An update on T2-toxins: metabolism, immunotoxicity mechanism and human assessment exposure of intestinal microbiota

T2毒素的最新进展:代谢、免疫毒性机制和人体肠道菌群暴露评估

阅读:1

Abstract

Mycotoxins are naturally produced secondary metabolites or low molecular organic compounds produced by fungus with high diversification, which cause mycotoxicosis (food contamination) in humans and animals. T-2 toxin is simply one of the metabolites belonging to fungi trichothecene mycotoxin. Specifically, Trichothecenes-2 (T-2) mycotoxin of genus fusarium is considered one of the most hotspot agricultural commodities and carcinogenic compounds worldwide. There are well-known examples of salmonellosis in mice and pigs, necrotic enteritis in chickens, catfish enteric septicemia and colibacillosis in pigs as T-2 toxic agent. On the other hand, it has shown a significant reduction in the Salmonella population's aptitude in the pig intestinal tract. Although the impact of the excess Fusarium contaminants on humans in creating infectious illness is less well-known, some toxins are harmful; for example, salmonellosis and colibacillosis have been frequently observed in humans. More than 20 different metabolites are synthesized and excreted after ingestion, but the T-2 toxin is one of the most protuberant metabolites. Less absorption of mycotoxins in intestinal tract results in biotransformation of toxic metabolites into less toxic variants. In addition to these, effects of microbiota on harmful mycotoxins are not limited to intestinal tract, it may harm the other human vital organs. However, detoxification of microbiota is considered as an alternative way to decontaminate the feed for both animals and humans. These transformations of toxic metabolites depend upon the formation of metabolites. This study is complete in all perspectives regarding interactions between microbiota and mycotoxins, their mechanism and practical applications based on experimental studies.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。