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Journal ArticleDOI

Protection against vanadium-induced testicular toxicity by testosterone propionate in rats

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TLDR
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.

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The toxicity of vanadium on gastrointestinal, urinary and reproductive system, and its influence on fertility and fetuses malformations.

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.
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Heat stress-induced hepatotoxicity and its prevention by resveratrol in rats.

TL;DR: The results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during heat stress may render liver more susceptible to oxidative damage, leading to their functional inactivation.
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Improvements in the corrosion resistance and biocompatibility of biomedical Ti–6Al–7Nb alloy using an electrochemical anodization treatment

TL;DR: In this paper, an electrochemical anodization surface treatment was applied to improve both the corrosion resistance and biocompatibility of Ti-6Al-7Nb alloy for implant applications.
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Androgens’ effects on cerebrovascular function in health and disease

TL;DR: A better understanding of androgens’ interactions with the cerebral vasculature under physiological and pathological conditions is of key importance.
References
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Journal Article

Protein Measurement with the Folin Phenol Reagent

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.
Book ChapterDOI

Microsomal lipid peroxidation.

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Journal ArticleDOI

The preparation of 131i-labelled human growth hormone of high specific radioactivity

TL;DR: The loss of immunological reactivity at high specific radioactivities or at high levels of chemical substitution with STAI/sup 127/!iodine is demonstrated.
Journal ArticleDOI

Selenium: Biochemical Role as a Component of Glutathione Peroxidase

TL;DR: When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H2O2, added glutathione failed to protect the hemoglobin from oxidative damage.
Journal ArticleDOI

Environmental Health Criteria

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