Halliwell B
Department of Biochemistry, University of London King's College, UK.
FASEB J. 1987 Nov;1(5):358-64.
Oxidant species such as superoxide radical (O.2-), hydrogen peroxide (H2O2), hydroxyl radical (HO.), and lipid peroxides (LOOH) are becoming increasingly implicated in human disease. However, the question of whether such oxidants are a major cause of tissue injury in human disease or are merely produced during such injury has been difficult to answer because of inadequate experimental techniques, and possibly because of an overemphasis on lipid peroxidation as a mechanism of oxidant injury. Recent developments in methodology, in our understanding of the primary mechanism of oxidant toxicity to cells, and in concepts of antioxidant protection are reviewed. Good evidence now exists for some role of oxidant damage to tissues in the pathology of several human diseases, including rheumatoid arthritis, reperfusion injury, immune injury to lung and kidney, and cerebral trauma or ischemia. These have led to promising suggestions for new therapeutic approaches.
诸如超氧阴离子自由基(O₂⁻)、过氧化氢(H₂O₂)、羟自由基(HO·)和脂质过氧化物(LOOH)等氧化物种越来越多地与人类疾病相关。然而,由于实验技术不足,也可能是由于过度强调脂质过氧化作为氧化损伤机制,这些氧化剂是人类疾病中组织损伤的主要原因还是仅仅在这种损伤过程中产生,这个问题一直难以回答。本文综述了方法学的最新进展、我们对氧化剂对细胞毒性的主要机制的理解以及抗氧化保护的概念。现在有充分的证据表明,氧化损伤在包括类风湿性关节炎、再灌注损伤、肺和肾的免疫损伤以及脑外伤或缺血在内的几种人类疾病的病理学中对组织起到了一定作用。这些发现为新的治疗方法带来了有前景的建议。