期刊
MOLECULAR REPRODUCTION AND DEVELOPMENT
卷 78, 期 2, 页码 69-79出版社
WILEY
DOI: 10.1002/mrd.21268
关键词
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资金
- Council of Scientific and Industrial Research (CSIR), New Delhi, India
- National Institute of Health and Family Welfare (NIHFW), New Delhi
The mechanism of H2O2 induced oxidative stress leading to male germ cell apoptosis was earlier reported from our laboratory. In the present study, we investigated the mechanisms by which N-acetyl-L-cysteine (NAC, which is highly cell specific with strong antioxidant and anti-genotoxic properties), stimulated cell survival under such conditions. Co-incubation with 5mM NAC significantly (P < 0.001) reduced the germ cell apoptosis induced by 10 mu M H2O2. Lipid peroxidation was brought down with significant restoration of activities of antioxidant enzymes, SOD, GST, and catalase. Expression of pro-apoptotic marker, Bax up-regulated following H2O2 exposure, was reversed back to control levels. In contrast, expression of anti-apoptotic Bcl-2 and phospho-Akt revealed a completely opposite trend. While caspase-8 activity remained unaffected, NAC successfully attenuated the increased activities of caspase-3 and -9 in the H2O2 treated cells. Simultaneously, the increased expression of caspase-9, phospho-JNK, and phospho-c-Jun after H2O2 treatment was down-regulated by NAC. The above findings indicate that the mechanism of inhibition of H2O2 induced male germ cell apoptosis by NAC is mediated through regulation of caspase-9 and JNK. Mol. Reprod. Dev. 78: 69-79, 2011. (c) 2010 Wiley-Liss, Inc.
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