Shiraz University of Medical Sciences, Faculty of Pharmacy, P.O. Box 71345-1583, Shiraz, Iran; Department of Pharmacology, School of Medicine, P. O. Box 13145-784, Medical Sciences/University of Tehran, Tehran, Iran.
Environ Toxicol Pharmacol. 2008 Jul;26(1):1-5. doi: 10.1016/j.etap.2008.02.009. Epub 2008 Feb 29.
Paraquat (PQ) is a relatively safe and effective herbicide used all over the world. PQ is very toxic to all living organisms; and many cases of acute poisoning and death have been reported over the past decade. The main suggested potential mechanism for PQ toxicity is the production of superoxide radicals from the metabolism of the PQ by microsomal enzyme systems, and by inducing mitochondrial toxicity. Mitochondria are considered to be a major source of reactive oxygen species in cells and according to this hypothesis, PQ, through suitable oxidation and reduction processes, is able to participate in the redox system in mitochondria. The potential ability of PQ to accept electrons from complex (I, II, III, IV) leads to rapid reaction with molecular oxygen to yield superoxide anion which can lead to the formation of more toxic reactive oxygen species, e.g., hydroxyl radical, often taken as the main toxicant. Lipid peroxidation due to PQ has been implicated in a number of deleterious effects such as increased membrane rigidity, osmotic fragility, decreased mitochondrial components, reduced mitochondrial survival and lipid fluidity. The biological effect of reactive oxygen species (ROS) is controlled by a wide spectrum of enzymatic and non-enzymatic defense mechanisms such as superoxide dismutas (SOD), catalase (CAT) and glutathione. According to this hypothesis, the chemical cascades lead to the reduction of PQ, which reacts quite rapidly with molecular oxygen to yield superoxide anion. The generation of free radicals and lipid peroxidation are the main factors that lead to mitochondrial damage.
百草枯（PQ）是一种在全球范围内广泛使用的相对安全且有效的除草剂。PQ 对所有生物都具有很强的毒性；在过去十年中，已报告了许多急性中毒和死亡的病例。PQ 毒性的主要潜在机制是通过微粒体酶系统代谢 PQ 产生超氧自由基，并通过诱导线粒体毒性。线粒体被认为是细胞中活性氧的主要来源，根据这一假设，PQ 通过适当的氧化还原过程，能够参与线粒体的氧化还原系统。PQ 从复合物（I、II、III、IV）接受电子的潜在能力导致其与分子氧迅速反应生成超氧阴离子，从而导致更具毒性的活性氧的形成，例如羟基自由基，通常被视为主要的毒物。PQ 引起的脂质过氧化作用与许多有害影响有关，例如增加膜刚性、渗透脆性、减少线粒体成分、降低线粒体存活率和脂质流动性。活性氧（ROS）的生物学效应受到广泛的酶和非酶防御机制的控制，例如超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽。根据这一假设，化学级联反应导致 PQ 的还原，它与分子氧反应迅速生成超氧阴离子。自由基的产生和脂质过氧化是导致线粒体损伤的主要因素。
