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Toxicological Sciences 69, 149-156 (2002)
Copyright © 2002 by the Society of Toxicology

MOLECULAR AND GENETIC TOXICOLOGY

Tea Catechins Protect against Lead-Induced Cytotoxicity, Lipid Peroxidation, and Membrane Fluidity in HepG2 Cells

Liuji Chen*, Xianqiang Yang*, Hongli Jiao{dagger} and Baolu Zhao{dagger},1

* Department of Tea Science, Zhejiang University, Hangzhou, China 310029; and {dagger} Laboratory of Visual Information Processing, Research Centers of Brain and Cognitive Science, Institute of Biophysics, Academia Sinica, 15 Datun Road, Chaoyang District, Beijing, China 100101

Recent studies have shown that lead causes oxidative stress by inducing the generation of reactive oxygen species (ROS) and reducing the antioxidant defense system of cells. This suggests that antioxidants may play an important role in the treatment of lead poisoning as a kind of excellent scavenger of free radicals and chelator of heavy metal. Whether tea catechins have protective effects against oxidative stress after lead treatment in cell systems remains unclear. The present study was designed to elucidate if tea catechins have any protective effects on lipid peroxidation damage in lead-exposed HepG2 cells. Exposure of HepG2 cells to Pb++ decreased cell viability and stimulated lipid peroxidation of cell membranes as measured by the thioburbituric acid reaction. Electron spin resonance (ESR) spin-labeling studies indicated that lead exposure could decrease the fluidity in the polar surface of cell membranes. Tea catechin treatment significantly increased cell viability, decreased lipid peroxidation levels, and protected cell membrane fluidity in lead-exposed HepG2 cells in a concentration-dependent manner. The galloylated catechins showed a stronger effect than nongalloylated catechins. Cotreatment with (-)-epigallocatechin gallate (EGCG) and (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), and (-)-epigallocatechin gallate (EGCG) showed a synergistically protective effect. The results suggest that tea catechin supplementation may have a role to play in modulating oxidative stress in lead-exposed HepG2 cells.

Key Words: tea; catechins; lead toxicity; lipid peroxidation; antioxidants; oxidative stress; ESR spin labeling; membrane fluidity.


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