Effects and mechanisms of aflatoxin B1 on oocytes and embryo development

IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES
Lang Li , Yangyong Dong , Jiafu Zhao , Yuemin Li , Zhenzhen Wang , Bin Liu , Jingyi Chen , Tongyao Wang , Huihui Gao , Xiong Xiao , Yongju Zhao , Xiaoyan Qiu
{"title":"Effects and mechanisms of aflatoxin B1 on oocytes and embryo development","authors":"Lang Li ,&nbsp;Yangyong Dong ,&nbsp;Jiafu Zhao ,&nbsp;Yuemin Li ,&nbsp;Zhenzhen Wang ,&nbsp;Bin Liu ,&nbsp;Jingyi Chen ,&nbsp;Tongyao Wang ,&nbsp;Huihui Gao ,&nbsp;Xiong Xiao ,&nbsp;Yongju Zhao ,&nbsp;Xiaoyan Qiu","doi":"10.1016/j.ecoenv.2025.118572","DOIUrl":null,"url":null,"abstract":"<div><div>Aflatoxin B1 (AFB1), a ubiquitous environmental contaminant, poses substantial threats to animal reproductive health. This review thoroughly described the damage effects and summarized the potential mechanisms of AFB1 on reproductive health. Following metabolic activation by cytochrome P450 to form aflatoxin B1–8, 9-epoxide (AFBO), AFB1 disrupts cellular architecture and impairs mitochondrial function. This impairment manifests as suppressed mitochondrial biogenesis, diminished membrane potential, and induction of mitochondrial DNA mutations. Consequently, energy metabolism dysregulation and arrested development occur in oocytes, embryonic cells, granulosa cells, and ovarian somatic cells. AFB1-induced oxidative stress activates apoptotic pathways and perturbs epigenetic reprogramming, thereby disrupting oocyte meiotic progression and gene expression. Furthermore, AFB1 inhibits GPX4 expression, upregulates TFRC and ACSL4 expression, and promotes iron accumulation, collectively driving lipid peroxidation and triggering ferroptosis. This cascade ultimately impedes oocyte maturation and compromises embryonic developmental competence. This study provides novel insights into the reproductive toxicity of AFB1 and establishes a scientific foundation for developing effective preventative and therapeutic strategies.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"302 ","pages":"Article 118572"},"PeriodicalIF":6.1000,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ecotoxicology and Environmental Safety","FirstCategoryId":"93","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0147651325009170","RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Aflatoxin B1 (AFB1), a ubiquitous environmental contaminant, poses substantial threats to animal reproductive health. This review thoroughly described the damage effects and summarized the potential mechanisms of AFB1 on reproductive health. Following metabolic activation by cytochrome P450 to form aflatoxin B1–8, 9-epoxide (AFBO), AFB1 disrupts cellular architecture and impairs mitochondrial function. This impairment manifests as suppressed mitochondrial biogenesis, diminished membrane potential, and induction of mitochondrial DNA mutations. Consequently, energy metabolism dysregulation and arrested development occur in oocytes, embryonic cells, granulosa cells, and ovarian somatic cells. AFB1-induced oxidative stress activates apoptotic pathways and perturbs epigenetic reprogramming, thereby disrupting oocyte meiotic progression and gene expression. Furthermore, AFB1 inhibits GPX4 expression, upregulates TFRC and ACSL4 expression, and promotes iron accumulation, collectively driving lipid peroxidation and triggering ferroptosis. This cascade ultimately impedes oocyte maturation and compromises embryonic developmental competence. This study provides novel insights into the reproductive toxicity of AFB1 and establishes a scientific foundation for developing effective preventative and therapeutic strategies.
黄曲霉毒素B1对卵母细胞和胚胎发育的影响及其机制
黄曲霉毒素B1 (AFB1)是一种普遍存在的环境污染物,对动物生殖健康构成重大威胁。本文综述了AFB1对生殖健康的损害作用,并对其潜在机制进行了综述。在细胞色素P450代谢激活形成黄曲霉毒素b1 - 8,9 -环氧化物(AFBO)后,AFB1破坏细胞结构并损害线粒体功能。这种损伤表现为抑制线粒体生物发生,降低膜电位,并诱导线粒体DNA突变。因此,能量代谢失调和发育受阻发生在卵母细胞、胚胎细胞、颗粒细胞和卵巢体细胞中。afb1诱导的氧化应激激活凋亡通路,扰乱表观遗传重编程,从而破坏卵母细胞减数分裂进程和基因表达。此外,AFB1抑制GPX4表达,上调TFRC和ACSL4表达,促进铁积累,共同驱动脂质过氧化,引发铁下垂。这种级联最终阻碍卵母细胞成熟,损害胚胎发育能力。本研究为AFB1的生殖毒性提供了新的认识,并为制定有效的预防和治疗策略奠定了科学基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
12.10
自引率
5.90%
发文量
1234
审稿时长
88 days
期刊介绍: Ecotoxicology and Environmental Safety is a multi-disciplinary journal that focuses on understanding the exposure and effects of environmental contamination on organisms including human health. The scope of the journal covers three main themes. The topics within these themes, indicated below, include (but are not limited to) the following: Ecotoxicology、Environmental Chemistry、Environmental Safety etc.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信