کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2595077 | 1132289 | 2006 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats](/preview/png/2595077.png)
Microbial infections, localized as well as systemic, are known to cause transitive or permanent male infertility. However, the mechanisms of infection-induced infertility are largely unknown. Earlier reports showed that steroidogenesis and spermatogenesis are affected during bacterial lipopolysaccharide (LPS)-induced acute inflammation. The present study used an LPS rat model to investigate the role of oxidative stress in spermatogenesis. Intraperitoneal administration of bacterial LPS (5 mg/kg body weight) to adult male albino rats elevated testicular malondialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE), and decreased the activities of testicular antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. The GSH/GSSG ratio also decreased significantly. Time series analysis revealed transitory oxidative stress and expression of inflammatory mediators such as interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) from 3 h to 12 h after LPS. Testicular expression of steroidogenic acute regulatory (StAR) protein decreased to 24 h, in correlation with damage to spermatogenesis. These data are consistent with oxidative stress as a major causal factor in altered steroidogenesis, spermatogenesis, and perhaps male infertility during endotoxin-induced acute inflammation.
Journal: Reproductive Toxicology - Volume 22, Issue 3, October 2006, Pages 493–500