DeLeve L D
Division of Gastrointestinal and Liver Disease and the USC Research Center for Liver Disease, University of Southern California School of Medicine, Los Angeles 90033, USA.
Semin Liver Dis. 1998;18(4):403-13. doi: 10.1055/s-2007-1007173.
Toxicity to nonparenchymal cells can result in disruption of the hepatic microcirculation, altered production of cytokines, and hepatic fibrosis. Many of the relevant insults produce oxidative stress or toxic metabolites that require glutathione detoxification. This article reviews the role of sinusoidal endothelial cell glutathione (GSH) in reperfusion injury, cytomegalovirus infection, and hepatic venoocclusive disease. The effects of oxidative stress and antioxidants on Kupffer cell production of cytokines and, in particular the potential benefit of antioxidants in the setting of reperfusion injury, are discussed. Oxidative stress upregulates collagen gene expression by stellate cells, and this is modulated by antioxidants. Current thinking on intrahepatic GSH and cysteine homeostasis is discussed. Finally, I review the published data on nonparenchymal GSH levels, glutathione S-transferase activity and isoenzyme pattern, and glutathione peroxidase activity.
对非实质细胞的毒性作用可导致肝微循环紊乱、细胞因子产生改变以及肝纤维化。许多相关损伤会产生氧化应激或需要谷胱甘肽解毒的毒性代谢产物。本文综述了肝血窦内皮细胞谷胱甘肽（GSH）在再灌注损伤、巨细胞病毒感染和肝静脉闭塞病中的作用。讨论了氧化应激和抗氧化剂对库普弗细胞产生细胞因子的影响，特别是抗氧化剂在再灌注损伤情况下的潜在益处。氧化应激会上调星状细胞的胶原基因表达，而抗氧化剂可对其进行调节。文中还讨论了目前关于肝内谷胱甘肽和半胱氨酸稳态的观点。最后，我回顾了已发表的关于非实质细胞谷胱甘肽水平、谷胱甘肽S -转移酶活性及同工酶模式，以及谷胱甘肽过氧化物酶活性的数据。
