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大鼠亚慢性暴露于马拉硫磷后唾液和血浆中的氧化应激与胆碱酯酶抑制作用

Oxidative stress and cholinesterase inhibition in saliva and plasma of rats following subchronic exposure to malathion.

作者信息

Abdollahi Mohammad, Mostafalou Sara, Pournourmohammadi Shirin, Shadnia Shahin

机构信息

Department of Toxicology and Pharmacology, Faculty of Pharmacy and Laboratory of Toxicology, Pharmaceutical Sciences Research Centre, Tehran University of Medical Sciences, Tehran 14155-6451, Iran.

出版信息

Comp Biochem Physiol C Toxicol Pharmacol. 2004 Jan;137(1):29-34. doi: 10.1016/j.cca.2003.11.002.

Abstract

The aim of this study was to examine whether malathion, a commonly used organophosphate (OP), might induce oxidative stress and cholinesterase (ChE) depression in saliva and plasma in rats following subchronic exposure mimicking human exposure. Malathion was administered orally at doses of 100, 500 and 1500 ppm for 4 weeks. Oxidative stress was determined by measuring the malondialdehyde concentration, the end product of lipid peroxidation, and assessing total antioxidant power. Four weeks oral administration of malathion at doses of 100 ppm, 500 ppm and 1500 ppm depressed plasma ChE activity to 45% (P<0.01), 48% (P<0.01) and 41% (P<0.01) of control, respectively. Malathion at doses of 100 ppm, 500 ppm and 1500 ppm depressed saliva ChE activity to 73% (P<0.01), 75% (P<0.01) and 78% (P<0.01) of control, respectively. Malathion at doses of 100 ppm, 500 ppm and 1500 ppm increased plasma antioxidant power by 33% (P<0.01), 59% (P<0.01) and 118% (P<0.01) of control, respectively. Malathion did not change saliva antioxidant power. Malathion at doses of 100 ppm, 500 ppm and 1500 ppm increased plasma thiobarbituric acid reactive substances (TBARS) by 61% (P<0.01), 69% (P<0.01) and 63% (P<0.01) of control, respectively. Malathion at doses of 500 ppm and 1500 ppm increased saliva TBARS by 19% (P<0.01) and 22% (P<0.01) of control, respectively. Malathion (100 ppm) did not change saliva TBARS level. We concluded that in OP subchronic exposure, depression of ChE is accompanied by induction of oxidative stress that might be beneficial in monitoring OP toxicity.

摘要

本研究的目的是检测常用有机磷酸酯(OP)马拉硫磷在模拟人类暴露的亚慢性暴露后,是否会在大鼠唾液和血浆中诱导氧化应激并导致胆碱酯酶(ChE)活性降低。以100、500和1500 ppm的剂量口服给予马拉硫磷,持续4周。通过测量脂质过氧化的终产物丙二醛浓度并评估总抗氧化能力来确定氧化应激。以100 ppm、500 ppm和1500 ppm的剂量口服给予马拉硫磷4周后,血浆ChE活性分别降至对照组的45%(P<0.01)、48%(P<0.01)和41%(P<0.01)。以100 ppm、500 ppm和1500 ppm的剂量给予马拉硫磷后,唾液ChE活性分别降至对照组的73%(P<0.01)、75%(P<0.01)和78%(P<0.01)。以100 ppm、500 ppm和1500 ppm的剂量给予马拉硫磷后,血浆抗氧化能力分别增加至对照组的33%(P<0.01)、59%(P<0.01)和118%(P<0.01)。马拉硫磷未改变唾液抗氧化能力。以100 ppm、500 ppm和1500 ppm的剂量给予马拉硫磷后,血浆硫代巴比妥酸反应性物质(TBARS)分别增加至对照组的61%(P<0.01)、69%(P<0.01)和63%(P<0.01)。以500 ppm和1500 ppm的剂量给予马拉硫磷后,唾液TBARS分别增加至对照组的19%(P<0.01)和22%(P<0.01)。马拉硫磷(100 ppm)未改变唾液TBARS水平。我们得出结论,在OP亚慢性暴露中,ChE活性降低伴随着氧化应激的诱导,这可能有助于监测OP毒性。

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