Nicotine diminishes testicular gametogenesis, steroidogenesis, and steroidogenic acute regulatory protein expression in adult albino rats: possible influence on pituitary gonadotropins and alteration of testicular antioxidant status.
The present study was done to evaluate the pituitary-testicular activities of rats subjected to chronic nicotine treatment. The testicular key androgenic enzymes activities, plasma and intratesticular testosterone (ITT) concentrations, and plasma concentration of gonadotropin were significantly reduced by nicotine treatment along with the decreased sperm counts and the disruption of spermatogenesis indicated by significant reduction in the number of different generations of germ cells at stage VII of the spermatogenesis cycle with increased sperm head abnormalities. The Western blot and the reverse transcriptase-PCR analysis revealed that the nicotine induced a marked decrease in the expression of testicular steroidogenic acute regulatory (StAR) protein, which helps in the transfer of cholesterol in mitochondria for the testosterone biosynthesis. The increased testicular lipid peroxidation, plasma concentration of corticosterone, with enhanced hydrogen peroxide and hydroxyl radical generations, as well as decreased glutathione level, reduced antioxidant enzymes activities, and mitochondrial membrane potential (Deltapsi(m)) of testis, were noted after nicotine treatment in rats. Human chorionic gonadotropin or taurine supplementation with nicotine prevented the degeneration of germ cells to some extent, restored spermatogenesis moderately with decreased sperm head abnormalities, and enhanced sperm counts, accompanied with increase in plasma and ITT concentrations, testicular StAR gene expression, and key androgenic enzymes activities. Moreover, taurine supplementation to nicotine-treated animals resulted in the diminution of testicular lipid peroxidation, hydrogen peroxide and hydroxyl radical generations, with the elevation in glutathione level as well as different antioxidant enzymes activities and Deltapsi(m) in testis. The results indicated that nicotine caused testicular toxicity by germ cell degeneration, inhibition of StAR gene expression along with androgen production in adult male rats probably by affecting pituitary gonadotropin, and/or modulating the extent of testicular antioxidant status.
Jana
Kuladip
K
Department of Surgery and Radiology, Faculty of Veterinary and Animal Sciences, West Bengal University of Animal and Fishery Sciences, Kolkata 700037, India. kuladip@bic.boseinst.ernet.in
Samanta
Prabhat Kumar
PK
De
Dipak Kumar
DK
D015067:17-Hydroxysteroid Dehydrogenases / Q000235:genetics; D015096:3-Hydroxysteroid Dehydrogenases / Q000235:genetics; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood; D004435:Eating / Q000187:drug effects; D006065:Gonadotropins, Pituitary / Q000097:blood*; D015227:Lipid Peroxidation; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D009538:Nicotine / Q000633:toxicity*; D009929:Organ Size / Q000187:drug effects; D010750:Phosphoproteins / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013076:Sperm Count; D013091:Spermatogenesis / Q000187:drug effects*; D013737:Testis / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013739:Testosterone / Q000096:biosynthesis / Q000097:blood; D000098682:Steroidogenic Acute Regulatory Protein
D000975:Antioxidants; D006065:Gonadotropins, Pituitary; D010750:Phosphoproteins; D017382:Reactive Oxygen Species; D000098682:Steroidogenic Acute Regulatory Protein; D013739:Testosterone; D009538:Nicotine; D015067:17-Hydroxysteroid Dehydrogenases; D015096:3-Hydroxysteroid Dehydrogenases; D003345:Corticosterone