ale Wistar Rats were treated with Endotoxin（Lipopolysacchride

LPS）by intraperitonealinjection（2mg/kg body welght）.Liver mitochondria damage and lipid peroxidation were investigatedat a tune course of 4、14、24、48 hrs followed Succinate dehydrogenase（SDH）activity decreasedmarkedly at 14-24 hr after LPS administration

thereafter tending to recover. The mitocondrialipoperox oxide level（expressed by Malonaldehyde fromed） elevated at 4 hr to 173.2% of thecontrol’s

but retruned to normal range after 48hrs

Superoxide dismutase （SOD）and glutathioneperoxidase（GSH-PX）activities in liver mitochondrla decreased initially and tended to increasethereafter.In coincidence with biocnemlcal alteration

electronic micrographs showed a markedhepatocyte damage at 14-24hr after LPS adininistration. Biochemical results and detectionmicrographs suggest that; 1)at the experunental LPS dose

hepatic injury was apparent butreversible

and mitochondria was one of the major organella attacked by LPS

2)SOD and GSH-PXactivities change suggested to be an induced effect

and put out previous studies together

weconsidered 3)lipid peroxidation and PLA

2

activation are two initial key steps leading to membranedamage and they play an important role in the interacting mechanism of liver toxicity induced byLPS.