Ultrastructural findings in murine seminiferous tubules as a consequence of subchronic vanadium pentoxide inhalation.
ABSTRACT Vanadium (V) is a transition metal emitted to the atmosphere during the combustion of fossil fuels. Its current status as an atmospheric pollutant increases the need for information about the effects that this element might have on the reproductive health of exposed populations. The present study investigated changes in testicular ultrastructure following inhalation exposure of male mice to V (as vanadium pentoxide). Tissue V level was constant during the 12-week time period. We observed necrosis of spermatogonium, spermatocytes and Sertoli cells, as well as pseudo-nuclear inclusion and disruption of cellular junctions. Our findings stressed the importance of the hemato-testicular barrier in supporting the function of Sertoli cells and suggest as a possible target of V, tight junction proteins. Further analysis is needed in order to identify the role that reactive oxidative species (ROS) might have on these cellular junctions, and if a specific protein is the target of its toxic effects. The relevance of this report concerns the impact that metal air pollution could have on male fertility in dense cities with vehicular traffic problems.
- [Show abstract] [Hide abstract]
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.Toxicology mechanisms and methods 07/2010; 20(6):306-15. · 1.37 Impact Factor
Article: Vanadium pentoxide inhalation[Show abstract] [Hide abstract]
ABSTRACT: Context: This mini-review describes the toxic effects of vanadium pentoxide inhalation principally in the workplace and associated complications with breathing and respiration. Although there are some material safety data sheets available detailing the handling, hazards and toxicity of vanadium pentoxide, there are only two reviews listed in PubMed detailing its toxicity. Aim: To collate information on the consequences of occupational inhalation exposure of vanadium pentoxide on physiological function and wellbeing. Materials and Methods: The criteria used in the current mini-review for selecting articles were adopted from proposed criteria in The International Classification of Functioning, Disability and Health. Articles were classified from an acute and chronic exposure and toxicity thrust. Results: The lungs are the principal route through which vanadium pentoxide enters the body. It can injure the lungs and bronchial airways possibly involving acute chemical pneumonotis, pulmonary edema and/or acute tracheobronchitis. It may adversely influence cardiac autonomic function. It stimulates the secretion of cytokines and chemokines by hepatocytes and disrupts mitochondria function. It disrupts the permeability of the epithelium and promotes access of inflammatory mediators to the underlying neuronal tissue causing injury and neuronal death. When renal brush border membrane vesicles are exposed to vanadium pentoxide, there is a time-dependent inhibition of citrate uptake and Na + K + ATPase in the membrane possibly contributing to nephrotoxicity. Exposure results in necrosis of spermatogonium, spermatocytes and Sertoli cells contributing to male infertility. Conclusion: Vanadium pentoxide certainly has adverse effects on the health and the well-being and measures need to be taken to prevent hazardous exposure of the like.Indian journal of occupational and environmental medicine 01/2007;
- [Show abstract] [Hide abstract]
ABSTRACT: Exposure to electromagnetic pulses in certain doses may lead to increase in the permeability of the blood testes barrier (BTB) in mice, which in turn affects spermatogenesis, penetration and spermiation. TGF-β3 is a key molecule involved in BTB permeability via regulation of tight junction proteins, and it participates in regulating spermatogenesis, synthesis of steroids and production of the extracellular matrix in testicular tissue. Therefore, it is hypothesized that TGF-β3 plays important roles in electromagnetic pulse (EMP)-induced changes in BTB permeability. In the present study, we carried out whole-body irradiation on mice using EMP of different intensities. No obvious pathological changes or significant increase in apoptosis was detected in testicular tissues after exposure to 100 and 200 pulses of intensity 200kV/m; however, with 400 pulses we observed the degeneration and shrinkage of testicular tissues along with a significant increase in apoptotic rate. Moreover, in the 100- and 200-EMP groups, a non-significant increase in TGF-β3 mRNA and protein expression was observed, whereas in the 400-EMP group a significant increase was observed (P < 0.05). These results indicate that increase in the apoptotic rate of testicular tissues and increase in TGF-β3 expression may be one of the mechanisms for EMP-induced increase in BTB permeability in mice.Toxicology 05/2013; · 4.02 Impact Factor