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驱蚊剂N,N-二乙基苯乙酰胺对小鼠、大鼠和家兔的急性经口毒性及戊巴比妥钠的保护作用

Acute oral toxicity of insect repellent N,N-diethylphenylacetamide in mice, rats and rabbits and protective effect of sodium pentobarbital.

作者信息

Rao S S, Kaveeshwar U, Purkayastha S S

机构信息

Biochemistry Division, Defence R&D Establishment, Gwalior, India.

出版信息

Indian J Exp Biol. 1993 Sep;31(9):755-60.

PMID:8276444
Abstract

Median lethal dose (LD50) of undiluted liquid insect repellent N,N-diethylphenylacetamide (DEPA) in male mice, rats and rabbits was 900, 825 and 635 mg/kg respectively when administered by gavage. Signs of DEPA intoxication point to stimulation of central nervous system (CNS). Acetazolamide (10 mg/kg), sodium bicarbonate (40 mg/kg), and atropine (5 mg/kg) when injected (ip) 5 min after a lethal oral dose of DEPA (1700 mg/kg) did not prevent mortality, while sodium pentobarbital (SPB; 20 mg/kg) when injected 5 min after or 15 min before DEPA provided greater protection to the animals. SPB pretreatment elevated the LD50 of DEPA to 1780 and 1535 mg/kg in mice and rats respectively and 85% rats survived when SPB was injected 5 min after acute oral exposure to DEPA (1000 mg/kg). Carboxylesterase (CaE) inhibition is not a factor in the protection mechanism of SPB. DEPA (1000 mg/kg) when given orally elevated blood PCO2 and reduced pH, O2 content and per cent O2 saturation, while administration of SPB after the same dose of DEPA reduced the degree of acidosis and raised PCO2, and increased the O2 content and per cent O2 saturation to near normal status. The CNS depressant action of SPB may be a crucial factor in protection of rats from DEPA poisoning.

摘要

通过灌胃给药时,未稀释的液体驱虫剂N,N-二乙基苯基乙酰胺(DEPA)对雄性小鼠、大鼠和兔子的半数致死剂量(LD50)分别为900、825和635毫克/千克。DEPA中毒的迹象表明中枢神经系统(CNS)受到刺激。在给予致死口服剂量的DEPA(1700毫克/千克)5分钟后腹腔注射乙酰唑胺(10毫克/千克)、碳酸氢钠(40毫克/千克)和阿托品(5毫克/千克)并不能防止死亡,而在DEPA给药前15分钟或给药后5分钟注射戊巴比妥钠(SPB;20毫克/千克)能为动物提供更好的保护。SPB预处理分别将小鼠和大鼠的DEPA LD50提高到1780和1535毫克/千克,当在急性口服暴露于DEPA(1000毫克/千克)后5分钟注射SPB时,85%的大鼠存活。羧酸酯酶(CaE)抑制不是SPB保护机制的一个因素。口服DEPA(1000毫克/千克)会使血液PCO2升高,pH值、O2含量和O2饱和度百分比降低,而在给予相同剂量的DEPA后给予SPB可减轻酸中毒程度,提高PCO2,并使O2含量和O2饱和度百分比增加至接近正常状态。SPB的中枢神经系统抑制作用可能是保护大鼠免受DEPA中毒的关键因素。

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