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Adjudin‐mediated germ cell depletion alters the anti‐oxidant status of adult rat testis
Author(s) -
Sarkar Oli,
Mathur P.P.
Publication year - 2009
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20928
Subject(s) - biology , androgen binding protein , oxidative stress , reactive oxygen species , superoxide dismutase , catalase , medicine , sertoli cell , glutathione peroxidase , endocrinology , spermatogenesis , glutathione , andrology , germ cell , biochemistry , enzyme , gene
Successful spermatogenesis is dependent on the proper attachment of developing germ cells to Sertoli cells. Manipulation of these interactions by drugs like Adjudin can hamper the development of germ cells and lead to conditions of temporary infertility. Although studies have shown the contraceptive potential of Adjudin, much is not known about its action in the testis. In this study, we sought to investigate the effect of Adjudin on the oxidative status of mammalian testis. Adult male rats were administered with a single dose of Adjudin (50 mg/kg body weight) by oral gavage and were killed at 1, 2, 4, 7, 15, or 30 days of treatment. Adjudin caused a significant increase in the production of hydrogen peroxide and lipid peroxidation from 4 to 7 days after treatment. There was a significant decrease in the activities of anti‐oxidant enzymes superoxide dismutase, catalase, glutathione peroxidase and glutathione S ‐transferase from 4 to 7 days after treatment with Adjudin. However, the state of oxidative stress was less pronounced from 15 to 30 days after Adjudin treatment. The level of androgen binding protein (ABP) remained unchanged following Adjudin treatment. These results show that there is an induction of oxidative stress accompanying adherens junction restructuring which suggests a role for reactive oxygen species in the regulation of these testicular junctions. However, transient elevation in reactive oxygen species levels did not affect androgen transport. Mol. Reprod. Dev. 76: 31–37, 2009. © 2008 Wiley‐Liss, Inc.