Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice.

Vanadium is a prevalent neurotoxic transition metal with therapeutic potentials in some neurological conditions. Hydrocephalus poses a major clinical burden in neurological practice in Africa. Its primary treatment (shunting) has complications, including infection and blockage; alternative drug-based therapies are therefore necessary. This study investigates the function and cytoarchitecture of motor and cerebellar cortices in juvenile hydrocephalic mice following treatment with varying doses of vanadium. Fifty juvenile mice were allocated into five groups (n = 10 each): controls, hydrocephalus-only, low- (0.15 mg/kg), moderate- (0.3 mg/kg), and high- (3.0 mg/kg) dose vanadium groups. Hydrocephalus was induced by the intracisternal injection of kaolin and sodium metavanadate administered by intraperitoneal injection 72hourly for 28 days. Neurobehavioral tests: open field, hanging wire, and pole tests, were carried out to assess locomotion, muscular strength, and motor coordination, respectively. The cerebral motor and the cerebellar cortices were processed for cresyl violet staining and immunohistochemistry for neurons (NeuN) and astrocytes (glial fibrillary acidic protein). Hydrocephalic mice exhibited body weight loss and behavioral deficits. Horizontal and vertical movements and latency to fall from hanging wire were significantly reduced, while latency to turn and descend the pole were prolonged in hydrocephalic mice, suggesting impaired motor ability; this was improved in vanadium-treated mice. Increased neuronal count, pyknotic cells, neurodegeneration and reactive astrogliosis were observed in the hydrocephalic mice. These were mostly mitigated in the vanadium-treated mice, except in the high-dose group where astrogliosis persisted. These results demonstrate a neuroprotective potential of vanadium administration in hydrocephalus. The molecular basis of these effects needs further exploration.

Proteomic alteration of albumen by dietary vanadium in commercial egg-type layers.

Vanadium (V) is an ultratrace metal with the insulin-tropic properties and is often researched as the diabetes drug. However, in animals, V has been reported to have toxic effects on the development, immunity, oxidation-reduction equilibrium, gastrointestinal function, and so forth. Especially in poultry, supplementation of more than 10 mg of V/kg in the layer diets has been shown to adversely affect the egg production and egg quality. In this study, we supplemented 0 mg of V/kg, 5 mg of V/kg, and 10 mg of V/kg in the layer diets for 35 D and examined the quantitative proteomics of albumen for finding the possible target signaling pathway and mechanism of V action and made the preliminary verification. In contrast to the control group, V resulted in a significant drop in the albumen height, and in oviduct ampulla, the activity of total antioxidant capacity and glutathione peroxidase significantly decreased (P = 0.01, P = 0.02), the content of malonic dialdehyde significantly increased (P = 0.01), and the apoptosis rate significantly increased in the 5-mg V/kg and 10-mg V/kg treatment groups (P ＜ 0.01). V affected 36 differentially accumulated proteins in albumen, with 23 proteins upregulated and 13 proteins downregulated. The expressions of innate protein albumen lysozyme (Q6LEL2), vitellogenin-2 (P02845), and the F1NWD0 protein in albumen belonged to the P53 family were significantly reduced, in contrast to the control (P < 0.05), and the expression of riboflavin-binding protein (P02752) was significantly improved (P < 0.05). The Hippo signaling pathway-fly, which is suitable for the key protein P53 as the most significantly affected network, might be important for discriminating V.

Global biogeochemical cycle of vanadium.

Synthesizing published data, we provide a quantitative summary of the global biogeochemical cycle of vanadium (V), including both human-derived and natural fluxes. Through mining of V ores (130 × 109 g V/y) and extraction and combustion of fossil fuels (600 × 109 g V/y), humans are the predominant force in the geochemical cycle of V at Earth's surface. Human emissions of V to the atmosphere are now likely to exceed background emissions by as much as a factor of 1.7, and, presumably, we have altered the deposition of V from the atmosphere by a similar amount. Excessive V in air and water has potential, but poorly documented, consequences for human health. Much of the atmospheric flux probably derives from emissions from the combustion of fossil fuels, but the magnitude of this flux depends on the type of fuel, with relatively low emissions from coal and higher contributions from heavy crude oils, tar sands bitumen, and petroleum coke. Increasing interest in petroleum derived from unconventional deposits is likely to lead to greater emissions of V to the atmosphere in the near future. Our analysis further suggests that the flux of V in rivers has been incremented by about 15% from human activities. Overall, the budget of dissolved V in the oceans is remarkably well balanced-with about 40 × 109 g V/y to 50 × 109 g V/y inputs and outputs, and a mean residence time for dissolved V in seawater of about 130,000 y with respect to inputs from rivers.

Selenium, Vanadium, and Chromium as Micronutrients to Improve Metabolic Syndrome.

Trace metals play an important role in the proper functioning of carbohydrate and lipid metabolism. Some of the trace metals are thus essential for maintaining homeostasis, while deficiency of these trace metals can cause disorders with metabolic and physiological imbalances. This article concentrates on three trace metals (selenium, vanadium, and chromium) that may play crucial roles in controlling blood glucose concentrations possibly through their insulin-mimetic effects. For these trace metals, the level of evidence available for their health effects as supplements is weak. Thus, their potential is not fully exploited for the target of metabolic syndrome, a constellation that increases the risk for cardiovascular disease and type 2 diabetes. Given that the prevalence of metabolic syndrome is increasing throughout the world, a simpler option of interventions with food supplemented with well-studied trace metals could serve as an answer to this problem. The oxidation state and coordination chemistry play crucial roles in defining the responses to these trace metals, so further research is warranted to understand fully their metabolic and cardiovascular effects in human metabolic syndrome.

[Metallosis: A Rare Cause of Autoimmune Hemolytic Anemia]. / Metalose: Causa Rara de Anemia Hemolítica Autoimune.

INTRODUCTION: Hemolytic anemia may be associated with multiple etiologies, including toxic substances, such as metals, which is a rare cause. CASE STUDY: 55-year-old male, who underwent a total arthroplasty of the right hip (uncemented prostheses with ceramic-ceramic articulation with an acetabular component consisting of a dome composed of an alloy of titanium, aluminum and vanadium into which fitted a ceramic 'insert'). Approximately 4 years after surgery the patient complained of noise originating from the prosthesis which occurred on movement. A surgical revision was performed and showed the presence of dark thick intracapsular fluid, fracture of the ceramic acetabular 'insert' and signs of wear of the acetabular metal dome. Extensive washing was carried out and the fractured ceramic 'insert' was replaced for a polyethylene 'insert'. Two months later he was referred to the Emergency Room due to worsening of his general health, floating in the right hip and mucocutaneous jaundice. Laboratory tests suggested autoimmune hemolytic anemia. Arthrocentesis was performed and a large volume of metal fluid was drained off. The CT scan showed a large heterogeneous pelvic cystic collection seeded with prosthesis fragments, suggestive of metallosis. Hemolytic anemia was explained as toxicity of the particles and metal ions caused by the wear of the prosthesis. The patient was started on a high-dose steroid treatment. Afterwards, when he was stable, prosthesis components replacement and drainage of pelvic debris fluid were carried out. DISCUSSION: After the fracture of the ceramic 'insert' the ceramic head began to articulate directly with the metallic acetabular component, causing noise and wear with release of particles and ions. This caused a cystic pelvic abscess, which went unnoticed on the first surgical revision. Surgical debridement lead to the cystic collection extending into the adjacent tissues and the systemic circulation, triggering serious systemic effects, such as autoimmune hemolytic anemia. The potential toxicity of each of the metal elements of this prosthesis is unknown, and there are still no available laboratory tests for its detection. CONCLUSION: Metallosis is a rare cause of autoimmune hemolytic anemia.

Introdução: A anemia hemolítica pode estar associada a múltiplas etiologias, nomeadamente a tóxicos, como os metais, sendo esta uma causa rara.Caso Clínico: Homem de 55 anos de idade, sujeito a artroplastia total da anca direita (prótese não cimentada com articulação cerâmica-cerâmica, cujo componente acetabular era constituído por uma cúpula metálica composta por uma liga de titânio, vanádio e alumínio na qual encaixava um insert cerâmico). Cerca de quatro anos após esta intervenção cirúrgica referia ruídos na prótese com os movimentos. Foi sujeito a revisão cirúrgica tendo-se constatado a presença de líquido espesso intracapsular de cor escura, fractura do insert acetabular cerâmico e sinais de desgaste da cúpula metálica acetabular. Procedeu-se a lavagem abundante e substituição do insert cerâmico fracturado por um insert de polietileno. Dois meses depois recorreu ao Serviço de Urgência por degradação do estado geral, flutuação na anca direita e icterícia muco-cutânea. Analiticamente evidenciava valores compatíveis com anemia hemolítica autoimune. Foi feita punção articular com saída de abundante líquido metalótico. A tomografia computorizada revelou extensa colecção heterogénea quística intrapélvica com múltiplos fragmentos de prótese no seu interior, sugestivos de metalose. A anemia hemolítica foi interpretada como consequência da toxicidade das partículas e iões metálicos oriundos do desgaste da prótese. Iniciou corticoterapia em altas doses e posteriormente quando houve condições procedeu-se à substituição de todos os componentes da prótese e drenagem do material acumulado intra-pélvico.Discussão: Após a fractura do insert cerâmico a cabeça cerâmica passou a articular directamente com o componente acetabular metálico, originando os ruídos e desgaste com libertação de partículas e iões. Este material formou uma coleção quística intrapélvica, que passou despercebida na primeira revisão cirúrgica. O desbridamento cirúrgico pôs em comunicação esta coleção com os tecidos adjacentes e com a circulação sistémica, desencadeando efeitos sistémicos graves, como anemia hemolítica auto-imune. Desconhece-se o potencial de toxicidade de cada um dos elementos metálicos desta prótese, não estando ainda disponíveis testes laboratoriais de detecção.Conclusão: A metalose é uma causa rara de anemia hemolítica auto-imune.

Harbour porpoises (Phocoena phocoena) stranded along the southern North Sea: an assessment through metallic contamination.

Throughout the last few years, the southern North Sea has witnessed an increase in the number of stranded marine mammals, particularly the harbour porpoise (Phocoena phocoena). This species is subject to several potential threats such as exposure to contaminants, changes in food supply, marine traffic and fishery by-catch. The aims of this study were to investigate potential associations between contaminants and health status and to analyze spatial and temporal trends of metal concentrations in harbour porpoises. Selected trace elements (As, Cd, Cr, Cu, Hg, Mn, Se, V and Zn) were measured in kidneys and livers of 105 harbour porpoises stranded along the southern North Sea (French and Belgian coasts from 2006 to 2013) and 27 stranded along the Bay of Biscay (French coast from 2009 to 2012). Porpoises that died from infectious disease displayed significant higher hepatic concentrations of Cd, Hg, Se and Zn compared to healthy porpoises that died from physical trauma. Adult porpoises displayed significant higher concentrations of Cd, Cr, Hg, Se and V in livers compared to juveniles. No spatial or temporal trends in metal concentrations were detected in our study. The results of the present study suggested that chemical contamination may represent one of many threats encountered by harbour porpoises, but it cannot explain alone the increase in the number of stranded individuals.

An evidence-based systematic review of vanadium by the Natural Standard Research Collaboration.

An evidence-based systematic review of vanadium by the Natural Standard Research Collaboration consolidates the safety and efficacy data available in the scientific literature using a validated, reproducible grading rationale. This article includes written and statistical analysis of clinical trials, plus a compilation of expert opinion, folkloric precedent, history, pharmacology, kinetics/dynamics, interactions, adverse effects, toxicology, and dosing.

Dietary high vanadium causes oxidative damage-induced renal and hepatic toxicity in broilers.

The purpose of this study was to investigate the renal and hepatic oxidative damage and toxicity caused by dietary high vanadium in broilers. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet (vanadium 0.073 mg/kg), and five high vanadium diets (vanadium 5 mg/kg, high vanadium group I; 15 mg/kg, high vanadium group II; 30 mg/kg, high vanadium group III; 45 mg/kg, high vanadium group IV; and 60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. The results showed that the renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxy radical, and malondialdehyde (MDA), glutathione, and vanadium contents were not significantly changed in high vanadium group I and II when compared with those of the control groups. However, the SOD and GSH-Px activities, ability to inhibit hydroxy radical, and GSH content were significantly decreased, and the MDA and vanadium contents were markedly increased in high vanadium groups III, IV, and V. At the same time, the lesions were also observed in the kidney and liver of high vanadium groups III, IV, and V. The renal tubular epithelial cells showed granular degeneration and vacuolar degeneration, and hepatocytes showed granular degeneration, vacuolar degeneration, and fatty degeneration. It was concluded that dietary vanadium in the range of 30-60 mg/kg could cause oxidative damage and vanadium accumulation, which induced renal and hepatic toxicity and lesions. The renal and hepatic function was finally impaired in boilers.

Comparison of hypoglycemic activity and toxicity of vanadium (IV) and vanadium (V) absorbed in fermented mushroom of Coprinus comatus.

This study was designed to evaluate the effect and toxicity of administration of vanadium (IV, V) absorbed by Coprinus comatus (VACC) on alloxan-induced and sucrosefed hyperglycemic mice, respectively. The blood glucose, lipid profile, and the organ masses of the mice were analyzed. After the mice were administered with VACC, the blood glucose and the lipid profile of hyperglycemic mice decreased, irrespective of the VACC produced by vanadium (IV) or vanadium (V). However, the organ masses of the mice were significantly different after the mice were treated with vanadium (IV) and vanadium (V) 9 weeks later. The results indicate both vanadium (IV) and vanadium (V) absorbed in C. comatus have hypoglycemic activity on hyperglycemic mice. However, vanadium (IV) absorbed in C. comatus is less toxic to mice than vanadium (V).

Evidence of multiple metabolic routes in vanadium's effects on layers. Ascorbic acid differential effects on prepeak egg production parameters following prolonged vanadium feeding.

The development of V toxicity was followed over a 28-d period in 25-wk-old Leghorn layers fed 20 mg ammonium metavanadate/kg diet (Days 1 to 14) followed by 30 mg/kg diet (Days 15 to 28). Then, over a second 28-d period, the responses to V and supplemental ascorbic acid (AA) fed at 500 or 1,000 mg/kg diet (Days 29 to 42) followed by 1,500 or 3,000 mg/kg diet (Days 43 to 56) were examined. Feed consumption, egg weight, Haugh units (HU), and BW measurements indicated that the response to V was multifactorial, but of differing intensities and time-frames for the variables. Haugh units were lowered rapidly (3 d, P < .05) in response to V feeding, but HU values decreased only slightly when dietary V was increased to 30 mg/kg. In contrast, egg production was decreased moderately by 20 mg V/kg and a considerable further reduction in egg production resulted from increasing the V to 30 mg/kg. Ascorbic acid supplementation differentially affected these responses: BW, egg production, and egg weight were improved significantly in the V-fed group receiving an AA supplement, as compared with those fed V only. Haugh unit values, however, were not improved by AA supplementation in groups receiving V. Foam functional properties, which also were changed by V feeding, were not corrected by AA feeding. The results suggest that the toxic effects of V are mediated through more than one physiological mechanism. One mechanism, which includes negative effects on BW, egg production, and egg weight, is responsive to the additional reducing equivalents provided by supplemental AA. Another mechanism, which is apparent from the effect of V on egg HU values, is not ameliorated by AA supplementation after toxicity developed.

Unusual occupational toxins.

Occupational and environmental medicine affords encounters with many unusual toxins, ranging from exotic metals to rocket fuels. Twelve of the most unusual industrial toxins are reviewed here and their clinical manifestations and treatments explored: acetonitrile, acrylonitrile, boron hydrides, dimethylaminopropionitrile, dimethylformamide, hydrazines, methyl isocyanate, 2-nitropropane, phosphine, Stalinon, tellurium, and vanadium.

[Blastomogenic action of heavy vanadium-rich petroleum and its processing products]. / Blastomogennoe deistvie tiazheloi vysokovanadievoi nefti i produktov ee pererabotki.

The contributors performed a study of the blastomogenic properties of the heavy high vanadium oil processed at different temperatures. Skin applications of the oil and oil products in hybrid mice induced skin tumours in 27.5 (48.7%), pregastric--6.4 (7.6%), genital--15.4 (21.1%) cases. It was established that high temperatures of oil sublimation increased the benzopyrene contents and the oil products' blastomogenic activity.

Induction of lesions of selenium-vitamin E deficiency in weanling swine fed silver, cobalt, tellurium, zinc, cadmium, and vanadium.

Forty-two weanling pigs were allotted to 7 groups and fed (for 10 weeks) a commercial ration that was adequate in selenium and vitamin E (Se-E) content, either alone or with supplements of Ag (3,000 mg/kg of feed, as acetate), Co (500 mg/kg, as chloride), Te (500 mg/kg, as tetrachloride), Zn (3,000 mg/kg, as sulfate), Cd (500 mg/kg, as sulfate), or V (200 mg/kg, as vanadate). The pigs fed the Ag supplement died after 25 to 39 days and had lesions characteristic of Se-E deficiency with accumulations of serous transudates in body cavities and hepatic and cardiac necrosis. In the pigs fed the Ag supplement, there was high hepatic Se content terminally; blood glutathione peroxidase (GSH-Px) activity decreased to low levels several weeks before the pigs died with lesions of Se-E deficiency. Macroscopic lesions of Se-E deficiency were not found in pigs fed Co, Te, Zn, Cd, or V. However, evidence of Se-E deficiency, as indicated by microscopically detected necrosis of cardiac and skeletal muscle, was present in 50% to 65% of the pigs fed Co or Te and occasionally in pigs fed Zn, Cd, and V supplements. The pigs fed Te had marked decrease of blood GSH-Px activity over the last 6 weeks of the feeding period. No consistently abnormal values for blood GSH-Px activity or terminal hepatic Se content were observed in pigs fed Co, Zn, Cd, or V. The pigs fed the Zn supplement grew as rapidly as the control pigs. Evidence of V toxicosis was observed as severe growth suppression, mortality, and marked enteritis and cystitis (with accompanying hydroureter in 1 pig).