Tokyay R, Kaya E, Gur E S, Tuncel P, Ozbek R, Ozturk E
Department of Surgery, Uludag University Medical School, Bursa, Turkey.
Surg Today. 1999;29(1):42-6. doi: 10.1007/BF02482968.
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.
本研究旨在确定前列腺素代谢是否导致腹膜炎诱导的早期肝脏氧化应激。脂质过氧化产物丙二醛（MDA）和共轭二烯（CD）用于监测氧化应激。给大鼠腹腔注射5毫升25%大鼠粪便悬液，然后腹腔注射生理盐水（腹膜炎组，n = 11）、维生素E（n = 6）或双氯芬酸（n = 6）。3小时后测量肝脏和血浆中的MDA和CD水平。腹膜炎组的血浆和肝脏MDA及CD水平显著高于对照组（n = 9）。前列腺素合成酶抑制剂（双氯芬酸）使肝脏和血浆中的MDA及CD保持在对照水平。因此发现抗氧化剂α生育酚（维生素E）在降低这些升高的MDA和CD水平方面无效。腹膜炎诱导的肝脏早期氧化应激似乎是由环氧化酶途径的非氧化依赖性激活介导的。
