Journal of Andrology
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Published-Ahead-of-Print August 23, 2006, DOI:10.2164/jandrol.106.000265

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Induction of oxidative stress by organic hydroperoxides in testis and epididymal sperm of rats in vivo

Thimappa R. Rajeshkumar and - Muralidhara *

* To whom correspondence should be addressed. E-mail: mura16{at}yahoo.com.

Abstract The present study describes the extent and pattern of oxidative stress induction in testis and epididymal sperm of rats following in vivo exposure to repeated sub-lethal doses of two model prooxidants viz., t-butyl hydroperoxide (tbHP) and cumene hydroperoxide (cHP). Single sub-lethal (1/40, 1/20 and 1/10 LD50) doses of hydroperoxides (HP) administered intraperitoneally to male rats (CFT- Wistar strain) failed to induce any significant increase in malondialdehyde or reactive oxygen species (ROS) levels in testis or epididymal sperm. However, repeated doses for 1 or 2 weeks induced a marked dose-related enhancement of lipid peroxidation (LPO) and ROS levels in both testis and epididymal sperm. Further evidences such as significant perturbations in both enzymic/ non-enzymic antioxidants and enhanced levels of protein carbonyls in testis suggested induction of oxidative stress. In testis, moderate depletion in reduced glutathione levels and marked diminution in ascorbic acid and a-tocopherol content were accompanied by increased activities of various antioxidant enzymes viz., glutathione peroxidase, glutathione- S-transferse and catalase in both the HP treatments. Furthermore, significant alterations in the specific activities of testicular enzymes such as LDH-X, G-6-PDH, and SDH indicated altered testicular physiology. Both HP at higher doses induced a significant DNA damage (determined by FADU assay) in testis and epididymal sperm. Increased total iron levels in testis of HP treated rats are indicative of the possible involvement of iron-mediated free radical reactions in this model. These findings provide an account of early oxidative damage in testis and epididymal sperm following short-term exposure to HP in vivo and this model is being further exploited for understanding the consequences of chronic oxidative stress-mediated alterations on the physiology of male reproductive system and its implications on fertility.


Key words: Epididymis • Sperm • Testis • DNA damage • Lipid peroxidation • Organic hdroperoxides • Oxidative stress • ROS levels






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