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Thymic apoptosis induced by T-2 toxin and its metabolites

机译:T-2毒素及其代谢产物诱导的胸腺细胞凋亡

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T-2 toxin (T-2), a trichothecene mycotoxin produced principally by Fusarium species, has been detected in a gretat number of field crops such as maize, wheat, and oats. T-2 causes several outbreaks of mycotoxicosis in humans and animals after accidental ingestion via contaminated foods. Although studies in animal models demonstrated that T-2 exhibits profound immunosuppressive effects, little is presently known regarding possible specific effects of this mycotoxin on resident thymocytes occupying the thymus. Recently, apoposis has been proposed to be involved in the thymic atrophy induced by chemicals including glucocorticoid. At present, however, little is known about the mechanism by which trichothecenes including T-2 induec toxic effects through apoptosis and about which structural component(s) is responsible for the potent apoptotic effect of T-2. We show here that T-2, its mammalian metabolites, and some other trichothecentes induce apoposis in the mouse thymus in vivo.
机译:T-2毒素(T-2)是一种主要由镰刀菌属物种产生的单端孢霉毒素,已经在玉米,小麦和燕麦等农作物的大量食用中检出。通过被污染的食物意外摄入后,T-2导致人和动物多次爆发霉菌毒素中毒。尽管在动物模型中的研究表明T-2表现出深远的免疫抑制作用,但对于这种霉菌毒素对占据胸腺的驻留胸腺细胞的可能特异性作用,目前知之甚少。最近,已提出凋亡参与由包括糖皮质激素在内的化学物质诱导的胸腺萎缩。然而,目前对于包括T-2的毛虫纤体通过细胞凋亡产生的毒性作用的机理以及哪个或哪些结构成分对T-2的有效凋亡作用负责的机制还知之甚少。我们在这里显示T-2,其哺乳动物的代谢产物和其他一些trichothecentes在体内诱导小鼠胸腺的凋亡。

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