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药物和代谢抑制剂对小鼠T-2毒素急性毒性的影响。

Effects of drugs and metabolic inhibitors on the acute toxicity of T-2 toxin in mice.

作者信息

Ryu J C, Shiraki N, Ueno Y

机构信息

Department of Toxicology and Microbial Chemistry, Faculty of Pharmaceutical Sciences, Science University of Tokyo, Japan.

出版信息

Toxicon. 1987;25(7):743-50. doi: 10.1016/0041-0101(87)90124-3.

Abstract

The antidotal effects of antiinflammatory agents, inhibitors of bioamine syntheses, an opioid antagonist and other pharmacological agents on lethal toxicity, leukocytosis and ear inflammation, were investigated in mice subcutaneously administered or topically exposed to T-2 toxin, a trichothecene mycotoxin of Fusarium species. The acute lethal toxicity of T-2 toxin was reduced by administration of the steroidal anti-inflammatory agents, prednisolone and dexamethasone, and prolongation of survival times was demonstrated with an antihistaminic agent, diphenhydramine, and an opioid antagonist, naloxone. Prednisolone also antagonized leukocytosis and the increment of ear weight caused by T-2 toxin. These findings suggest that the action site(s) of steroidal anti-inflammatory agents is involved in the development of the toxic actions of T-2 toxin, and the implications of the results with bioamines and opioids are also discussed.

摘要

研究了抗炎药、生物胺合成抑制剂、阿片类拮抗剂及其他药理剂对经皮下注射或局部暴露于T-2毒素(镰刀菌属的一种单端孢霉烯族霉菌毒素)的小鼠的致死毒性、白细胞增多和耳部炎症的解毒作用。给予甾体抗炎药泼尼松龙和地塞米松可降低T-2毒素的急性致死毒性,给予抗组胺药苯海拉明和阿片类拮抗剂纳洛酮可延长存活时间。泼尼松龙还可拮抗T-2毒素引起的白细胞增多和耳部重量增加。这些发现表明,甾体抗炎药的作用位点参与了T-2毒素毒性作用的发展,同时还讨论了生物胺和阿片类药物研究结果的意义。

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