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伏马菌素B暴露通过触发氧化应激途径和诱导相关细胞色素P450同工酶导致肠道组织损伤。

Fumonisin B Exposure Causes Intestinal Tissue Damage by Triggering Oxidative Stress Pathways and Inducing Associated CYP Isoenzymes.

作者信息

Cao Changyu, Hua Weiping, Xian Runxi, Liu Yang

机构信息

College of Animal Science and Technology, Foshan University, Foshan 528225, China.

Foshan University Veterinary Teaching Hospital, Foshan 528231, China.

出版信息

Toxins (Basel). 2025 May 12;17(5):239. doi: 10.3390/toxins17050239.

DOI:10.3390/toxins17050239
PMID:40423322
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12116071/
Abstract

Fumonisin B (FB) is considered the most toxic fumonisin produced by fungi and is commonly found in contaminated feed and crops. Fumonisin and its metabolites extensively exist in feed and crops, where FB-polluted crop ingestion can do harm to livestock and poultry, causing poultry intestinal toxicity in the latter. For investigating FB-mediated intestinal toxicity, we assessed the function of FB exposure in quail intestines and explored its possible molecular mechanisms. In total, 120 quail pups were classified into two groups, where those in the control group were given a typical control diet, and those in the experimental group were given a typical diet that contained 30 mg/kg FB. We evaluated the histopathological and ultrastructural changes in quails' intestines on days 14, 28, and 42, and studied the molecular mechanisms by assessing oxidative stress, inflammation, and nuclear xenobiotic receptors (NXRs). Our results suggest that FB exposure causes intestinal inflammation by triggering oxidative stress pathways and modulating NXRs to induce Cytochrome P450 proteins (CYP) isoforms, leading to intestinal histopathological damage. The results of this study shed novel light on the molecular mechanism underlying FB-induced intestinal injury in juvenile quails.

摘要

伏马菌素B(FB)被认为是真菌产生的毒性最强的伏马菌素,常见于受污染的饲料和农作物中。伏马菌素及其代谢产物广泛存在于饲料和农作物中,摄入受FB污染的农作物会对畜禽造成危害,导致家禽肠道中毒。为了研究FB介导的肠道毒性,我们评估了FB暴露对鹌鹑肠道的作用,并探讨了其可能的分子机制。总共120只鹌鹑幼崽被分为两组,对照组给予典型的对照饮食,实验组给予含有30毫克/千克FB的典型饮食。我们在第14天、28天和42天评估了鹌鹑肠道的组织病理学和超微结构变化,并通过评估氧化应激、炎症和核异生素受体(NXRs)来研究分子机制。我们的结果表明,FB暴露通过触发氧化应激途径和调节NXRs以诱导细胞色素P450蛋白(CYP)同工型,从而导致肠道炎症,进而造成肠道组织病理学损伤。本研究结果为FB诱导幼年鹌鹑肠道损伤的分子机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/166383f2c436/toxins-17-00239-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/92a7087ed5f0/toxins-17-00239-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/1c714b15553f/toxins-17-00239-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/33a51e3448df/toxins-17-00239-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/82c1edc38d00/toxins-17-00239-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/6eac017baec6/toxins-17-00239-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/fa128fb543ae/toxins-17-00239-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/166383f2c436/toxins-17-00239-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/92a7087ed5f0/toxins-17-00239-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/1c714b15553f/toxins-17-00239-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/33a51e3448df/toxins-17-00239-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/82c1edc38d00/toxins-17-00239-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/6eac017baec6/toxins-17-00239-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/fa128fb543ae/toxins-17-00239-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9aa/12116071/166383f2c436/toxins-17-00239-g007.jpg

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Vet Res Commun. 2025 Apr 8;49(3):161. doi: 10.1007/s11259-025-10728-6.
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Immune evasion and persistence in enteric bacterial pathogens.肠道细菌病原体的免疫逃逸与持续存在。
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Tissular Genomic Responses to Oral FB1 Exposure in Pigs.猪口腔暴露于 FB1 后的组织基因组反应。
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