Format

Send to

Choose Destination
See comment in PubMed Commons below
Toxicol In Vitro. 2012 Sep;26(6):841-8. doi: 10.1016/j.tiv.2012.04.028. Epub 2012 May 8.

Polychlorinated biphenyl quinone metabolites lead to oxidative stress in HepG2 cells and the protective role of dihydrolipoic acid.

Author information

1
Key Laboratory of Luminescence and Real-Time Analysis, Ministry of Education, College of Pharmaceutical Sciences, Southwest University, Chongqing 400715, People's Republic of China.

Abstract

Parent polychlorinated biphenyls (PCBs) have been shown to induce cellular oxidative stress. However, the effects of PCB active metabolites have not been extensively investigated. Parent PCBs are first converted to hydroquinone metabolites via cytochrome P-450-catalyzed hydroxylation, and the hydroquinone metabolites are then further oxidized into the corresponding quinone metabolites. Quinones are responsible for a wide range of toxic effects because of their high reactivity. Previous studies have suggested that reactive oxygen species (ROS) play important roles in multiple toxic mechanisms. In this context, the present study was undertaken to investigate oxidative stress resulting from treatment with PCB quinones in HepG2 cells. The protective effects resulting from co-administration of dihydrolipoic acid (DH-LA) were also investigated. We have found that exposure to PCB quinones leads to: (1) a decrease in cell viability; (2) an increase in both the total ROS production and superoxide production; (3) only 3Cl-PCBQ caused significant increase in the thiobarbituric acid reactive substances (TBARS) level; (4) an increase in SOD activity and a decrease in catalase activity; and (5) a decrease in GST activity and GSH level. We have also found that quinones possessing a higher number of chlorine atoms on the quinone ring display a greater activity and that DH-LA is an effective protective agent as it diminishes PCB quinone-induced cellular oxidative stress.

PMID:
22580158
DOI:
10.1016/j.tiv.2012.04.028
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center