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毒死蜱对大鼠组织中硫代巴比妥酸反应性物质、清除酶和谷胱甘肽的影响。

Effect of chlorpyrifos on thiobarbituric acid reactive substances, scavenging enzymes and glutathione in rat tissues.

作者信息

Verma Radhey S, Srivastava Nalini

机构信息

School of Studies in Biochemistry, Jiwaji University, Gwalior 474 11, India.

出版信息

Indian J Biochem Biophys. 2003 Dec;40(6):423-8.

Abstract

The present study showed that exposure of chlorpyrifos, O,O'-diethyl-O-3,5,6-trichloro-2-pyridyl phosphorothionate (CPF), a widely used pesticide in rats caused significant inhibition of acetylcholinesterase (AChE) activity in different tissues viz., liver, kidney and spleen. CPF exposure also generated oxidative stress in the body, as evidenced by increase in thiobarbituric acid reactive substances (TBARS), decrease in the levels of superoxide scavenging enzymes viz., superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in liver, kidney and spleen at all doses. Malondialdehyde levels were increased by 14%, 31% and 76% in liver, 11%, 31% and 64% in kidney and 32%, 75% and 99.9% in spleen when 50 mg, 100 mg and 200 mg/kg body wt. CPF was administered for three days. SOD and CAT activities were decreased in liver, kidney and spleen, while GPx activity showed slight increase in kidney at 50 mg and 100 mg dose, and decreased on further increase in dose of CPF. Liver and spleen showed dose-dependent decrease in GPx activity. The levels of reduced glutathione (GSH) was decreased, while oxidized glutathione (GSSG) was increased, thus a marked fall in GSH/GSSG ratio was observed in all tissues. A maximum decrease of 83% was observed in liver, followed by kidney and spleen, which showed 78% and 57% decrease, respectively in group given 200 mg/kg CPF. The levels of glucose-6-phosphate dehydrogenase (G6PDH) and glutathione reductase (GR) were also decreased in liver and kidney, while spleen showed increase at lower doses, but decrease at high dose of CPF. The data provide evidence for induction of oxidative stress on CPF exposure.

摘要

本研究表明,毒死蜱(O,O'-二乙基-O-3,5,6-三氯-2-吡啶基硫代磷酸酯,CPF)是一种广泛使用的杀虫剂,在大鼠体内的暴露会导致不同组织(即肝脏、肾脏和脾脏)中的乙酰胆碱酯酶(AChE)活性受到显著抑制。CPF暴露还会在体内产生氧化应激,这在所有剂量下肝脏、肾脏和脾脏中硫代巴比妥酸反应性物质(TBARS)增加、超氧化物清除酶(即超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx))水平降低中得到了证实。当以50mg、100mg和200mg/kg体重的剂量连续三天给予CPF时,肝脏中的丙二醛水平分别增加了14%、31%和76%,肾脏中分别增加了11%、31%和64%,脾脏中分别增加了32%、75%和99.9%。肝脏、肾脏和脾脏中的SOD和CAT活性降低,而在50mg和100mg剂量下,肾脏中的GPx活性略有增加,随着CPF剂量的进一步增加而降低。肝脏和脾脏中的GPx活性呈现剂量依赖性降低。还原型谷胱甘肽(GSH)水平降低,而氧化型谷胱甘肽(GSSG)水平升高,因此在所有组织中均观察到GSH/GSSG比值显著下降。在给予200mg/kg CPF的组中,肝脏中GSH/GSSG比值最大下降了83%,其次是肾脏和脾脏,分别下降了78%和57%。肝脏和肾脏中的葡萄糖-6-磷酸脱氢酶(G6PDH)和谷胱甘肽还原酶(GR)水平也降低,而脾脏在较低剂量下升高,但在高剂量CPF时降低。这些数据为CPF暴露诱导氧化应激提供了证据。

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