Fretham Stephanie Jb, Caito Samuel, Martinez-Finley Ebany J, Aschner Michael
Department of Pediatrics and Department of Pharmacology, and the Kennedy Center for Research on Human Development, Vanderbilt University Medical Center, Nashville, TN, USA.
Toxicol Res (Camb). 2012 Jul 1;1(1):32-38. doi: 10.1039/C2TX20010D. Epub 2012 May 2.
The neurotoxic consequences of methylmercury (MeHg) exposure have long been known, however a complete understanding of the mechanisms underlying this toxicity is elusive. Recent epidemiological and experimental studies have provided many mechanistic insights, particularly into the contribution of genetic and environmental factors that interact with MeHg to modify toxicity. This review will outline cellular processes directly and indirectly affected by MeHg, including oxidative stress, cellular signaling and gene expression, and discuss genetic, environmental and nutritional factors capable of modifying MeHg toxicity.
长期以来,人们一直知晓甲基汞(MeHg)暴露会产生神经毒性后果,然而,对这种毒性背后的机制仍缺乏全面的了解。最近的流行病学和实验研究提供了许多机制方面的见解,特别是关于与甲基汞相互作用以改变毒性的遗传和环境因素的作用。本综述将概述甲基汞直接和间接影响的细胞过程,包括氧化应激、细胞信号传导和基因表达,并讨论能够改变甲基汞毒性的遗传、环境和营养因素。