Vanadium-induced testicular toxicity and its prevention by oral supplementation of zinc sulphate.
TL;DR: The results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during vanadium exposure may render testis more susceptible to oxidative damage, leading to their functional inactivation, and zinc sulphate supplementation can be an effective antidote in the treatment of vanadium poisoning.
Abstract: Transition metal vanadium has been shown to modulate the cellular redox potential and catalyze the generation of reactive oxygen intermediates. Since free radical production and lipid peroxidation are potentially important mediators in testicular physiology and pathophysiology, the present study was conducted to elucidate the vanadium-induced oxidative damages in rat testis and the ameliorative role of zinc sulphate against such adverse effects of vanadium. Adult male rats were dosed for 26 days with daily intraperitoneal injection of 0.4 mg V/kg body weight as sodium metavanadate. One group of rats was treated with zinc sulphate orally simultaneously with vanadium for 26 days, while the other group was treated with zinc sulphate alone. Changes in testicular and accessory sex organ weight, different varieties of germ cells at stage VII of spermatogenic cycle, epididymal sperm count, and enzymatic (Delta(5)3beta- HSD, 17beta- HSD, SOD, catalase), lipid peroxidation, and hormonal milieu were monitored. Vanadium treatment resulted in a significant increase in the testicular lipid peroxidation and caused a marked inhibition in the activities of antioxidant and steroidogenic enzymes. Histopathological examination revealed inhibition of spermatogenesis and the preferential loss of maturing and elongated spermatids. However, coadministration of zinc sulphate to vanadium-treated animals resulted in normalizing these parameters appreciably, emphasizing the therapeutic potentials of zinc. Taken together, the results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during vanadium exposure may render testis more susceptible to oxidative damage, leading to their functional inactivation. However, zinc sulphate supplementation can be an effective antidote in the treatment of vanadium poisoning.
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TL;DR: The harmful effects of vanadium on the morphology and physiology of both animal and human tissues, including the digestive system, the urinary tract, and the reproductive system are described.
Abstract: Vanadium is a transition metal that has a unique and beneficial effect on both humans and animals. For many years, studies have suggested that vanadium is an essential trace element. Its biological properties are of interest due to its therapeutic potential, including in the treatment of diabetes mellitus. Vanadium deficiencies can lead to a range of pathologies. However, excessive concentration of this metal can cause irreversible damage to various tissues and organs. Vanadium toxicity mainly manifests in gastrointestinal symptoms, including diarrhea, vomiting, and weight reduction. Vanadium also exhibits hepatotoxic and nephrotoxic properties, including glomerulonephritis and pyelonephritis. Vanadium compounds may also lead to partial degeneration of the seminiferous epithelium of the seminiferous tubules in the testes and can affect male fertility. This paper describes the harmful effects of vanadium on the morphology and physiology of both animal and human tissues, including the digestive system, the urinary tract, and the reproductive system. What is more, the following study includes data concerning the correlation between the above-mentioned metal and its influence on fertility and fetus malformations. Additionally, this research identifies the doses of vanadium which lead to pathological alterations becoming visible within tissues. Moreover, this study includes information about the protective efficacy of some substances in view of the toxicity of vanadium.
55 citations
TL;DR: The proposed CPE of V using 8-hydroxyquinoline (oxine) as complexing reagent and mediated by nonionic surfactant (Triton X-114) was investigated and successfully applied to the determination of trace quantity of V in various pharmaceutical preparations with satisfactory results.
Abstract: A cloud point extraction (CPE) method has been developed for the determination of trace quantity of vanadium ions in pharmaceutical formulations (PF), dialysate (DS) and parenteral solutions (PS). The CPE of vanadium (V) using 8-hydroxyquinoline (oxine) as complexing reagent and mediated by nonionic surfactant (Triton X-114) was investigated. The parameters that affect the extraction efficiency of CPE, such as pH of sample solution, concentration of oxine and Triton X-114, equilibration temperature and time period for shaking were investigated in detail. The validity of CPE of V was checked by standard addition method in real samples. The extracted surfactant-rich phase was diluted with nitric acid in ethanol, prior to subjecting electrothermal atomic absorption spectrometry. Under these conditions, the preconcentration of 50 mL sample solutions, allowed raising an enrichment factor of 125-fold. The lower limit of detection obtained under the optimal conditions was 42 ng/L. The proposed method has been successfully applied to the determination of trace quantity of V in various pharmaceutical preparations with satisfactory results. The concentration ranges of V in PF, DS and PS samples were found in the range of 10.5-15.2, 0.65-1.32 and 1.76-6.93 microg/L, respectively.
42 citations
TL;DR: Data suggest that dietary antioxidants including ascorbic acid, vitamin E, polyphenols, phytosterols, and extracts from medicinal plants can bring a beneficial effect in vanadium toxicity.
Abstract: Vanadium (V) in its inorganic forms is a toxic metal and a potent environmental and occupational pollutant and has been reported to induce toxic effects in animals and people. In vivo and in vitro data show that high levels of reactive oxygen species are often implicated in vanadium deleterious effects. Since many dietary (exogenous) antioxidants are known to upregulate the intrinsic antioxidant system and ameliorate oxidative stress-related disorders, this review evaluates their effectiveness in the treatment of vanadium-induced toxicity. Collected data, mostly from animal studies, suggest that dietary antioxidants including ascorbic acid, vitamin E, polyphenols, phytosterols, and extracts from medicinal plants can bring a beneficial effect in vanadium toxicity. These findings show potential preventive effects of dietary antioxidants on vanadium-induced oxidative stress, DNA damage, neurotoxicity, testicular toxicity, and kidney damage. The relevant mechanistic insights of these events are discussed. In summary, the results of studies on the role of dietary antioxidants in vanadium toxicology appear encouraging enough to merit further investigations.
38 citations
Cites background from "Vanadium-induced testicular toxicit..."
...Oral supplementation of zinc sulfate prevented lipid peroxidation and normalized the activities of antioxidant enzymes in the testis of sodium metavanadate-exposed rats [121]....
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TL;DR: In this article, a mouse model with vanadium pentoxide (V 2 O 5 ) inhalation was used to investigate the effect of V 2 O5 on the alveoli, pulmonary capillaries, and systemic circulation.
Abstract: Vanadium pentoxide (V 2 O 5 ) is one of the compounds bound to the suspended material found in the atmosphere and classified as particulate matter. The main source of these pollutants is the incomplete combustion of fossil fuels. Some of these fuels are rich in vanadium, such as Mexican, Venezuelian and Kuwaity petroleum, and after the incomplete combustion, carbon-core particles are liberated to the atmosphere, with V 2 O 5 adsorbed to its surface. These particles, about 2.5 μm in diameter, are inhaled reaching the alveoli, the pulmonary capillaries, arriving to the systemic circulation and to every system and organ producing different effects. Here we report our findings on a mouse model with V 2 O 5 inhalation. It is important to notice that the toxic effects differ drastically between systems and organs. Some of our findings support the presence of increased vascular events in urban areas with high particulate pollution.
34 citations
TL;DR: It is established that vanadium is a testicular toxicant that perturbs the male reproductive system adversely, however, hormone replacement therapy by testosterone propionate may provide partial protection.
Abstract: Vanadium is a well recognized industrial hazard known to adversely affect male reproductive functions. The intricate mechanistic aspects of this metal and the role of oxidative stress in the deterioration of testicular functions are investigated in the current study. The experiment also focused on the effects of testosterone propionate in testicular and sperm functions in the rat intoxicated with vanadate. Vanadium exposure resulted in a more prominent spermatogenic arrest and consistently abolished the conversion of round to mature spermatids along with decreased epididymal sperm number and increased percentage of abnormal sperm. This is followed by a precipitous decline in the level of serum testosterone and gonadotropins and consequently the testicular steroidogenic and antioxidant enzymes were inhibited. Vanadium induces degeneration in the genital organs of rats and exhibits high indices of lipid oxidative damage. In response to exogenous testosterone propionate (TP) administration, spermatogonial cell populations remained suppressed, while the spermatogenesis was restored quantitatively. In contrast, the hormone treatment had no effect on the dramatically decreased serum FSH level after vanadate treatment. Moreover, TP could ameliorate the toxicity, as indicated by decreased testicular lipid peroxidation with marginal but significant increase in the activities of all the measured enzymes following vanadate-treatment. Taken together all these studies establish that vanadium is a testicular toxicant that perturbs the male reproductive system adversely. However, hormone replacement therapy by testosterone propionate may provide partial protection. The results suggest the feasibility of using endocrine regimens to impede deleterious effects of vanadium on the male reproductive system.
34 citations
Cites background or methods from "Vanadium-induced testicular toxicit..."
...Group II: rats received i.p. injection of sodium metavanadate (NaVO 3 ) dissolved in sterile distilled water at a dose of 0.4 mgV/kg body weight daily for 26 days (Chandra et al. 2007b)....
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...The animals were fed on standardized normal diet (20% protein) which consisted of 70% wheat, 20% Bengal gram, 5% fish meal powder, 4% dry yeast powder, 0.75% refined til oil, and 0.25% shark liver oil and water ad libitum (Chandra et al. 2007a)....
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...4 mgV/kg body weight daily for 26 days (Chandra et al. 2007b)....
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...It has been reported in the previous study (Chandra et al. 2007c) that plasma testosterone and FSH suppression following vanadium treatment resulted in disordered spermatogonial proliferation and disordered progression through meiosis and spermatid development, with evidence for FSHspecific effects…...
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...This might be due to an increase in the number of germ cells apoptosis, as a consequence of adverse effects on Sertoli cells and germ cell interactions (Chandra et al. 2007a; Jain et al. 2007)....
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References
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Journal Article•
TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
Abstract: Since 1922 when Wu proposed the use of the Folin phenol reagent for the measurement of proteins, a number of modified analytical procedures utilizing this reagent have been reported for the determination of proteins in serum, in antigen-antibody precipitates, and in insulin. Although the reagent would seem to be recommended by its great sensitivity and the simplicity of procedure possible with its use, it has not found great favor for general biochemical purposes. In the belief that this reagent, nevertheless, has considerable merit for certain application, but that its peculiarities and limitations need to be understood for its fullest exploitation, it has been studied with regard to effects of variations in pH, time of reaction, and concentration of reactants, permissible levels of reagents commonly used in handling proteins, and interfering substances. Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
289,852 citations
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TL;DR: This chapter discusses microsomal lipid peroxidation, a complex process known to occur in both plants and animals that involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and the eventual destruction of membrane lipids.
Abstract: Publisher Summary This chapter discusses microsomal lipid peroxidation Lipid peroxidation is a complex process known to occur in both plants and animals It involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and the eventual destruction of membrane lipids, producing a variety of breakdown products, including alcohols, ketones, aldehydes, and ethers Biological membranes are often rich in unsaturated fatty acids and bathed in an oxygen-rich, metal-containing fluid Lipid peroxidation begins with the abstraction of a hydrogen atom from an unsaturated fatty acid, resulting in the formation of a lipid radical The formation of lipid endoperoxides in unsaturated fatty acids containing at least 3 methylene interrupted double bonds can lead to the formation of malondialdehyde as a breakdown product Nonenzymic peroxidation of microsomal membranes also occurs and is probably mediated in part by endogenous hemoproteins and transition metals The direct measurement of lipid hydroperoxides has an advantage over the thiobarbituric acid assay in that it permits a more accurate comparison of lipid peroxide levels in dissimilar lipid membranes
11,945 citations
"Vanadium-induced testicular toxicit..." refers methods in this paper
...Lipid peroxidation (LPO) was measured by the method of Buege and Aust (1978)....
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4,344 citations
"Vanadium-induced testicular toxicit..." refers methods in this paper
...All the counts (crude counts) of the germ cells were corrected for differences in the nuclear diameter by the formula of Abercrombie (1946): true count = (crude count × section thickness)/ (section thickness—nuclear diameter of germ cell) The nuclear diameter of each variety of germ cell was…...
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TL;DR: Some mechanisms associated with the toxicities of metal ions are very similar to the effects produced by many organic xenobiotics, related to differences in solubilities, absorbability, transport, chemical reactions, and the complexes that are formed within the body.
Abstract: The role of reactive oxygen species, with the subsequent oxidative deterioration of biological macromolecules in the toxicities associated with transition metal ions, is reviewed. Recent studies have shown that metals, including iron, copper, chromium, and vanadium undergo redox cycling, while cadmium, mercury, and nickel, as well as lead, deplete glutathione and protein-bound sulfhydryl groups, resulting in the production of reactive oxygen species as superoxide ion, hydrogen peroxide, and hydroxyl radical. As a consequence, enhanced lipid peroxidation. DNA damage, and altered calcium and sulfhydryl homeostasis occur. Fenton-like reactions may be commonly associated with most membranous fractions including mitochondria, microsomes, and peroxisomes. Phagocytic cells may be another important source of reactive oxygen species in response to metal ions. Furthermore, various studies have suggested that the ability to generate reactive oxygen species by redox cycling quinones and related compounds may require metal ions. Recent studies have suggested that metal ions may enhance the production of tumor necrosis factor alpha (TNF alpha) and activate protein kinase C, as well as induce the production of stress proteins. Thus, some mechanisms associated with the toxicities of metal ions are very similar to the effects produced by many organic xenobiotics. Specific differences in the toxicities of metal ions may be related to differences in solubilities, absorbability, transport, chemical reactivity, and the complexes that are formed within the body. This review summarizes current studies that have been conducted with transition metal ions as well as lead, regarding the production of reactive oxygen species and oxidative tissue damage.
4,084 citations
"Vanadium-induced testicular toxicit..." refers background in this paper
...Certain inorganic salts of vanadium have been shown to modulate cellular redox potential and to catalyze the generation of reactive oxygen intermediates (Shi et al. 1996; Stohs and Bagchi 1995; Jounes and Strobelt 1991)....
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Book•
01 Jan 1963TL;DR: Sir Ronald A. Fisher and Frank Yates: Statistical Tables for Biological, Agricultural and Medical Research.
Abstract: Sir Ronald A. Fisher and Frank Yates: Statistical Tables for Biological, Agricultural and Medical Research. Edinburgh and London: Oliver and Boyd, 1953. Pp. xi + 126. 21s.
3,315 citations
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...05 was interpreted as statistically significant (Fisher and Yates, 1974)...
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...A value of p <0.05 was interpreted as statistically significant (Fisher and Yates, 1974)...
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