Prostaglandin synthetase inhibition reduces peritonitis-induced early liver oxidant stress.

Abstract

This study was undertaken to determine whether or not the prostanoid metabolism contributes to peritonitis-induced early liver oxidant stress. Lipid peroxidation products, malondialdehyde (MDA) and conjugated dienes (CD), were used to monitor oxidant stress. The rats were given a 5-cc intraperitoneal (i.p.) injection of 25% rat feces suspension and then received either i.p. saline (peritonitis group, n = 11), vitamin E (n = 6), or diclofenac (n = 6). The liver and plasma MDA and CD levels were measured after 3 h. The plasma and liver MDA and CD levels were significantly higher in the peritonitis group than in the control (n = 9). Prostaglandin synthetase inhibitor (diclofenac) kept the liver and plasma MDA and CD at control levels. Antioxidant alpha tacopherol (vitamin E) was thus found not to be effective in reducing these increased MDA and CD levels. Peritonitis-induced early oxidant stress in the liver seems to be mediated by the oxidant-independent activation of the cyclooxygenase pathway.