Sprague G L, Castles T R
Life Sci. 1987 May 4;40(18):1777-81. doi: 10.1016/0024-3205(87)90088-9.
The oral LD50 for bis(trichloromethyl) sulfone (N-1386 Biocide) in male rats was 691 mg/kg. Deaths occurred 1-5 days after treatment and signs of toxicity suggestive of an anticholinesterase effect were noted. However, neither plasma cholinesterase nor brain acetylcholinesterase was inhibited 2, 4 or 24 hours after a single, oral dose of 500 mg/kg. Atropine (300 mg/kg, s.c.) or scopolamine (670 mg/kg, s.c.) pretreatments did not protect against the acute lethality of bis(trichloromethyl) sulfone although signs of toxicity were alleviated by both pretreatments. Bis(trichloromethyl) sulfone produced in vitro inhibition of rat plasma cholinesterase and brain acetylcholinesterase. The inhibition was competitive in brain. IC50's for these 2 enzymes were 8 microM in plasma and 25 microM in brain. In summary, bis(trichloromethyl) sulfone produced in vitro cholinesterase inhibition not demonstrated in vivo. Doses of anticholinergic compounds that ameliorated many toxic signs did not protect against lethality produced by bis(trichloromethyl) sulfone.
双（三氯甲基）砜（N - 1386杀菌剂）对雄性大鼠的经口半数致死剂量为691毫克/千克。给药后1 - 5天出现死亡，并观察到提示抗胆碱酯酶作用的毒性迹象。然而，单次口服500毫克/千克剂量后2、4或24小时，血浆胆碱酯酶和脑乙酰胆碱酯酶均未受到抑制。阿托品（300毫克/千克，皮下注射）或东莨菪碱（670毫克/千克，皮下注射）预处理虽能缓解毒性迹象，但不能预防双（三氯甲基）砜的急性致死作用。双（三氯甲基）砜在体外可抑制大鼠血浆胆碱酯酶和脑乙酰胆碱酯酶。在脑中这种抑制作用具有竞争性。这两种酶的半数抑制浓度在血浆中为8微摩尔，在脑中为25微摩尔。总之，双（三氯甲基）砜在体外产生胆碱酯酶抑制作用，但在体内未得到证实。能改善多种毒性迹象的抗胆碱能化合物剂量并不能预防双（三氯甲基）砜产生的致死作用。
