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Induction of oxidative stress by organic hydroperoxides in testis and epididymal sperm of rats in vivo.
J Androl. 2007 Jan-Feb; 28(1):77-85.JA

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 sublethal doses of 2 model pro-oxidants, namely, t-butyl hydroperoxide (tbHP) and cumene hydroperoxide (cHP). Single sublethal (1/40, 1/20, and 1/10 LD(50)) 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 evidence, such as significant perturbations in both enzymic and nonenzymic 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 alpha-tocopherol content were accompanied by increased activities of various antioxidant enzymes, namely glutathione peroxidase, glutathione-S-transferase, 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 significant DNA damage (determined by fluorimetric analysis of DNA unwinding 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 for the physiology of male reproductive system and its implications for fertility.

Authors+Show Affiliations

Scientist, Department of Biochemistry & Nutrition, CFTRI, Mysore-570 020, India.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16928893

Citation

Kumar, Thimmappa R., and Muralidhara. "Induction of Oxidative Stress By Organic Hydroperoxides in Testis and Epididymal Sperm of Rats in Vivo." Journal of Andrology, vol. 28, no. 1, 2007, pp. 77-85.
Kumar TR, Muralidhara . Induction of oxidative stress by organic hydroperoxides in testis and epididymal sperm of rats in vivo. J Androl. 2007;28(1):77-85.
Kumar, T. R., & Muralidhara, . (2007). Induction of oxidative stress by organic hydroperoxides in testis and epididymal sperm of rats in vivo. Journal of Andrology, 28(1), 77-85.
Kumar TR, Muralidhara . Induction of Oxidative Stress By Organic Hydroperoxides in Testis and Epididymal Sperm of Rats in Vivo. J Androl. 2007 Jan-Feb;28(1):77-85. PubMed PMID: 16928893.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Induction of oxidative stress by organic hydroperoxides in testis and epididymal sperm of rats in vivo. AU - Kumar,Thimmappa R, AU - Muralidhara,, Y1 - 2006/08/23/ PY - 2006/8/25/pubmed PY - 2007/3/22/medline PY - 2006/8/25/entrez SP - 77 EP - 85 JF - Journal of andrology JO - J. Androl. VL - 28 IS - 1 N2 - 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 sublethal doses of 2 model pro-oxidants, namely, t-butyl hydroperoxide (tbHP) and cumene hydroperoxide (cHP). Single sublethal (1/40, 1/20, and 1/10 LD(50)) 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 evidence, such as significant perturbations in both enzymic and nonenzymic 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 alpha-tocopherol content were accompanied by increased activities of various antioxidant enzymes, namely glutathione peroxidase, glutathione-S-transferase, 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 significant DNA damage (determined by fluorimetric analysis of DNA unwinding 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 for the physiology of male reproductive system and its implications for fertility. SN - 0196-3635 UR - https://www.unboundmedicine.com/medline/citation/16928893/Induction_of_oxidative_stress_by_organic_hydroperoxides_in_testis_and_epididymal_sperm_of_rats_in_vivo_ L2 - https://doi.org/10.2164/jandrol.106.000265 DB - PRIME DP - Unbound Medicine ER -