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
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Publication
Data
Paper received:
25 March 2014
Revised received:
01 December 2014
Accepted:
25 February 2015
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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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