Eaton David L, Williams David E, Coulombe Roger A
Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA 98195, USA.
Environmental and Molecular Toxicology, College of Agricultural Sciences, Oregon State University, Corvalis, OR 97331, USA.
Toxins (Basel). 2025 Jan 9;17(1):30. doi: 10.3390/toxins17010030.
It has been known since the early days of the discovery of aflatoxin B1 (AFB1) that there were large species differences in susceptibility to AFB1. It was also evident early on that AFB1 itself was not toxic but required bioactivation to a reactive form. Over the past 60 years there have been thousands of studies to delineate the role of ~10 specific biotransformation pathways of AFB1, both phase I (oxidation, reduction) and phase II (hydrolysis, conjugation, secondary oxidations, and reductions of phase I metabolites). This review provides a historical context and substantive analysis of each of these pathways as contributors to species differences in AFB1 hepatoxicity and carcinogenicity. Since the discovery of AFB1 as the toxic contaminant in groundnut meal that led to Turkey X diseases in 1960, there have been over 15,000 publications related to aflatoxins, of which nearly 8000 have addressed the significance of biotransformation (metabolism, in the older literature) of AFB1. While it is impossible to give justice to all of these studies, this review provides a historical perspective on the major discoveries related to species differences in the biotransformation of AFB1 and sets the stage for discussion of other papers in this Special Issue of the important role that AFB1 metabolites have played as biomarkers of exposure and effect in thousands of human studies on the toxic effects of aflatoxins. Dr. John Groopman has played a leading role in every step of the way-from initial laboratory studies on specific AFB1 metabolites to the application of molecular biomarkers in epidemiological studies associating dietary AFB1 exposure with liver cancer, and the design and conduct of chemoprevention clinical trials to reduce cancer risk from unavoidable aflatoxin exposures by alteration of specific AFB1 biotransformation pathways. This article is written in honor of Dr. Groopman's many contributions in this area.
自黄曲霉毒素B1(AFB1)被发现之初,人们就知道不同物种对AFB1的易感性存在很大差异。早期也很明显,AFB1本身并无毒性,但需要生物活化成一种活性形式。在过去60年里,已经进行了数千项研究来阐明AFB1的约10种特定生物转化途径的作用,包括I相(氧化、还原)和II相(水解、结合、I相代谢产物的二次氧化和还原)。本综述提供了这些途径的历史背景和实质性分析,这些途径是导致AFB1肝毒性和致癌性物种差异的因素。自1960年发现AFB1是导致火鸡X病的花生粕中毒性污染物以来,已有超过15000篇与黄曲霉毒素相关的出版物,其中近8000篇涉及AFB1生物转化(在早期文献中称为代谢)的意义。虽然不可能对所有这些研究都进行全面介绍,但本综述提供了一个历史视角,介绍了与AFB1生物转化物种差异相关的主要发现,并为本期特刊中其他论文讨论AFB1代谢产物在数千项关于黄曲霉毒素毒性影响的人体研究中作为暴露和效应生物标志物所起的重要作用奠定了基础。约翰·格罗普曼博士在每一步都发挥了主导作用——从对特定AFB1代谢产物的初步实验室研究,到将分子生物标志物应用于将膳食AFB1暴露与肝癌联系起来的流行病学研究,以及设计和开展化学预防临床试验以通过改变特定AFB1生物转化途径降低不可避免的黄曲霉毒素暴露导致的癌症风险。本文是为纪念格罗普曼博士在这一领域的诸多贡献而撰写的。