Chemical toxicity and reactive oxygen species.
Chemical toxicity and reactive oxygen species.
复制标题
化学毒性和活性氧。
DOI：
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发表时间：
1996
影响因子：
2
通讯作者：
A. Sapota
中科院分区：
文献类型：
--
作者：
Parke Dv;A. Sapota
活性氧（ROS）具有细胞毒性，可引起炎症性疾病，包括组织坏死、器官衰竭、动脉粥样硬化、不孕症、出生缺陷、早衰、突变和恶性肿瘤。在药物和工业化学品的代谢过程中，ROS通过(i)单电子过氧化物酶氧化形成阳离子自由基，（ii）细胞色素P450代谢为自由基产物，（iii） ROS生成器CYP2E1的稳定，以及（iv）其他细胞色素P450的无效循环产生。ROS的产生引发炎症，如果不加以抑制，可能导致慢性炎症疾病状态，如肝炎、肾炎、肌炎、硬皮病、红斑狼疮、多系统器官衰竭。ROS的猝灭受氧化还原缓冲液、谷胱甘肽（GSH）、抗氧化剂、抗坏血酸、生育酚、类维生素a以及氧化还原酶、谷胱甘肽还原酶、谷胱甘肽过氧化物酶、过氧化氢酶和超氧化物歧化酶的影响。许多因接触有毒化学品而出现全身性炎症症状的工业工人被诊断为患有类风湿关节炎、病毒感染或其他微生物病变，这主要是因为许多医生不知道接触某些化学品会引发炎症性疾病状态。
Reactive oxygen species (ROS) are cytotoxic, causing inflammatory disease, including tissue necrosis, organ failure, atherosclerosis, infertility, birth defects, premature aging, mutations and malignancy. ROS are produced in the metabolism of drugs and industrial chemicals by (i) one-electron peroxidase oxidations to form cation radicals, (ii) cytochrome P450 metabolism to free radical products, (iii) stabilisation of the ROS-generator, CYP2E1, and (iv) futile cycling of other cytochromes P450. ROS production initiates inflammation which unless quenched may result in chronic inflammatory disease states, e.g. hepatitis, nephritis, myositis, scleroderma, lupus erythematosus, multiple system organ failure. Quenching of ROS is affected by the redox buffer, glutathione (GSH), and the antioxidants, ascorbic acid, tocopherols, retinoids, in conjunction with the redox enzymes, GSH reductase, GSH peroxidase, catalase and superoxide dismutase. Many industrial workers with symptoms of systemic inflammation, resulting from exposure to toxic chemicals, are diagnosed as having rheumatoid arthritis, virus infections, or other microbial lesions, largely because many physicians are unaware that exposure to certain chemicals can initiate inflammatory disease states.