Vitamin E-supplementation protect chromium (VI)-induced spermatogenic and steroidogenic disorders in testicular tissues of rats.
Excess chromium (Cr) exposure is associated with various pathological conditions including reproductive dysfunction. Generation of oxidative stress is one of the plausible mechanisms behind Cr induced cellular deteriorations. The efficacy of vitamin E to combat Cr induced oxidative damage in adult rat testis has investigated in the current study. Adult male rats exposed to hexavalent Cr (intraperitoneal injection with 0.4 mg K(2)Cr(2)O(7)/ kg bw/day) for 26 days resulted in decreased accessory sex organs weight compared to controls. Development of oxidative stress in testis was evidenced by increased lipid peroxidation along with decreased superoxide dismutase (SOD) and catalase activities than control animals. Marked reduction in the activities of testicular steroidogenic enzymes; Delta(5)3beta-hydroxysteroid dehydrogenase (HSD), 17beta-HSD, serum testosterone and Leutinizing Hormone (LH) levels were observed. However significant increase in serum Follicle Stimulating Hormone (FSH) level was observed with Cr treated group. Histological evaluation of testis revealed degeneration of stage VII spermatogenic cycle along with decrease in epithelial cell height in epididymis and seminiferous tubules; number of different germ cells per seminiferous tubule and seminiferous tubular diameter reduced after Cr exposure. Simultaneous oral supplementation of vitamin E (50mg/kg bw/day) in Cr exposed rats showed less oxidative damage and restored the otherwise altered testicular activities. Epididymal sperm number was also restored in vitamin E-supplemented group than Cr induced rats. This study implicates vitamin E as a possible protective agent against Cr induced spermatogenic and steroidogenic alteration.
Chandra
Amar K
AK
Department of Physiology, Endocrinology and Reproductive Physiology Laboratory, University of Calcutta, Kolkata, West Bengal, India. amark_chandra@yahoo.co.in
Chatterjee
Aparajita
A
Ghosh
Rituparna
R
Sarkar
Mahitosh
M
D015067:17-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D002857:Chromium / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D004797:Enzyme-Linked Immunosorbent Assay; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013076:Sperm Count; D013256:Steroids / Q000096:biosynthesis*; D013482:Superoxide Dismutase / Q000378:metabolism; D013733:Testicular Diseases / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D013737:Testis / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D013739:Testosterone / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology*
D000975:Antioxidants; D013256:Steroids; D017392:Thiobarbituric Acid Reactive Substances; D002857:Chromium; D014810:Vitamin E; D013739:Testosterone; D015067:17-Hydroxysteroid Dehydrogenases; D015096:3-Hydroxysteroid Dehydrogenases; D002374:Catalase; D013482:Superoxide Dismutase