Liu Xiang-Tao, Hu Jian
Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing 100083, China.
World J Gastroenterol. 2002 Jun;8(3):413-7. doi: 10.3748/wjg.v8.i3.413.
In this paper, we summarize the main progresses made in our group in the field of the mechanism of pigment gallstone formation. It was found that after treatment with free radicals, bilirubin (BR) was changed into free radical itself, and a semiquinone free radical and a superoxide free radical bound with metal were recognized, which was detected by ESR (electron spin resonance). By the means of NMR (nuclear magnetic resonance) and IR (Infra-red spectra), it was postulated that bilirubin polymerized through the reaction between the vinyl group and the hydroxyl group under the attack of free radicals. It was also found that bilirubin free radical were liable to calcify in a kinetic study. Because of its chemical properties, bilirubin free radical was shown to be cytotoxic to hepatocyte, which was demonstrated based on the following facts: induction of phospholipid peroxidation (LPO), leakage of lactate dehydrogenase (LDH) and decrease of glutathione. As to the mechanism of bilirubin-induced cytotoxicity, it was postulated that the main target of bilirubin free radical was the cell membrane, including phospholipid and membrane bound proteins, especially spectrin, a content of cytoskeleton. Based on the results mentioned above, it was deduced that bilirubin free radical is the key factor that initiates and promotes the formation of pigment gallstone, which is consistent with other researches in recent years.
在本文中,我们总结了本研究小组在色素胆结石形成机制领域取得的主要进展。研究发现,胆红素(BR)经自由基处理后自身转变为自由基,通过电子自旋共振(ESR)检测到一种半醌自由基和一种与金属结合的超氧自由基。借助核磁共振(NMR)和红外光谱(IR)推测,胆红素在自由基攻击下通过乙烯基与羟基之间的反应发生聚合。在动力学研究中还发现胆红素自由基易于钙化。基于其化学性质,胆红素自由基对肝细胞具有细胞毒性,这基于以下事实得以证明:诱导磷脂过氧化(LPO)、乳酸脱氢酶(LDH)泄漏以及谷胱甘肽减少。关于胆红素诱导细胞毒性的机制,推测胆红素自由基的主要靶点是细胞膜,包括磷脂和膜结合蛋白,尤其是细胞骨架成分血影蛋白。基于上述结果推断,胆红素自由基是启动和促进色素胆结石形成的关键因素,这与近年来的其他研究结果一致。