Protection against vanadium-induced testicular toxicity by testosterone propionate in rats.
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.
Endocrinology & Reproductive Physiology Laboratory, Department of Physiology, University of Calcutta, 92 Acharya Prafulla Chandra Road, Kolkata, West Bengal, India. amark_chandra@yahoo.co.in
Amar K
AK
Chandra
Rituparna
R
Ghosh
Aparajita
A
Chatterjee
Mahitosh
M
Sarkar
D015067:17-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D004797:Enzyme-Linked Immunosorbent Assay; D005640:Follicle Stimulating Hormone / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013076:Sperm Count; D013737:Testis / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D013739:Testosterone / Q000097:blood; D043343:Testosterone Propionate / Q000494:pharmacology*; D014018:Tissue Distribution; D014638:Vanadates / Q000493:pharmacokinetics / Q000633:toxicity*
D000975:Antioxidants; D014638:Vanadates; D013739:Testosterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D015067:17-Hydroxysteroid Dehydrogenases; D015096:3-Hydroxysteroid Dehydrogenases; C031954:delta(5)-3 beta-hydroxysteroid dehydrogenase; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase; D043343:Testosterone Propionate