Search

Objectives: To define the vitamin B12 levels and other micronutrients status in severe acute malnutrition (SAM) children. Methods: This was a prospective hospital based cross-sectional study. Inclusion criteria: Children with severe acute malnutrition as per WHO criteria. Exclusion criteria: (i) Pernicious anemia (ii) Autoimmune gastritis (iii) SAM children on exclusive vitamin B12 supplementation. All enrolled children underwent a detailed clinical history, general physical examination with more emphasis on clinical features of vitamin B12 and other micronutrients deficiencies. Three ml of venous blood was collected to estimate vitamin B12 and other micronutrients. Primary outcome was percentage of deficiency of serum vitamin B12, zinc, copper, selenium, manganese, molybdenum and cobalt in SAM children. Results: Fifty children were included in the study. The mean age of children was 15.60±12.90 mo with male to female ratio 0.85:1. The common clinical presentation in order of frequency were upper respiratory infection (URI) symptoms 35 (70%), hepatomegaly 24 (48%), Hyperpigmentation 17 (34%), angular cheilitis 14 (28%), tremors 11 (22%), edema 07 (14%), and hypotonia 05 (10%). Anemia was found in 44 (88%) children. Prevalence of vitamin B12 deficiency was 34%. Other micronutrient deficiencies observed were cobalt 24 (100%), copper 05 (12%), zinc 04 (9.5%), and molybdenum 03 (12.5%). No statistical significance was found between clinical symptoms and levels of vitamin B12 with different age and sex. Conclusions: Prevalence of low vitamin B12 and cobalt were more common than other micronutrients. [ABSTRACT FROM AUTHOR]

Simple Summary: Cobalt (Co) is an essential element with ubiquitous dietary exposure and possible incremental exposure due to dietary supplements, occupations, and medical devices. The main function of Co in humans is based on its role in vitamin B12 (cobalamin). This review provides an extended overview of Co in relation to its effects on health and biological processes. Cobalt (Co) is an essential trace element for humans and other animals, but high doses can be harmful to human health. It is present in some foods such as green vegetables, various spices, meat, milk products, seafood, and eggs, and in drinking water. Co is necessary for the metabolism of human beings and animals due to its key role in the formation of vitamin B12, also known as cobalamin, the biological reservoir of Co. In high concentrations, Co may cause some health issues such as vomiting, nausea, diarrhea, bleeding, low blood pressure, heart diseases, thyroid damage, hair loss, bone defects, and the inhibition of some enzyme activities. Conversely, Co deficiency can lead to anorexia, chronic swelling, and detrimental anemia. Co nanoparticles have different and various biomedical applications thanks to their antioxidant, antimicrobial, anticancer, and antidiabetic properties. In addition, Co and cobalt oxide nanoparticles can be used in lithium-ion batteries, as a catalyst, a carrier for targeted drug delivery, a gas sensor, an electronic thin film, and in energy storage. Accumulation of Co in agriculture and humans, due to natural and anthropogenic factors, represents a global problem affecting water quality and human and animal health. Besides the common chelating agents used for Co intoxication, phytoremediation is an interesting environmental technology for cleaning up soil contaminated with Co. The occurrence of Co in the environment is discussed and its involvement in biological processes is underlined. Toxicological aspects related to Co are also examined in this review. [ABSTRACT FROM AUTHOR]

Cobalt can be toxic and the way cells adapt to its presence is largely unknown. Here we carried out a transcriptomic analysis of Escherichia coli exposed to cobalt. A limited number of genes were either up- or downregulated. Upregulated genes include the isc and the nfuA genes encoding Fe/S biogenesis assisting factors, and the rcnA gene encoding a cobalt efflux system. Downregulated genes are implicated in anaerobic metabolism (narK, nirB, hybO, grcA), metal transport (feoB, nikA), sulfate/thiosulfate import (cysP), and one is of unknown function (yeeE). Cobalt regulation of isc, nfuA, hybO, cysP and yeeE genes was found to involve IscR, a Fe/S transcriptional regulator. Previously, the Suf Fe/S biogenesis machinery was found to be important for cobalt stress adaptation, but suf genes did not show up in the microarray analysis. Therefore, we used qRT-PCR analysis and found that cobalt induced the suf operon expression. Moreover, kinetic analysis of the cobalt-mediated induction of the suf operon expression allowed us to propose that cobalt toxicity is caused first by impaired Fe/S biogenesis, followed by decreased iron bioavailability and eventually oxidative stress., (© 2010 Society for Applied Microbiology and Blackwell Publishing Ltd.)

Cobalt is essential for growth of Salmonella enterica and other organisms, yet this metal can be toxic when present in excess. Wild-type Salmonella exhibits several metabolic defects when grown in the presence of cobalt, some of which generate visible growth consequences. Work herein identifies sulfur assimilation, iron homeostasis, and Fe-S cluster metabolism as targets for cobalt toxicity. In each case it is proposed that cobalt exerts its effect by one of two mechanisms: direct competition with iron or indirectly through a mechanism that involves the status of reduced thiols in the cell. Cobalt toxicity results in decreased siroheme production, increased expression of the Fur regulon, and decreased activity of Fe-S cluster proteins. The consequences of reduced sulfite reductase activity in particular are exacerbated by the need for glutathione in cobalt resistance. Significantly, independent metabolic perturbations could be detected at cobalt concentrations below those required to generate a detectable growth defect.

Background: It has been estimated that more than 1 million workers in the United States are exposed to cobalt. Occupational exposure to 59 Co occurs mainly via inhalation and leads to various lung diseases. Cobalt is classified by the IARC as a possible human carcinogen (group 2B). Although there is evidence for in vivo and in vitro toxicity, the mechanisms of cobalt-induced lung toxicity are not fully known. The purpose of this work was to identify potential signatures of acute cobalt exposure using a toxicogenomic approach. Data analysis focused on some cellular processes and protein targets that are thought to be relevant for carcinogenesis, transport and biomarker research., Results: A time course transcriptome analysis was performed on A549 human pulmonary cells, leading to the identification of 85 genes which are repressed or induced in response to soluble 59 Co. A group of 29 of these genes, representing the main biological functions, was assessed by quantitative RT-PCR. The expression profiles of six of them were then tested by quantitative RT-PCR in a time-dependent manner and three modulations were confirmed by Western blotting. The 85 modulated genes include potential cobalt carriers (FBXL2, ZNT1, SLC12A5), tumor suppressors or transcription factors (MAZ, DLG1, MYC, AXL) and genes linked to the stress response (UBC, HSPCB, BNIP3L). We also identified nine genes coding for secreted proteins as candidates for biomarker research. Of those, TIMP2 was found to be down-regulated and this modulation was confirmed, in a dose-dependent manner, at protein level in the supernatant of exposed cells., Conclusion: Most of these genes have never been described as related to cobalt stress and provide original hypotheses for further study of the effects of this metal ion on human lung epithelial cells. A putative biomarker of cobalt toxicity was identified.

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 Ca(2+), Mg(2+), Na(+), K(+) ions and pH independently affect cobalt toxicity to barley was studied. With increasing activities of Mg(2+), and to a lesser extent also K(+), the 4-d EC50(Co2+) increased linearly, while Ca(2+), Na(+) and H(+) activities did not affect Co(2+) toxicity. Stability constants for the binding of Co(2+), Mg(2+) and K(+) to the biotic ligand were obtained: logK(CoBL)=5.14, logK(MgBL)=3.86 and logK(KBL)=2.50. Limited validation of the model with one standard artificial soil and one standard field soil showed that the 4-d EC50(Co2+) could only be predicted within a factor of four from the observed values, indicating further refinement of the BLM is needed.

Cobalt is suspected to cause memory deficit in humans and was reported to induce neurotoxicity in animal models. We have studied the effects of cobalt in primary cultures of mouse astrocytes. CoCl(2) (0.2-0.8mM) caused dose-dependent ATP depletion, apoptosis (cell shrinkage, phosphatidylserine externalization and chromatin rearrangements) and secondary necrosis. The mitochondria appeared to be a main target of cobalt toxicity, as shown by the loss of mitochondrial membrane potential (DeltaPsi(m)) and release from the mitochondria of apoptogenic factors, e.g. apoptosis inducing factor (AIF). Pre-treatment with bongkrekic acid reduced ATP depletion, implicating the involvement of the mitochondrial permeability transition (MPT) pore. Cobalt increased the generation of oxygen radicals, but antioxidants did not prevent toxicity. There was also an impaired response to ATP stimulation, evaluated as a lower raise in intracellular calcium. Similarly to hypoxia and dymethyloxallyl glycine (DMOG), cobalt triggered stabilization of the alpha-subunit of hypoxia-inducible factor HIF-1 (HIF-1alpha). This early event was followed by an increased expression of HIF-1 regulated genes, e.g. stress protein HO-1, pro-apoptotic factor Nip3 and iNOS. Although all of the three stimuli activated the HIF-1alpha pathway and decreased ATP levels, the downstream effects were different. DMOG only inhibited cell proliferation, whereas the other two conditions caused cell death by apoptosis and necrosis. This points to cobalt and hypoxia not only inducing HIF-1alpha regulated genes but also affecting similarly other cellular functions, including metabolism.

High field 1H NMR spectroscopy demonstrated that addition of Co(II) ions to osteoarthritic knee-joint synovial fluid (SF) resulted in its complexation by a range of biomolecules, the relative efficacies of these complexants/chelators being citrate >> histidine - threonine >> glycine - glutamate - glutamine - phenylalanine tyrosine > formate > lactate >> alanine > valine > acetate > pyruvate > creatinine, this order reflecting the ability of these ligands to compete for the available Co(II) in terms of (1) thermodynamic equilibrium constants for the formation of their complexes and (2) their SF concentrations. Since many of these SF Co(II) complexants (e.g. histidinate) serve as powerful *OH scavengers, the results acquired indicate that any of this radical generated from the Co(II) source in such complexes via Fenton or pseudo-Fenton reaction systems will be "site-specifically" scavenged. The significance of these observations with regard to cobalt toxicity and the in vivo corrosion of cobalt-containing metal alloy joint prostheses (e.g. CoCr alloys) is discussed.

Metal-on-metal hip arthroplasty has been performed with increasing frequency throughout the world, particularly in younger and more active patients, including women of childbearing age. The potential toxicity of cobalt exposure on fetus is concerned since cobalt ions generated by metal-on-metal bearings can traverse the placenta and be detected in fetal blood and amniotic fluid. This study examined the effects of cobalt exposure on early embryonic development and the mechanisms underlying its toxicity. Zebrafish embryos were exposed to a range of cobalt concentrations (0-100 mg/L) between 1 and 144 h postfertilization. The survival and early development of embryos were not significantly affected by cobalt at concentrations <100 μg/L. However, embryos exposed to higher concentrations (>100 μg/L) displayed reduced survival rates and abnormal development, including delayed hatching, aberrant morphology, retarded growth, and bradycardia. Furthermore, this study examined oxidative stress and apoptosis in embryos exposed to cobalt at concentrations of 0-500 μg/L. Lipid peroxidation levels were increased in cobalt-treated embryos at concentrations of 100 and 500 μg/L. The mRNA levels of catalase, superoxide dismutase 2, p53, caspase-3, and caspase-9 genes were upregulated in a dose-dependent manner. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assays also revealed abnormal apoptotic signals in the brain, trunk, and tail when treated with 500 μg/L cobalt. These data suggest that oxidative stress and apoptosis are associated with cobalt toxicity in zebrafish embryos. [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.

Chronic cobalt exposure is characterized by severe cardiac insufficiency. Since the mechanisms of cobalt toxicity are not yet clear, we analysed the effects of chronic cobalt exposure on antioxidant enzyme activities and myocardial mitochondrial ATP production rate in a rat model. One group of rats was fed a conventional diet and another a cobalt supplemented diet for 24 weeks. The manganese-superoxide dismutase activity was markedly reduced in the cobalt rats (18+/-4.7 U/mg protein) compared to the control rats (100+/-22 U/mg protein; p <0.001). Activity in the respiratory chain enzymes succinate-cytochrome c reductase, NADH-cytochrome c reductase and cytochrome c oxidase was also reduced in the cobalt rats (p<0.01). Glutamate dehydrogenase activity, located in the mitochondrial matrix, was unchanged. The mitochondrial ATP production rate in relation to myocardial mass was lower in the cobalt rats for all substrates tested except palmitoyl-l-carnitine + malate. In conclusion, 24 weeks of chronic cobalt exposure induces a marked decrease in manganese-superoxide dismutase activity, a moderate decrease in mitochondrial ATP production rate and a general reduction in the capacity of the respiratory chain. The impairment in mitochondrial ATP production might be secondary to the decreased manganese-superoxide dismutase activity, causing inactivation of mitochondrial factors susceptible to superoxide radicals.

Copyright of Canadian Journal of Surgery is the property of CMA Impact Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Despite the wide use of nanoscale materials in several industrial applications as well as in biology and medicine, very little research has been carried out on the potential toxicity of nanoparticles. We had previously obtained 10 differentially expressed mRNAs in BALB3T3 fibroblasts exposed to different forms of cobalt, i.e., microparticles, nanoparticles, and ions. Those genes represented candidate biomarkers for indicating specific cellular effects after cobalt nanoparticle exposure. In the present paper, we have further evaluated the expression of those genes by real-time RT-PCR after exposure to different forms of cobalt. Moreover, we also tested some genes associated with cobalt toxicity, such as VEGF, HIF-1α, and Bnip3. We identified biomarkers that are sensitive to cobalt ions that we think to be the reactive form. Our data, in fact, are consistent with the possibility that Co-nano, due to their large surface area, once inside the cell dissolve and act as ions. [ABSTRACT FROM AUTHOR]

Tomato ( Lycopersicon esculentum L.) cv. Alivikas was grown in refined sand at two levels of phosphorus (P): 1.5 mM (adequate) and 3.0 mM (high); 0.5 mM cobalt (Co) was supplied at each P level after 35 days of growth. Visible symptoms of Co toxicity appeared as interveinal chlorosis of young leaves after 8 days of metal supply. Biomass was depressed at both P levels with excess Co, although less at the high P level. Discontinuation of high P or Co or additional iron (Fe) supply also increased the biomass. The fresh weight of fruits was decreased, but dry weight was increased in high P supply. Quality of fruits was poor with Co‐treated plants as Co depressed the fruit fresh weight and dry weight, volume and size of fruits, concentrations of chlorophyll a, b and carotene, ascorbic acid, lycopene, reducing sugars, and starch, and increased acidity and phenols. These effects were greater with adequate vs. high P. High P (without Co) improved fruit quality by increasing fruit dry weight, volume, and size of fruits, ascorbic acid content, and reducing sugars and by decreasing acidity. Accumulation of cobalt in leaves and fruits was greater, and these plant parts developed visible Co toxicity symptoms. Fruits developed black patches with prolonged Co supply. New fruits developed after the discontinuation of the Co supply appeared green and normal, but were few in number compared with increased vegetative growth of plants (cobalt supplied with the normal level of phosphorus). Earlier flowering, fruiting, and ripening were observed in plants with high phosphorus rather than adequate P. Brown spots in fruits developed after 18–20 days of Co supply, and in the most severe case, young emerging fruits were totally brown. Amelioration of cobalt toxicity was better with discontinuation of Co than withdrawal of high P with additional Fe. [ABSTRACT FROM AUTHOR]

Purpose of the Study: The purpose of this study was to measure the serum cobalt levels and their correlation with clinical and radiological findings in patients with metal on metal hip articulating surfaces., Method: Forty-one patients with metal on metal hip arthroplasty were reviewed retrospectively at mean follow-up of 12.9 months. Serum cobalt levels were determined for each patient by atomic absorption spectrometry at the maximal follow-up and were compared to a control group (19 patients). Two patients and one control subjects also performed exercise on a treadmill in order to appreciate the influence of physical activity on serum cobalt levels., Results: The metal on metal group presented higher serum cobalt levels than those of the control group (p < 0.0001). There was no correlation between serum cobalt and clinical and radiological findings at the exception of patient age (n = 40, r = 0.37). However, when the follow-up was greater than 18 months, mean serum cobalt was significantly higher compared to a follow-up less than 18 months. The physical exercise test led to a moderate elevation (around 10 p. 100) of cobalt in the two patients but not in the control subject., Discussion and Conclusion: The interpretation of an elevated cobalt serum level is difficult. Cobalt-containing drugs, other implants, excess of activity and diseases (renal failure) may influence serum cobalt level. In this study, the high serum cobalt levels seem not linked to a failure of the implant, mainly because of the short follow-up. They could rather be attributed to an increase of the patient activity beginning 18 months after the surgery. Because potential long-term cobalt toxicity and carcinogenicity is not well known, careful medical follow-up should be emphasized specially in young patients.

The absorption and disposition of inorganic cobalt salts after oral administration have not been well characterized. The objectives of this study were to compare in vivo results with cobalt transport through the in vitro everted small intestine and to relate the disposition results to a biochemical indicator of cobalt toxicity. Cobalt chloride was given to male Fischer 344 rats orally at 33.3 mg Co(II)/kg or intravenously at 4.16 mg Co(II)/kg. By 36 h, 74.5% of the oral dose was eliminated in the feces. The liver, kidney, and heart accumulated cobalt to the greatest extent. Following the single oral dose, the blood cobalt concentration-time curve was triphasic, peaked at 3.2 h, and had an absorptive half-life of 0.9 h, an elimination phase half-life of 3.9 h, and a terminal elimination half-life of 22.9 h. Following intravenous administration, 10.1% of the dose was excreted in the feces, indicating that cobalt can be secreted in the bile. Following a single intravenous injection, the concentration-time curve displayed three segments. The first segment, which occurred during the first 4 h, had a rapid half-life of 1.3 h. The second phase, from 4 to 12 h, demonstrated a slower clearance rate with a half-life of 4.3 h. The final and slowest phase, from 12 to 36 h, had a half-life of 19 h. Intestinal jejunal ring experiments indicated that cobalt transport has both active and passive components; however, cobalt transport through the in vitro rat everted duodenum indicated that cobalt transport had almost exclusively passive components with facilitated diffusion. The finding that uptake was saturable may explain the small extent of absorption following oral dosing. Heme oxygenase studies following subcutaneous and intravenous administration resulted in an increase in activity (twofold) over controls, while oral administration did not. We concluded that the extent of cobalt absorption across the gastrointestinal tract is incomplete, and that the concentration administered and the route of exposure may determine its systemic toxicity.

Cobalt is a relatively rare magnetic element with properties similar to iron and nickel. The two valance states are cobaltous (II) and cobaltic (III) and the former is the most common valance used in the chemical industry. Cobalt occurs in nature primarily as arsenides, oxides, and sulfides. Most of the production of cobalt involves the metallic form used in the formation of cobalt superalloys. The term "hard metal" refers to compounds containing tungsten carbide (80-95%) combined with matrices formed from cobalt (5-20%) and nickel (0-5%). For the general population, the diet is the main source of exposure to cobalt. In the occupational setting, exposure to cobalt alone occurs primarily during the production of cobalt powders. In other industrial exposures (e.g., hard metal, diamond polishing), additional agents (tungsten) modulate the toxicity of cobalt. Cobalt is an essential element necessary for the formation of vitamin B12 (hydroxocobalamin); however, excessive administration of this trace element produces goiter and reduced thyroid activity. In 1966, the syndrome "beer drinker's cardiomyopathy" appeared in Quebec City, Canada, and was characterized by pericardial effusion, elevated hemoglobin concentrations, and congestive heart failure. An interstitial pulmonary fibrosis has been associated with industrial exposure to hard metal dust (tungsten and cobalt), but not to cobalt alone. Exposure to cobalt alone produces an allergic contact dermatitis and occupational asthma. Treatment of cobalt toxicity is primarily supportive.

Total joint arthroplasty (TJA) implants are composed of metals, ceramics, and/or polyethylene. Studies suggest that the debris released from metal implants may possess neurotoxic properties with reports of neuropsychiatric symptoms and memory deficits, which could be relevant to Alzheimer's disease and related dementias. This exploratory study examined the cross-sectional correlation of blood metal concentrations with cognitive performance and neuroimaging findings in a convenience sample of 113 TJA patients with history of elevated blood metal concentrations of either titanium, cobalt and/or chromium. Associations with neuroimaging measures were observed but not with cognitive scores. Larger studies with longitudinal follow-up are warranted. [ABSTRACT FROM AUTHOR]

Due to advances in surgical procedures and the biocompatibility of materials used in total joint replacement, more and younger patients are undergoing these procedures. Although state-of-the-art joint replacements can last 20 years or longer, wear and corrosion is still a major risk for implant failure, and patients with these implants are exposed for longer to these corrosive products. It is therefore important to investigate the potential effects on the whole organism. Released nanoparticles and ions derived from commonly used metal implants consist, among others, of cobalt, nickel, and chromium. The effect of these metallic products in the process of osteolysis and aseptic implant loosening has already been studied; however, the systemic effect on other cell types, including neurons, remains elusive. To this end, we used human iPSC-derived motoneurons to investigate the effects of metal ions on human neurons. We treated human motoneurons with ion concentrations regularly found in patients, stained them with MitoSOX and propidium iodide, and analyzed them with fluorescence-assisted cell sorting (FACS). We found that upon treatment human motoneurons suffered from the formation of ROS and subsequently died. These effects were most prominent in motoneurons treated with 500 μM of cobalt or nickel, in which we observed significant cell death, whereas chromium showed fewer ROS and no apparent impairment of motoneurons. Our results show that the wear and corrosive products of metal implants at concentrations readily available in peri-implant tissues induced ROS and subsequently cell death in an iPSC-derived motoneuron cell model. We therefore conclude that monitoring of neuronal impairment is important in patients undergoing total joint replacement. [ABSTRACT FROM AUTHOR]

Improving angiogenesis is the key to the success of most regenerative medicine approaches. However, how and to which extent this may be performed is still a challenge. In this regard, cobalt (Co)-doped bioactive glasses show promise being able to combine the traditional bioactivity of these materials (especially bone-bonding and osteo-stimulatory properties) with the pro-angiogenic effect associated with the release of cobalt. Although the use and local delivery of Co2+ ions into the body have raised some concerns about the possible toxic effects on living cells and tissues, important biological improvements have been highlighted both in vitro and in vivo. This review aims at providing a comprehensive overview of Co-releasing glasses, which find biomedical applications as various products, including micro- and nanoparticles, composites in combination with biocompatible polymers, fibers and porous scaffolds. Therapeutic applications in the field of bone repair, wound healing and cancer treatment are discussed in the light of existing experimental evidence along with the open issues ahead. [ABSTRACT FROM AUTHOR]

Cobalt-containing hip prosthesis may cause systemic toxicity due to the release of cobalt from metal-on-metal (MoM) joint arthroplasty into the bloodstream. High cobalt blood levels can lead to a variety of clinical manifestations, mimicking other disorders, especially autoimmune, hematologic, and infectious diseases. Our purpose is to describe a clinical case of cobalt hip prosthesis intoxication mimicking an autoimmune disease, with systemic inflammation signs, arthro-myalgias unrelated to overt synovitis, and multiple autoantibody positivity. A 69-years-old woman presented with a 1-year history of right coxalgia, recurrent fever, arthro-myalgias, mediastinal and right iliac reactive lymphadenopathy. She underwent hip replacement surgery seven years earlier. The physical examination was unremarkable except for right hip pain. Laboratory tests showed markedly increased inflammatory indices and microbiological tests were all negative. Ultrasound-guided arthrocentesis of right hip yielded limpid fluid with negative cultures. Increased cobalt levels in plasma and urine showed metal intoxication. Magnetic resonance imaging with metal artifact reduction sequence (MARS) confirmed a periprosthetic mass as usually seen in reaction to metal debris. Prosthesis substitution was performed with a resolution of the clinical picture and normalization of cobalt levels. [ABSTRACT FROM AUTHOR]

Exposure to cobalt can give rise to adverse health effects related to various organs or tissues, such as the respiratory organs, the skin, the hematopoietic tissues, the myocardium, the thyroid gland, as well as teratogenic and carcinogenic effects. In occupational and environmental health, it is important to identify effects that occur at relatively low exposure, i.e. the critical effects which are crucial for preventive action. The limited database available on cobalt toxicity makes it difficult to select critical effects. For dermal exposures, allergic dermatitis may be regarded as such an effect, even if this is a reversible condition and dose-response relationships need to be defined. For inhalation exposures, effects on the respiratory tract can be considered as critical effects. Evidence of cobalt carcinogenicity in humans is inadequate and cannot be evaluated quantitatively but an extra safety factor to be added on exposures estimated from other effects may well be needed. Risks for development of pneumoconiosis are likely to be dependent on physical and chemical characteristics of airborne cobalt containing particles, but such information is lacking in most studies. It has been recognised for many years that there is an excess risk of pneumoconiosis when exposure to cobalt containing dust exceeds 100 micrograms/m3. Recently considerably lower concentrations occurring in the cobalt diamond industry have given rise to such effects. Irritation of mucous membranes may occur at 5-10 micrograms/m3.

Cobalt toxicity was evaluated in the dominant lethal assay (DLA) to determine whether the detrimental effects of cobalt on spermatozoa would have an impact on offspring. Male B6C3F1 mice were treated with cobaltous chloride (400 ppm Co) for 10 weeks and mated. Neither the stage nor rate of development in vitro of 2-cell embryos to blastocyst from cobalt-treated males was affected. There was an increase in preimplantation losses and a decrease in total and live births, but no change in postimplantation losses from litters at day 19 of gestation. Fertility of the males was maintained during the 10-week cobalt treatment period, decreased during the DLA, and recovered over the next 6 weeks. Sperm parameters at the end of DLA and the recovery period showed that cobalt decreased all parameters measured at 12 weeks, but these parameters, except concentration, recovered to control levels by 18 weeks. Tissue concentrations of cobalt measured by atomic absorption analysis were increased in liver, kidney, testis, and epididymis after 12 weeks of cobalt treatment. We conclude that cobalt affected preimplantation losses in the DLA by compromising the fertility of treated males.

The COT1 gene of Saccharomyces cerevisiae has been isolated as a dosage-dependent suppressor of cobalt toxicity. Overexpression of the COT1 gene confers increased tolerance to cobalt and rhodium ions but not other divalent cations. Strains containing null alleles of COT1 are viable yet more sensitive to cobalt than are wild-type strains. Transcription of COT1 responds minimally to the extracellular cobalt concentration. Addition of cobalt ions to growth media results in a twofold increase in COT1 mRNA abundance. The gene encodes a 48-kDa protein which is found in mitochondrial membrane fractions of cells. The protein contains six possible membrane-spanning domains and several potential metal-binding amino acid residues. The COT1 protein shares 60% identity with the ZRC1 gene product, which confers resistance to zinc and cadmium ions. Cobalt transport studies indicate that the COT1 product is involved in the uptake of cobalt ions yet is not solely responsible for it. The increased tolerance of strains containing multiple copies of the COT1 gene is probably due to increased compartmentalization or sequestration of the ion within mitochondria.

In this study, cobalt neurotoxicity was investigated in human astrocytoma and neuroblastoma (SH-SY5Y) cells using proliferation assays coupled with LC–MS-based metabolomics and transcriptomics techniques. Cells were treated with a range of cobalt concentrations between 0 and 200 µM. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay revealed cobalt cytotoxicity and decreased cell metabolism in a dose and time-dependent manner was observed by metabolomics analysis, in both cell lines. Metabolomic analysis also revealed several altered metabolites particularly those related to DNA deamination and methylation pathways. One of the increased metabolites was uracil which can be generated from DNA deamination or fragmentation of RNA. To investigate the origin of uracil, genomic DNA was isolated and analyzed by LC–MS. Interestingly, the source of uracil, which is uridine, increased significantly in the DNA of both cell lines. Additionally, the results of the qRT-PCR showed an increase in the expression of five genes Mlh1, Sirt2, MeCP2, UNG, and TDG in both cell lines. These genes are related to DNA strand breakage, hypoxia, methylation, and base excision repair. Overall, metabolomic analysis helped reveal the changes induced by cobalt in human neuronal-derived cell lines. These findings could unravel the effect of cobalt on the human brain. [ABSTRACT FROM AUTHOR]

This study investigated the impact of cobalt and cesium stresses on two hulless barley varieties through a hydroponic experiment. The plants were exposed to 200 μM cobalt chloride (Co), 200 μM cesium chloride (Cs), or with concurrent exposure to 100 μM Co + 100 μM Cs. The findings revealed that exposure to Co and Cs, either alone or in combination, caused a substantial reduction in plant growth and weight. Interestingly, the hulless barley seedlings were found to be more resilient to Cs stress, attributed to its lower Cs enrichment factor. The stressed seedlings demonstrated increased oxidative stress levels (malondialdehyde, proline, and content), but also displayed increased activity of antioxidant enzymes (POD and SOD), active oxygen scavenging capacity (GSH and GSSG content), and gene expression (GSH2, POD and SOD), reflecting a plant defense mechanism. Moreover, the expression of PAL and P5CS genes was significantly enhanced in seedlings under Co, Cs, and (Co + Cs) treatments, providing a basis for the physiological mechanism of heavy metal resistance in hulless barley. The results of this study provide valuable insights into the mechanisms of heavy metal resistance in hulless barley, indicating the plant's potential for phytoremediation. [ABSTRACT FROM AUTHOR]

Cobalt ferrite (CoFe2O4) nanopowder was successfully synthesised by the coprecipitation method. For the entire experiment, natural iron sand from the Bengawan Solo River is used as an iron (Fe) cation source. The effect of the annealing temperature of a coprecipitated CoFe2O4 sample from natural iron sand was investigated. The presence of strong metal oxide bond groups at the tetrahedral and octahedral sites is revealed by fourier transform infrared (FTIR) spectral results, owing to the CoFe2O4 characteristic. Then the X-ray diffraction (XRD) pattern confirmed the formation of a single-phase CoFe2O4 with face centred cubic (FCC) crystal structure closely matched to reference data ICDD221086. The crystalline parameters such as lattice parameter and crystallite size modify with the increase of annealing temperature. The saturation magnetisation (Ms) decreases as the annealing temperature rises. In addition, the coercive fields (Hc) increases as the annealing temperature rises. As a result, the annealing temperature affects the performance of the CoFe2O4 photocatalyst. The photocatalytic performance of the annealing temperature sample at 300°C was found to be the best. [ABSTRACT FROM AUTHOR]

The present systematic review investigated the concentration of chromium (Cr) and cobalt (Co) in serum in patients who have undergone total hip arthroplasty (THA). The first outcome of interest was to investigate the mean concentration in serum of Cr and Co using different material combinations and to verify whether their concentrations change significantly using different patterns of head and liner in THA. The second outcome of interest was to investigate whether the time elapsed from the index surgery to the follow-up, BMI, sex, and side exert an influence on the mean concentration of Cr and Co in serum in patients who have undergone THA. The following material combinations were investigated (head-liner): Ceramic-Co Cr (CoCr), CoCr-CoCr, CoCr-Polyethylene, CoCr high carbide-CoCr high carbide. Data from 2756 procedures were retrieved. The mean length of follow-up was 69.3 ± 47.7 months. The ANOVA test evidenced good comparability in age, length of follow-up, BMI, and sex (P > 0.1). In patients who have undergone THA, the mean concentration in the serum of Co ranged between 0.5 µg/L and 3.5 µg/L, and the mean concentration of Cr from 0.6 to 2.6 µg/L. The difference in the concentration of Co and Cr in serum is strictly related to the implant configuration, with the coupling CoCr-CoCr showing the highest and CoCr-Polyethylene showing the lowest concentration. Patient characteristics, BMI, sex, side and the time elapsed from the index surgery to the last follow-up did not exert a significant influence on the concentration of Co and Cr in serum in patients who have undergone total hip arthroplasty (THA). [ABSTRACT FROM AUTHOR]

Objective(s): Cobalt toxicity has become a health concern in recent years, due to overexposure resulting in neurological impairments. 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 neurotoxicity. Materials and Methods: We treated rats with CoCl2 or CoCl2 in combination with aqueous PA seed extract (PAE) orally for 14 days. Control rats received distilled water for the same period. Following treatments, behavioral experiments, analysis for oxidative stress, inflammation, and histological and immunohistochemical analysis were performed. Results: 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 inflammation.

Simple Summary: We review the role of cobalt and vitamin B12 in animals, especially in ruminants. Vitamin B12 is an essential part of the enzyme systems involved in multiple metabolic reactions and mainly in the formation of energy from ruminal fermentation. Signs of deficiency, as well as cobalt toxicity, in animals are described. The level of cobalt in ruminants can be assessed by measuring the blood or tissue concentrations of cobalt or vitamin B12, as well as the level of some metabolites such as malonate, homocysteine or transobolamine in blood or methylmalonic acid in urine. The requirement for cobalt (Co) is around 0.11 ppm (mg/kg) dry matter (DM) in the diet, although current recommendations advise supplementing the diet up to 0.20 mg Co/kg DM, which seems to increase animal production, especially in dairy cattle. Cobalt, as a trace element, is essential for rumen microorganisms for the formation of vitamin B12. In the metabolism of mammals, vitamin B12 is an essential part of two enzymatic systems involved in multiple metabolic reactions, such as in the metabolism of carbohydrates, lipids, some amino acids and DNA. Adenosylcobalamin and methylcobalamin are coenzymes of methylmalonyl coenzyme A (CoA) mutase and methionine synthetase and are essential for obtaining energy through ruminal metabolism. Signs of cobalt deficiency range from hyporexia, reduced growth and weight loss to liver steatosis, anemia, impaired immune function, impaired reproductive function and even death. Cobalt status in ruminant animals can be assessed by direct measurement of blood or tissue concentrations of cobalt or vitamin B12, as well as the level of methylmalonic acid, homocysteine or transcobalamin in blood; methylmalonic acid in urine; some variables hematological; food consumption or growth of animals. In general, it is assumed that the requirement for cobalt (Co) is expressed around 0.11 ppm (mg/kg) in the dry matter (DM) diet; current recommendations seem to advise increasing Co supplementation and placing it around 0.20 mg Co/kg DM. Although there is no unanimous criterion about milk production, fattening or reproductive rates in response to increased supplementation with Co, in some investigations, when the total Co of the diet was approximately 1 to 1.3 ppm (mg/kg), maximum responses were observed in the milk production. [ABSTRACT FROM AUTHOR]

Although cobalt is a required nutrient, it is toxic due to its ability to generate reactive oxygen species (ROS) and damage DNA. ROS generation by Co2+ often has been compared to that of Fe2+ or Cu+, disregarding the reduction potential differences among these metal ions. In plasmid DNA damage studies, a maximum of 15% DNA damage is observed with Co2+/H 2 O 2 treatment (up to 50 μM and 400 μM, respectively) significantly lower than the 90% damage observed for Fe2+/H 2 O 2 or Cu+/H 2 O 2 treatment. However, when ascorbate is added to the Co2+/H 2 O 2 system, a synergistic effect results in 90% DNA damage. DNA damage by Fe2+/H 2 O 2 can be prevented by polyphenol antioxidants, but polyphenols both prevent and promote DNA damage by Cu+/H 2 O 2. When tested for cobalt-mediated DNA damage affects, eight of ten polyphenols (epicatechin gallate, epigallocatechin gallate, propyl gallate, gallic acid, methyl-3,4,5-trihydroxybenzoate, methyl-4,5-dihydroxybenzoate, protocatechuic acid, and epicatechin) prevent cobalt-mediated DNA damage with IC 50 values of 1.3 to 27 μM and two (epigallocatechin and vanillic acid) prevent little to no DNA damage. EPR studies demonstrate cobalt-mediated formation of •OH, O 2 •ˉ, and •OOH, but not 1O 2 in the presence of H 2 O 2 and ascorbate. Epigallocatechin gallate and methyl-4,5-dihydroxybenzoate significantly reduce ROS generated by Co2+/H 2 O 2 /ascorbate, consistent with their prevention of cobalt-mediated DNA damage. Thus, while cobalt, iron, and copper are all d -block metal ions, cobalt ROS generation and its prevention is significantly different from that of iron and copper. In contrast to Fe(II), Co(II) does not damage DNA in the presence of hydrogen peroxide alone. Instead, it generates reactive oxygen species (ROS) and damages DNA in the presence of both hydrogen peroxide and ascorbate. Some polyphenols can bind Co(II) and scavenge these ROS to prevent cobalt-mediated DNA damage. [Display omitted] • Unlike Fe(II), Co(II) does not damage DNA in the presence of only hydrogen peroxide. • With H 2 O 2 and ascorbate, Co(II) generates hydroxyl and ascorbyl radicals to damage DNA. • Some polyphenols prevent Co-mediated DNA damage and compete with ascorbate to bind Co(II). • Antioxidant-metal binding may be one way to prevent cobalt toxicity. [ABSTRACT FROM AUTHOR]

This paper puts forward the use of "low-cost/low-end" hydroxyapatite-based adsorbing materials prepared from Tambaqui fish cleaning residues (i.e., bones) by grinding and/or thermal annealing. The nature of raw materials and treatments practically resulted in a "zero-cost" adsorbent for atrazine pesticide and Co2+ ion remediation in an aqueous solution. Despite the distinctive character of the two contaminants, all adsorptions were found to follow pseudo-second order kinetics and Freundlich isotherm models. Pristine hydroxyapatite proved to be more effective in adsorbing atrazine at low concentrations due to interactions with collagen residues. Conversely, heat-treated materials demonstrated better adsorption performances for cobalt due to the removal of organic residues hindering access to the surface. On the other hand, lower adsorption affinities resulted into a faster and more efficient Co2+ release into water. The different behavior in terms of phosphate and cobalt release shown by the three hydroxyapatite-based absorbents can be exploited for differential liberation of targeted nutrients, with high seed germination rates. Considering circular economic principles, waste-derived hydroxyapatites may be potentially attractive for removing ionic species, minimizing water pollution stemming from heavy industry, and for their subsequent targeted release to edible plants, enhancing agricultural availability of mineral nutrients for soil fertilization. [ABSTRACT FROM AUTHOR]

A carbon dot-functionalized solution-gated graphene transistor (CD-SGGT) was designed and prepared via the modification of CDs on the gate of SGGT. The above CDs were hydrothermally synthesized using DL-thioctic acid and triethylenetramine as C, N and S sources. The average size of CDs was ~6.2 nm, and there were many amino and carboxyl groups on the CDs' surfaces. The CDs was then used as a probe for preparation of CD-SGGT sensor for the cobalt(II) (Co2+) ions detection. The CD-SGGT sensor showed excellent sensitivity and high selectivity. Remarkably, the limit of detection (LOD) reached 10−19 M. The linear detection range was obtained from 10−19 to 10−15 M. Additionally, the CD-SGGT also showed fast response and good stability. [ABSTRACT FROM AUTHOR]

Purpose The persistent and alarming rates of increase in cardiovascular and renal diseases caused by chemicals such as cobalt chloride (CoCl2) in mammalian tissues have led to the use of various drugs for the treatment of these diseases. This study aims at evaluating the nephron-protective action of Naringin (NAR), a metal-chelating antioxidant against CoCl2-induced hypertension and nephrotoxicity. Methods Forty-two male Wistar rats were randomly distributed to seven rats of six groups and classified into Group A (Control), Group B (300 part per million; ppm CoCl2), Group C (300 ppm CoCl2 + 80 mg/kg NAR), Group D (300 ppm CoCl2 + 160 mg/kg NAR), Group E (80 mg/kg NAR), and Group F (160 mg/kg NAR). NAR and CoCl2 were administered via oral gavage for seven days. Biomarkers of renal damage, oxidative stress, antioxidant status, blood pressure parameters, immunohistochemistry of renal angiotensin-converting enzyme and podocin were determined. Results Cobalt chloride intoxication precipitated hypertension, renal damage, and oxidative stress. Immunohistochemistry revealed higher expression of angiotensin-converting enzyme (ACE) and podocin in rats administered only CoCl2. Conclusion Taken together, the antioxidant and metal-chelating action of Naringin administration against cobalt chloride-induced renal damage and hypertension could be through abrogation of angiotensin-converting enzyme and podocin signalling pathway. [ABSTRACT FROM AUTHOR]

Biogenic metals and their various inorganic, organometallic, and coordination compounds are comprehensively studied and extensively used in medical practice. Since the biogenic metals have various chemical properties corresponding to their position in the periodic table, their biological functions are different. Almost all of the discussed biogenic elements have an ability to form coordination complexes. Furthermore, the different accessible oxidation states occupied by most of these elements enables the body to catalyze oxy-reduction interactions, depending on the biological conditions. As they are biogenic in nature, their deficiency or their excess in the body leads to numerous pathological obstructions. The application of metal-based compounds as medications is connected with the oxy-reduction properties and the capability to form coordination complexes, which are involved in many bioreactions. The usefulness of these metals as therapeutic and diagnostic agents is also pointed out. [ABSTRACT FROM AUTHOR]

Cobalt (Co) bioaccumulation, contamination, and toxicity in the soil environment, plant growth, and cattles' health are becoming a severe matter that can cause unembellished consequences in environmental safety and human health. The present research was conducted for the assurance of cobalt (Co) amassing in three forage plant species (Zea mays, Sorghum bicolor, Trifolium alaxandrium), from four ecological sites, and sewage water and in buffaloes blood was investigated. The analysis of variance showed significant differences for Co concentration in the soil and sewage water collected from all ecological sites. Meanwhile, summer and winter seasons and forage ecotypes significantly influenced the quantity of Co. The forage pastures also vary significantly in the concentration of Co in the above-ground parts. The highest Co level was present in Trifolium alaxandrium at ecological site-5. Cobalt taken from wastewater had a higher concentration in Trifolium alaxandrium during the winter. The samples which are collected from site-V and site-IV have the maximum concentration of Co because these areas receive highly contaminated water for irrigation. Cobalt tends to be bioaccumulated in the food chain and can cause serious problems in humans and animals. Bioaccumulation of cobalt in collected samples could be accredited to anthropogenic activities. Pollution load index values for all samples fell in the range below 1. The health risk index indicated the probability of health damage caused by the ingestion of contaminated fodder. An increase of Co concentration in soil, fodder, and blood owing to wastewater irrigation to crops was indicated as an outcome of this investigation. The results indicate that the Co toxicity in forage crops is attributed to Co bioaccumulation, transfer, and pollution load in the soil–water-cattle triangle. Efforts should be extended to avoid contamination of the food chain via Co-rich sewage water. Other nonconventional water resources should be used for forage irrigation. [ABSTRACT FROM AUTHOR]

Emerging and low-carbon technologies and innovations are driving a need for domestic sources, sustainable use, and availability of critical minerals (CMs)—those vital to the national and economic security of the United States. Understanding the known and potential health effects of exposures to such mineral commodities can inform prudent and environmentally responsible handling and harvesting. We review the occurrence, use, predominant exposure pathways, and adverse outcome pathways (AOP) for human and fish receptors of those CMs that are nutritionally essential trace metals (specifically, cobalt, chromium, manganese, nickel, and zinc), as well as the rare earth elements. Biological responses to some elements having comparable biogeochemistry can sometimes be similar. Candidate quantifiable biomarkers for assessing potential AOP are conveyed. [ABSTRACT FROM AUTHOR]

Background: Cobalt, a versatile transition metal, has widespread industrial applications, but its potential link to cancer has raised concerns. This systematic review and meta-analysis protocol aims to investigate the relationship between cobalt exposure and cancer incidence, addressing its implications for public health and occupational safety. Methods: A comprehensive literature search will be conducted in PubMed, Scopus, and Web of Science databases up to August 2023. Eligible studies will include human participants exposed to cobalt, with cancer incidence as an outcome. Both observational and analytical study designs will be considered. Results: Quantitative meta-analysis will be performed using random-effects models to calculate pooled Incidence Rate Ratios (IRRs). Subgroup and sensitivity analyses will explore heterogeneity and potential bias. Findings will be compared with prior research to assess consistency and support. Conclusion: This systematic review and meta-analysis protocol aims to provide a comprehensive assessment of the potential association between cobalt exposure and cancer incidence. The outcomes could have significant implications for occupational health, public safety, and policy decisions. [ABSTRACT FROM AUTHOR]

Iron and cobalt are micronutrients that play an important role in the regulation of cellular processes, being part of the centre of catalases, peroxidases, cytochromes and metalloproteins such as hemoglobin and myoglobin (Fe). Cobalt primarily functions as a component of hydroxycobalamin, which is essential for regulating red blood cell production. Maintaining normal levels of cobalt and iron in the human body is important, as a deficiency can lead to anaemia. These elements are also involved in reactions during which oxidative stress occurs and are therefore considered to be a cause of tumor formation. This paper will discuss aspects of the influence of cobalt and iron on mechanisms that may contribute to the growth of gynecological tumors, as well as other obstetric-gynecological disease entities, by altering the conditions of the microenvironment. In addition, the following review also highlights the role of cobalt and iron in the treatment of gynecological tumors. [ABSTRACT FROM AUTHOR]

In the present study, the assessment of heavy metal contaminant migration from fresh mine tailings was conducted using the electrokinetic remediation technique (EKR). In this sense, a pilot EKR cell was designed to evaluate the recovery potential of copper, nickel, and cobalt species. In particular, the focus was on the impacts of electric field intensity and pH in initial mixture and testing their interaction in copper, nickel, and cobalt migration. Experiments were made using a 22 factorial experimental design with a central point, using DC electric fields from 1.0 to 2.0 V cm−1 and H2SO4 pretreatment solutions from 1.0 to 2.0 mol L−1, along with an ANOVA test with error reduction. The metal removal rates were approximately 7% for cobalt, neglectable for copper, and 6% for nickel. In the best cases, the highest concentrations by migration at the cathodic zone were 11%, 31%, and 30%, respectively. According to ANOVA tests, factor interaction was proven for each metal in the half cell near the cathode and the closest zone from the cathode specifically. Both factors affected metal concentrations, which indicates that when the goal aims for species accumulation in a narrower section, each factor has a significant effect, and their interaction makes a proven enhancement. Thus, using 2.0 V cm−1 and 2.0 mol L−1 showed a high improvement in metal concentration in the cathodic zone. [ABSTRACT FROM AUTHOR]

By decreasing root 1-aminocyclopropane-1-carboxylate (ACC) content and plant ethylene production, the microbial enzyme ACC deaminase is a widespread beneficial trait of plant growth-promoting rhizobacteria (PGPR), ameliorating ethylene-mediated root growth inhibition. However, relatively little is known about whether bacterial ACC deaminase modulates root architecture and root hair traits. Thus the dwarf tomato (Solanum lycopersicum) cultivar Micro-Tom was inoculated in vitro with Pseudomonas brassicacearum Am3, its ACC deaminase deficient mutant T8-1, a known PGPR strain Variovorax paradoxus 5C-2 or chemically treated with agents that promoted or inhibited ethylene production or sensitivity (Ag+, Co2+, and ACC). ACC treatment reduced both root elongation and the number of lateral roots, while ethylene inhibitors (Ag+, Co2+) and V. paradoxus 5C-2 promoted primary root elongation, but differentially affected lateral root length and number. Ag+ stimulated lateral root development, while Co2+ and V. paradoxus 5C-2 did not. Inoculation with P. brassicacearum Am3 and T8-1 inhibited elongation of the primary and lateral roots at a high inoculum concentration (106 cells cm3). All bacterial strains significantly increased the length and number of root hairs, with these effects more pronounced in P. brassicacearum Am3 than in the mutant T8-1. Treatment with Ag+ inhibited root hair formation and elongation, while Co2+ had the opposite effects. ACC treatment had no effect on root hair elongation but increased root hair density. While root growth inhibition caused by P. brassicacearum Am3 was independent of ACC deaminase, the promotion of root hair elongation and density by this strain was augmented by ACC deaminase activity. Thus ACC deaminase can modulate the morphological impacts of bacteria on root hair response by affecting plant ethylene content. [ABSTRACT FROM AUTHOR]

Zirconium oxide nanoparticles (ZrO2NPs) were green synthesized for the first time using an aqueous peppermint extract as a precipitating and capping agent. Addition of the extract to Zr4+ solution was followed by calcination of the resulting precipitate at 570 and 700 °C to form ZrO2NPs570 and ZrO2NPs700, respectively. These oxides were characterized using X-ray diffraction, transmission electron microscopy, and BET surface area analysis, and used as adsorbents for cobalt ions (Co2+) in water. The effects of pH, initial Co2+ concentration, ZrO2NPs mass, and contact time on adsorption efficiency were studied. Characterization results showed formation of cubic ZrO2 with average crystallite sizes (XRD data) of 6.27 and 7.26 nm for ZrO2NPs570 and ZrO2NPs700, respectively. TEM images of the two oxides exhibited nearly spherical nanoparticles and BET surface area measurements indicated the formation of mesoporous oxides having surface areas of 94.8 and 62.4 m2/g, respectively. The results of the adsorption study confirmed that the synthesized ZrO2NPs can be efficiently used for the adsorption of Co2+ from water. The uptake of Co2+ from the treated solution is favored at pH values higher than its point of zero charge (6.0). In addition, the adsorption of Co2+ by ZrO2 follows a pseudo-second order kinetics (R2 = 1.0) and can be explained by the Langmuir adsorption isotherm (R2 = 0.973). [ABSTRACT FROM AUTHOR]

The focus of this article is to understand the application and the factors influencing magnetic hyperthermia using cobalt ferrite nanoparticles. Intrinsic properties, such as particle size, specific absorption rate, and magnetic saturation, are correlated with the material’s property to generate hyperthermia. External factors, such as the magnitude of applied field frequency, also influence the rate of hyperthermia generated by magnetic nanoparticles. Quantitative analysis of Pennes bioheat equation and finite element analysis (FEA) using COMSOL are used to understand the transient increase in temperature at the tumor site using magnetic nanoparticles. The required temperature for generating hyperthermia using nanoparticles is approximately 315 K or 42 °C. Due to the intrinsic high rate of metabolism in tumor cells, the required magnetic field to induce transient increase at the malignant cell site is less than its surrounding healthier cells. This principle can therefore be applied for inducing selective hyperthermia in tumor cells by the application of a lower threshold external magnetic field. This article focuses on the Pennes bioheat equation to understand the phenomenon of heat transfer as a function of both the time and the applied field magnitude. It compares the difference in the rate of heat transfer for 1) cobalt ferrite and cobalt ferrite–barium titanate and 2) hyperthermia in healthier and tumor sites using magnetic nanoparticles. An FEA is performed in conjunction to understand the rate of temperature profile change occurring at a simulated cell site. [ABSTRACT FROM AUTHOR]

Infectious diseases remain the most serious public health issue, which requires the development of more effective strategies for infectious control. As a kind of ultra-trace element, cobalt is essential to the metabolism of different organisms. In recent decades, nanotechnology has attracted increasing attention worldwide due to its wide application in different areas, including medicine. Based on the important biological roles of cobalt, cobalt nanomaterials have recently been widely developed for their attractive biomedical applications. With advantages such as low costs in preparation, hypotoxicity, photothermal conversion abilities, and high drug loading ability, cobalt nanomaterials have been proven to show promising potential in anticancer and anti-infection treatment. In this review, we summarize the characters of cobalt nanomaterials, followed by the advances in their biological functions and mechanisms. More importantly, we emphatically discuss the potential of cobalt nanomaterials as anti-infectious agents, drug carriers, and immunomodulators for anti-infection treatments, which might be helpful to facilitate progress in future research of anti-infection therapy. [ABSTRACT FROM AUTHOR]

Novel antimicrobial compounds can be added to foods directly or incorporated into packaging materials in order to improve food safety and shelf life. One such potential antimicrobial compound is the bioinorganic complex Co(II)-citrate (NH4)4[Co(C6H5O7)2] (Co-cit). Its antimicrobial activity against Listeria monocytogenes, Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa was investigated in solution, both alone and in combination with existing preservatives. The antimicrobial activity of poly(lactic acid) films (PLA) with incorporated Co-cit (23.3% w/w) against L. monocytogenes was determined using culture medium and model foods (slices of turkey ham and smoked salmon). In nutrient broth, without preservatives, all four bacteria were significantly (p < 0.05) inhibited by 0.5 mM Co-cit, and L. monocytogenes and P. aeruginosa were the most sensitive. The addition of preservatives to the broth increased the antimicrobial activity of Co-cit in many cases, but not in a way that was consistent between the different bacteria investigated and was likely due to additional physiological stress exerted on the cells rather than any effect on the activity of the Co-cit itself. PLA films with Co-cit were bacteriostatic against L. monocytogenes on artificial media and on foods. However, in the latter case, the PLA film itself was the main contributor to the inhibition. Composite PLA-(Co-cit) films exhibited antimicrobial activity against foodborne bacteria and have potential application as active packaging materials to enhance food safety. [ABSTRACT FROM AUTHOR]

Extrinsic factors play a significant role during aquaculture feed manufacturing practices. Herein, a 90-day feeding trial was designed in triplicate under controlled environmental conditions to evaluate the efficiency of different chemical forms of dietary cobalt at different dosage levels on growth performance, hematological, and immunological indices of Tor putitora fingerlings. Firstly, cobalt chloride nanoparticles (Co-NPs) and cobalt methionine chelated complex (Co-Met) were synthesized via physical and chemical methods respectively and then characterized for their size, surface morphology, and elemental composition analysis by using X-rays diffraction spectroscopy (XRD), scanning electron microscopy (SEM), and energy dispersive spectroscopy (EDS). Results indicated the crystalline nature of Co-NPs with spherical shape having an average size < 20 nm while Co-Met appeared as an amorphous complex with a honey-comb-like octahedral structure with an average size of 82.69 nm. Afterward, a feeding experiment was executed and fish were divided into three groups, i.e., control group (CG; fed 40% crude protein diet with no mineral added), while the other two groups were fed graded levels (0.5–3 mg/kg; increment of 0.5 mg Co/group) of Co-NPs and Co-Met supplemented diets. Statistical analysis of results by using two-way ANOVA indicated significant (P < 0.001) effect of both chemical forms, dosage levels, and their interaction level on fish indicating a dose-dependent significant effect of different chemical forms of dietary cobalt on fish. Additionally, Co-Met supplemented group of fish at supplementation level of 3 mg/kg diet showed highest growth performance, and improved hemato-immunological as compared to other experimental and control group of fish. [ABSTRACT FROM AUTHOR]

Cobalt (Co) and nickel (Ni) are beneficial and essential elements for plants, respectively, with the latter required for urease activity, which hydrolyzes urea into ammonium in plants. However, excess Co and Ni are toxic to plants and their transport mechanisms in rice are unclear. Here, we analyzed an ethyl methanesulfonate (EMS)-mutagenized rice mutant, 1187_n, with increased Co and Ni contents in its brown rice and shoots. 1187_n has a mutation in OsFPN1, which was correlated with a high Co and Ni phenotype in F2 crosses between the parental line and mutant. In addition, CRISPR/Cas9 mutants exhibited a phenotype similar to that of 1187_n, demonstrating that OsFPN1 is the causal gene of the mutant. In addition to the high Co and Ni in brown rice and shoots, the mutant also exhibited high Co and Ni concentrations in the xylem sap, but low concentrations in the roots, suggesting that OsFPN1 is involved in the root-to-shoot translocation of Co and Ni. The growth of 1187_n and CRISPR/Cas9 lines were suppressed under high Co and Ni condition, indicating OsFPN1 is required for the normal growth under high Co and Ni. An OsFPN1-green fluorescent protein (GFP) fusion protein was localized to the Golgi apparatus. Yeast carrying GFP-OsFPN1 increased sensitivity to high Co contents and decreased Co and Ni accumulation. These results suggest that OsFPN1 can transport Co and Ni and is vital detoxification in rice. [ABSTRACT FROM AUTHOR]

aima I Abdel Hamid,1 Mohamed E Attia,2 Jon M Hirshon,3,4 Mohamed El-Shinawi,5,6 Moustafa El-Hussaini,7 Maged El-Setouhy7,81Forensic Medicine and Clinical Toxicology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 2Orthopedics Departments, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 3Department of Emergency Medicine, University of Maryland, School of Medicine, Baltimore, MD, USA; 4Department of Epidemiology and Public Health, University of Maryland, School of Medicine, Baltimore, MD, USA; 5Department of General Surgery, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 6Galala University, Galala City, Suez, Egypt; 7Department of Community, Environmental and Occupational Medicine, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 8Department of Family and Community Medicine, Faculty of Medince, Jazan University, Jazan, Kingdom of Saudi ArabiaCorrespondence: Omaima I Abdel Hamid, Forensic Medicine and Clinical Toxicology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt, Tel +201001664310, Email [email protected] Introduction: Hip arthroplasty (HA) using implantable metal components is among the commonest orthopedic interventions. However, it can be followed by several complications following corrosion and the release of metal ions. Several studies proved that damaged genomic DNA may contribute to the pathophysiology of mental disorders. Aim: The current work aims to evaluate the psychiatric disorders in metal on polyethylene hip arthroplasty (MOP-HA) patients and its correlation to cobalt/chromium (Co/Cr) levels and genotoxicity. Methods: The work was a longitudinal follow-up study including 34 adults with unilateral primary MOP-HA meeting the inclusion and exclusion criteria. Preoperatively, 6, 12-months-postoperatively, patients were examined for cognitive impairment using mini-mental-state-examination (MMSE), depression using major-depressive-inventory (MDI), and blood samples were collected for estimation of Co/Cr, detection of genotoxicity by single-cell-gel-electrophoresis (comet assay) and serum 8-hydroxy-2'–deoxyguanosine (8-OHdG). Results: Cognitive impairment was reported in 18.5% and 14.8% at 6-months, and 12-months postoperative, respectively. Depressive disorder was recorded in 22.2% at 6-months and 14.8% at 12-months postoperative. The marginal homogeneity tests proved a non-significant difference. There was a non-significant difference in preoperative, 6-months, 12-months postoperative MMSE, and MDI scores. There were significantly increased Co/Cr levels at 6-months postoperative. The levels decreased at 12-months postoperative, however, still significantly higher than preoperative values. There was a significant increase in serum 8-OHdG and the levels were positively correlated to cobalt levels at both 6 and 12-months-postoperative. There was a non-significant difference among preoperative, 6-months, and 12-months postoperative comet assay measurements. Conclusion: From previous findings, we can conclude that will-functioning MOP hip arthroplasty can induce increased ion levels and positively correlated increase in biochemical markers of genotoxicity (8-OHdG). [ABSTRACT FROM AUTHOR]