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预先用新霉素和头孢氨苄抑制肠道细菌丛后，Ｔ２毒素在灌流小肠袢内的代谢速度明显减慢，ｔ１／２β由正常的２６ｍｉｎ延长为１３１ｍｉｎ．主要代谢产物ＨＴ２的生成减少．Ｔ２毒素羟化生成３′－羟基ＨＴ２的反应被抑制．当Ｔ２毒素对预先用二异丙基氟磷酸酯抑制酯酶的小肠袢进行肠系膜一门脉血管灌流时．Ｔ２毒素的ｔ１／２β由正常的４７ｍｉｎ延长至１２０ｍｉｎ，ＨＴ２的生成部分被抑制，而３′－ＯＨＨＴ２的生成量显著增加．同时抑制肠道细菌丛和酯酶．Ｔ２毒素在小肠中的代谢转化基本被阻断．实验结果表明，Ｔ２毒素在大鼠小肠中的代谢转化反应主要在肠道细菌丛酶系统和非特异性羧酸酯酶的共同作用下进行．抑制肠道细菌丛酶系统可同时减少Ｔ２毒素在小肠中的水解和羟化反应．而抑制酯酶仅能减少水解反应．与此同时轻化产物增加．
After pretreatment with neomycin and cephalexin against bacterial flora in the intestine, the metabolic rate of T2 toxin in the perfused intestinal loop was significantly slowed down and t1 / 2β was extended from normal 26min to 131min. The production of the major metabolite HT2 is reduced. The reaction of T2 toxins hydroxylation to 3’-hydroxyl HT2 is inhibited. When T2 toxin was pre-treated with diisopropylfluorophosphate esterase inhibition of small intestine 肠 a mesenteric portal vein perfusion. The t1 / 2β of T2 toxin was prolonged from 47min to 120min, the formation of HT2 was inhibited and the production of 3’-OHHT2 was significantly increased. While inhibiting intestinal bacterial flora and esterase. The metabolic transformation of T2 toxin in the small intestine is essentially blocked. The experimental results showed that the metabolic transformation of T2 toxin in the rat small intestine was mainly carried out by the combination of intestinal bacterial cellar enzyme system and non-specific carboxylesterase. Inhibition of intestinal bacterial catabolite system can simultaneously reduce the T2 toxin in the small intestine hydrolysis and hydroxylation. Inhibition of esterase can only reduce the hydrolysis reaction. At the same time, light products increase.