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Journal of Environmental Biology

pISSN: 0254-8704 ; eISSN: 2394-0379 ; CODEN: JEBIDP

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    Abstract - Issue May 2015, 36 (3)                                     Back


nstantaneous and historical temperature effects on a-pinene

Bisphenol-A induced oxidative stress and apoptosis in

kidney of male rats 

 

Mai A. Elobeid* and Zeinab K. Hassan

Department of Zoology, Center for Scientific and Medical Female Colleges, King Saud University, Riyadh-11495, Saudi Arabia

*Corresponding Author?s E-mail: maielobeid@gmail.com

 

 

 

 Publication Data

Paper received:

25 March 2014

 

Revised received:

01 December 2014

 

Accepted:

25 February 2015

 

Abstract

Bisphenol-A (BP-A) is known to be toxic to mammalian cells. The present study investigated the ability of bisphenol-A to cause nephrotoxicity via aberration in the expression of apoptotic genes and oxidative stress in male rats kidney. Four groups of male Wistar rats were orally administered bisphenol-A at a dose of 0.1, 1, 10 and 50 mg kg-1 day-1 for 4 weeks. The fifth group was given water with vehicle. Significant increase in blood urea nitrogen and creatinine levels was observed in the group administered 50 mg kg-1 day-1 as compared to other groups and control. CAT activity increased insignificantly with increasing cumulative doses (10.5?0.09, 11.1?0.46, 12.6?0.34, 16.9?0.06) as compared to control (10.5?0.12). Group exposed to 50 mg BP-A (2.27?0.03*) showed significant reduction in GSH activity. Bax (1.7 ?0.02*) and Bad (2.1 ?0.01*) genes expression levels were suppressed in the group exposed to 50 mg BP-A. BclX gene expression was not affected by BPA in all groups. Bcl2 gene expression was significantly up-regulated in group exposed to 50 mg BP-A (4.8 ?0.02*) as compared to control. The study showed that bisphenol-A induced nephrotoxicity through oxidative stress and by altering the apoptotic pathway involved. ?    

 

 

 Key words

Apoptosis, Bisphenol-A, Nephrotoxicity, Oxidative stress

 

 

 

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