Influence of malathion pretreatment on the toxicity of anilofos in male rats: a biochemical interaction study
Influence of malathion pretreatment on the toxicity of anilofos in male rats: a biochemical interaction study
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DOI：
10.1016/s0300-483x(02)00574-7
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发表时间：
2003-03-14
期刊：
影响因子：
4.5
通讯作者：
Malik, JK
中科院分区：
文献类型：
--
作者：
Hazarika, A;Sarkar, SN;Malik, JK
有机磷的毒性主要来自于乙酰胆碱酯酶（ACNE）抑制引起的乙酰胆碱积累。过量乙酰胆碱的后果取决于乙酰胆碱与胆碱能受体相互作用引发的事件。有机磷诱导的脂质过氧化（LPO）似乎也通过胆碱能受体介导。胺硫磷是一种广泛使用的硫代有机磷除草剂，而马拉硫磷是一种硫代有机磷杀虫剂。硫代有机磷酸酯经混合功能氧化酶（MFO）催化活化为氧合酶，可引起哺乳动物胆碱能危象。因此，可以假定改变MFO活性的因素（例如暴露于某些异生物质）会影响这些有机磷酸酯的毒性。在大鼠中研究了马拉硫磷作为MFO的抑制剂是否可以改变莎稗磷的毒性，检查了血液、脑和肝脏中的某些生化特征。马拉硫磷或莎稗磷及其组合未产生任何明显的毒性迹象。马拉硫磷并不影响莎稗磷在血液、脑和肝脏中的抗胆碱酯酶作用。莎稗磷、马拉硫磷及二者合用均使红细胞、脑和肝组织LPO升高。在马拉硫磷预处理的大鼠脑中的脂质过氧化物的生产给予苯胺硫磷显着大于在大鼠单独给予苯胺硫磷。马拉硫磷可降低肝脏和血液中谷胱甘肽（GSH）含量。谷胱甘肽-S-转移酶（GST）的活性下降，在肝脏与马拉硫磷及其组合与苯胺硫磷。总腺苷三磷酸酶（ATP酶）活性不受影响。结果表明，农药混配可显著提高肝脏和红细胞中Mg ~（2+）-ATPase和Na ~+ -K ~+ -ATPase的活性。马拉硫磷及其与莎稗磷合用可降低血浆中蛋白质水平，但仅在肝脏中联合使用。研究结果表明，马拉硫磷预处理可能不会从根本上改变莎稗磷的抗胆碱酯酶作用，但可能会增强莎稗磷介导的氧化损伤。(C)2002爱思唯尔科学爱尔兰有限公司保留所有权利。
Toxicity of organophosphates stems mainly from the accumulation of acetylcholine due to inhibition of acetylcholinesterase (ACNE). The consequences of excess acetylcholine depend on the events initiated by the interaction of acetylcholine with cholinergic receptors. Lipid peroxidation (LPO) induced by organophosphates also seems to be mediated via cholinergic receptors. Anilofos is a widely used thionoorganophosphate herbicide, while malathion is a thionoorganophosphate insecticide. Thionoorganophosphates undergo mixed function oxidase (MFO)-catalyzed bioactivation to oxons and can induce cholinergic crisis in mammals. Thus, factors (e.g. exposure to certain xenobiotics) which alter the MFO activity, can be assumed to affect the toxicity of these organophosphates. It was investigated in rats if malathion as an inhibitor of MFO can alter the toxicity of anilofos, examining certain biochemical traits in blood, brain and liver. Malathion or anilofos and their combination did not produce any obvious signs of toxicity. Malathion did not alter the anticholinesterase action of anilofos in blood, brain and liver. LPO was increased in erythrocytes, brain and liver with anilofos or malathion and their combination. Production of lipid peroxide in brain of malathion-pretreated rats given anilofos was significantly greater than in rats given anilofos alone. Malathion decreased glutathione (GSH) contents of liver and blood. Glutathione-S-transferase (GST) activity was decreased in the liver with malathion and its combination with anilofos. Total adenosine triphosphatase (ATPase) activity was not affected. Activities of Mg2+-ATPase and Na+ -K+ -ATPase were increased in the liver and erythrocytes, respectively, with the pesticide combination. Protein level in plasma was decreased with malathion and its combination with anilofos, but only with the combination in the liver. Results of the study indicate that malathion pretreament may not essentially alter the anticholinesterase action of anilofos, but may enhance anilofos-mediated oxidative damage to rat brain. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.