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H2O2 at physiological concentrations modulates Leydig cell function inducing oxidative stress and apoptosis.

Authors: Gautam, DK  Misro, MM  Chaki, SP  Sehgal, N 
Citation: Gautam DK, etal., Apoptosis. 2006 Jan;11(1):39-46.
Pubmed: (View Article at PubMed) PMID:16374549
DOI: Full-text: DOI:10.1007/s10495-005-3087-1

H(2)O(2) is one of the active reactive oxygen species secreted by macrophages that are seen closely aligned with Leydig cells in the testicular interstitium. The present study was initiated to investigate the role of H(2)O(2) on Leydig cell function in vitro at physiological concentrations. Significant decrease in both testosterone production (p < 0.05) and 3 beta-hydroxysteroid dehydrogenase activity (p < 0.05) in adult Leydig cells were observed even with H(2)O(2) at low concentrations (30 - 50 microM). H(2)O(2) exposure increased oxidative stress in Leydig cells with the rise in lipid peroxidation and fall in the activities of the antioxidant enzymes; superoxide dismutase (SOD), catalase (CAT) & glutathione-s-transferase (GST). There was also a marginal increase (approximately 8%) in cell apoptosis accompanied by rise in FasL expression and caspase-3 activation. The above findings indicate that H(2)O(2) as a bio-molecule modulates Leydig cell function at or below physiological concentrations through a variety of actions like decrease in steroidogenic enzyme activity and increase in oxidative stress and apoptosis.

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CRRD Object Information
CRRD ID: 4889541
Created: 2010-12-06
Species: All species
Last Modified: 2010-12-06
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.