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肠道微生物群对苦杏仁苷代谢毒性及潜在解毒作用的影响

Impact of intestinal microbiota on metabolic toxicity and potential detoxification of amygdalin.

作者信息

Wen Qiuyu, Yu Shen, Wang Shanshan, Qin Yan, Xia Quan, Wang Sheng, Chen Guanjun, Shen Chenlin, Song Shuai

机构信息

School of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, China.

The Grade 3 Pharmaceutical Chemistry Laboratory of State Administration of Traditional Chinese Medicine, Hefei, China.

出版信息

Front Microbiol. 2022 Nov 24;13:1030516. doi: 10.3389/fmicb.2022.1030516. eCollection 2022.

DOI:10.3389/fmicb.2022.1030516
PMID:36504787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9730245/
Abstract

Amygdalin (Amy) is metabolized into cyanide , which may lead to fatal poisoning after oral administration. The defense mechanisms against toxic cyanide have not yet been adequately studied. In this study, comparative toxicokinetics study of Amy was performed in normal and pseudo germ-free rats. The efficiency of cyanide release was significant higher in normal group when given a single oral dose of 440 mg/kg (50% median lethal dose). Thiocyanate, the detoxification metabolite, was firstly detected in feces, caecum, and intestinal microbiota incubation enzymic system. The results suggest intestinal microbiota is involved in bidirectional regulation of toxicity and detoxification of Amy. We further identified the species related to cyanogenesis of Amy with metagenomic sequencing, such as , , and . Functional analysis of microbiota reveals the detoxification potential of intestinal microbiota for cyanide. Sulfurtransferase superfamily, such as rhodanese, considered as main detoxification enzymes for cyanide, are largely found in , , , etc. Besides, cyanoamino acid metabolism pathway dominated by may contribute to the detoxification metabolism of cyanide. In summary, intestinal microbiota may be the first line of defense against the toxicity induced by Amy.

摘要

苦杏仁苷(Amy)可代谢生成氰化物,口服后可能导致致命中毒。针对有毒氰化物的防御机制尚未得到充分研究。在本研究中,对正常大鼠和伪无菌大鼠进行了苦杏仁苷的比较毒代动力学研究。给予单次口服剂量440 mg/kg(50%半数致死剂量)时,正常组的氰化物释放效率显著更高。解毒代谢产物硫氰酸盐首先在粪便、盲肠和肠道微生物群孵育酶系统中被检测到。结果表明,肠道微生物群参与了苦杏仁苷毒性和解毒的双向调节。我们通过宏基因组测序进一步鉴定了与苦杏仁苷氰化作用相关的物种,如……。微生物群的功能分析揭示了肠道微生物群对氰化物的解毒潜力。硫转移酶超家族,如硫氰酸酶,被认为是氰化物的主要解毒酶,大量存在于……等中。此外,以……为主的氰基氨基酸代谢途径可能有助于氰化物的解毒代谢。总之,肠道微生物群可能是抵御苦杏仁苷诱导毒性的第一道防线。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1965/9730245/d400fb050b10/fmicb-13-1030516-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1965/9730245/97e92bae35ea/fmicb-13-1030516-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1965/9730245/0e2399f2cdb5/fmicb-13-1030516-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1965/9730245/d400fb050b10/fmicb-13-1030516-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1965/9730245/97e92bae35ea/fmicb-13-1030516-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1965/9730245/0e2399f2cdb5/fmicb-13-1030516-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1965/9730245/d400fb050b10/fmicb-13-1030516-g010.jpg

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Amygdalin protects against acetaminophen-induced acute liver failure by reducing inflammatory response and inhibiting hepatocyte death.苦杏仁苷通过减少炎症反应和抑制肝细胞死亡来预防对乙酰氨基酚引起的急性肝衰竭。
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