living in Cerro de Pasco, Peru (altitude 4300 m), and compared them with controls living in Lima, Peru (at sea-level). Toxic serum cobalt concentrations were detected in 11 of 21 (52%) study participants with excessive erythrocytosis, but were undetectable in high altitude or sea-level controls. In the mining community of Cerro de Pasco, cobalt toxicity might be an important contributor to excessive erythrocytosis. [Copyright &y& Elsevier]

Abstract: Modularity in arthroplasty components has increased options for solving complex issues in primary and revision procedures. However, this technology introduces the risk of accelerated metal ion release as a result of fretting or passive crevice corrosion within the Morse taper junction. Cobalt toxicity locally and systemically has been described with hip metal bearing surfaces and may be accentuated with ion release from Morse tapers. This is a case report of a knee adverse local tissue response lesion associated with corrosion within the Morse taper of a revision knee arthroplasty in the absence of systemic metal allergy. [Copyright &y& Elsevier]