Please use this identifier to cite or link to this item: http://nopr.niscpr.res.in/handle/123456789/4564
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dc.contributor.authorVerma, Yeshvandra-
dc.contributor.authorRana, S V S-
dc.date.accessioned2009-06-15T11:29:51Z-
dc.date.available2009-06-15T11:29:51Z-
dc.date.issued2008-08-
dc.identifier.issn0975-1009 (Online); 0019-5189 (Print)-
dc.identifier.urihttp://hdl.handle.net/123456789/4564-
dc.description568-572en_US
dc.description.abstractBilateral castration increased lipid peroxidation and consequently reduced glutathione in both liver and kidney. Testosterone administration reduced lipid peroxidation in the liver of castrated and benzene treated rats, however, reduced glutathione status could not be restored. Benzene depleted CYP4502E1 in castrated rats, however, the enzyme was restored in liver and kidney both after testosterone treatment. The results suggest that testosterone affects the metabolism and disposition of benzene by influencing CYP4502E1. Other hormonal and cellular/molecular factors may also alter the actions of testosterone. Testosterone dependent mechanism of toxicity of benzene in the liver and kidney has been discussed.en_US
dc.language.isoen_USen_US
dc.publisherCSIRen_US
dc.sourceIJEB Vol.46(08) [August 2008]en_US
dc.subjectBenzeneen_US
dc.subjectCastrationen_US
dc.subjectGSHen_US
dc.subjectKidneyen_US
dc.subjectLiveren_US
dc.subjectLipid peroxidationen_US
dc.subjectTestosteroneen_US
dc.titleModulation of CYP4502E1 and oxidative stress by testosterone in liver and kidney of benzene treated ratsen_US
dc.typeArticleen_US
Appears in Collections:IJEB Vol.46(08) [August 2008]

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