铁代谢紊乱和其它致病因素介导的肝氧化损伤及抗氧化保护策略研究进展

Progress on Hepatic Oxidative Damage Mediated by Iron Homeostasis Disregulation and Other Detrimental Factors and Antioxidative Protection Strategy

铁是人体所必需的微量元素,独特的化学活性使其成为血红蛋白和多种酶类的重要组成部分,同时,铁也可以催化产生各种自由基分子。作为铁的主要储存器官,肝脏在维持机体铁稳态中起着中心枢纽作用。当肝脏发生铁调节紊乱或者受到各种肝脏致病因素(丙型肝炎病毒、乙型肝炎病毒和酒精)侵袭时,都会造成自由基分子的过量生成。若机体的抗氧化防御系统不能将这些自由基及时清除,将会导致氧化应激损伤介导的肝损伤。目前的研究表明,针对肝脏疾病患者进行去铁及抗氧化治疗是一种有效的治疗模式。因此,研究肝脏铁代谢及各种肝脏疾病致病因素引起的氧化应激具有重要的理论和临床意义。

Iron is an essential metal in human nutrition. The unique activities of iron make it an important component of hemoglobin and various enzymes. However, excess iron can damage tissues by catalyzing the conversion of hydrogen peroxide to hydroxyl radicals, via the so-called Fenton reaction. The resulting free radicals would attack cell membranes, proteins, and DNA. As the major iron storage organ, liver plays a central role in maintenance of human iron homeostasis. Genetic disorder of iron metabolism in liver or external factors （i.e. infections of hepatitis C virus, hepatitis B virus and over-consumption of alcohol） will result in over-production of reactive oxygen species （ROS）. The excess ROS would lead to oxidative stress and consequently result liver damage. Clinical studies have showed that patients with liver diseases administered with iron chelators or antioxidants may be effective treatment modalities. Therefore, study of iron metabolism and liver oxidative stress caused by iron overload or association with other risk factors will be of great clinical significance.