Methylmercury (MeHg) is a long-lasting organic environmental pollutant that poses a great threat to human health. Ingestion of seafood containing MeHg is the most important way by which it comes into contact with human body, where the central nervous system (CNS) is the primary target of MeHg toxicity. During periods of pre-plus postnatal, in particular, the brain of offspring is vulnerable to specific developmental insults that result in abnormal neurobehavioral development, even without symptoms in mothers. While many studies on neurotoxic effects of MeHg on the developing brain have been conducted, the mechanisms of oxidative stress in MeHg-induced neurodevelopmental toxicity is less clear. Hitherto, no single process can explain the many effects observed in MeHg-induced neurodevelopmental toxicity. This review summarizes the possible mechanisms of oxidative stress in MeHg-induced neurodevelopmental toxicity, highlighting modulation of Nrf2/Keap1/Notch1, PI3K/AKT, and PKC/MAPK molecular pathways as well as some preventive drugs, and thus contributes to the discovery of endogenous and exogenous molecules that can counteract MeHg-induced neurodevelopmental toxicity.

甲基汞 (MeHg) 是一种持久的有机环境污染物，对人类健康构成巨大威胁。摄入含有甲基汞的海鲜是其与人体接触的最重要方式，其中中枢神经系统 (CNS) 是甲基汞毒性的主要目标。特别是在产前和产后期间，后代的大脑很容易受到特定的发育损伤，导致异常的神经行为发育，即使母亲没有症状。虽然已经对甲基汞对发育中的大脑的神经毒性作用进行了许多研究，但甲基汞诱导的神经发育毒性中氧化应激的机制尚不清楚。迄今为止，没有单一的过程可以解释在甲基汞诱导的神经发育毒性中观察到的许多影响。