Bisphenol A Induces Hepatotoxicity through Oxidative Stress in Rat Model

Oxidative Medicine and Cellular Longevity - Tập 2012 - Trang 1-6 - 2012
Zeinab Hassan1,2, Mai Elobeid2, Promy Virk2, Sawsan A. Omer2, Maha H. Elamin2, Maha H. Daghestani2, Ebtisam M. Al-Olayan2
1Cancer Biology Department, National Cancer Institute, Cairo University, Cairo 11796, Egypt
2Zoology Department, College of Science, King Saud University, Riyadh 11451, Saudi Arabia

Tóm tắt

Reactive oxygen species (ROS) are cytotoxic agents that lead to significant oxidative damage. Bisphenol A (BPA) is a contaminant with increasing exposure to it and exerts both toxic and estrogenic effects on mammalian cells. Due to limited information concerning the effect of BPA on liver, this study investigates whether BPA causes hepatotoxicity by induction of oxidative stress in liver. Rats were divided into five groups: The first four groups, BPA (0.1, 1, 10, 50 mg/kg/day) were administrated orally to rats for four weeks. The fifth group was taken water with vehicle. The final body weights in the 0.1 mg group showed a significant decrease compared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase activity were found in the 50 mg BPA group compared to control groups. High dose of BPA (50 mg/kg) significantly increased the biochemical levels of ALT, ALP and total bilirubin. BPA effect on the activity of antioxidant genes was confirmed by real time PCR in which the expression levels of these genes in liver tissue were significantly decrease compared to control. Data from this study demonstrate that BPA generate ROS and reduce the antioxidant gene expression that causes hepatotoxicity.

Từ khóa


Tài liệu tham khảo

10.1289/ehp.11579

10.1097/MED.0b013e32830ce95c

10.1080/10937400701724303

10.1016/j.reprotox.2007.05.008

10.1016/j.fct.2010.07.019

10.1038/sj.bjp.0705520

10.1210/en.2006-0561

10.1093/toxsci/68.1.121

10.1002/bdrb.20155

10.1093/toxsci/kfq025

10.1016/S0013-9351(03)00062-8

10.1080/10715769900300841

10.1016/S0300-483X(03)00056-8

10.1016/j.lfs.2003.07.060

2010, Oxidative Medicine and Cellular Longevity, 3, 428, 10.4161/oxim.3.6.14416

2011, PLoS ONE, 6

1974, Journal of Biological Chemistry, 249, 7130, 10.1016/S0021-9258(19)42083-8

10.1006/niox.2000.0319

10.1136/jcp.54.5.356

1976, Analytical Biochemistry, 72, 248, 10.1016/0003-2697(76)90527-3

10.1016/S0890-6238(03)00103-5

10.1002/bdrb.20147

10.1007/s00204-001-0319-1

10.1016/S0300-483X(02)00160-9

10.1016/j.brainresbull.2004.11.013

10.1016/j.aquatox.2004.04.004

10.1074/jbc.272.30.18515

10.1007/s11010-005-6630-z

2011, Environmental Toxicology and Chemistry, 30, 2335, 10.1002/etc.634

10.1007/s00204-002-0372-4

10.1016/j.tox.2008.04.002

10.3109/01480540903286468

10.4161/oxim.3.4.12714

1965, The Biochemical Journal, 95, 35, 10.1042/bj0950035

2004, Oncology Reports, 12, 921

10.1016/j.tox.2005.02.013

10.1089/152308604322899350

10.1016/0304-4165(93)90011-V

10.1074/jbc.271.23.13422

Thông tin
Thông tin xuất bản

Oxidative Medicine and Cellular Longevity

Tập 2012

1-6

Thông tin tác giả