Department of Neurology, National Hospital Organization Nishiniigata Chuo Hospital, Niigata 950-2085, Japan.
Department of Neurology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.
Int J Mol Sci. 2019 May 16;20(10):2435. doi: 10.3390/ijms20102435.
Methylmercury (MeHg) causes severe damage to the central nervous system, and there is increasing evidence of the association between MeHg exposure and vascular dysfunction, hemorrhage, and edema in the brain, but not in other organs of patients with acute MeHg intoxication. These observations suggest that MeHg possibly causes blood-brain barrier (BBB) damage. MeHg penetrates the BBB into the brain parenchyma via active transport systems, mainly the l-type amino acid transporter 1, on endothelial cell membranes. Recently, exposure to mercury has significantly increased. Numerous reports suggest that long-term low-level MeHg exposure can impair endothelial function and increase the risks of cardiovascular disease. The most widely reported mechanism of MeHg toxicity is oxidative stress and related pathways, such as neuroinflammation. BBB dysfunction has been suggested by both in vitro and in vivo models of MeHg intoxication. Therapy targeted at both maintaining the BBB and suppressing oxidative stress may represent a promising therapeutic strategy for MeHg intoxication. This paper reviews studies on the relationship between MeHg exposure and vascular dysfunction, with a special emphasis on the BBB.
甲基汞（MeHg）会对中枢神经系统造成严重损害，越来越多的证据表明，MeHg 暴露与血管功能障碍、脑出血和脑水肿有关，但与急性 MeHg 中毒患者的其他器官无关。这些观察结果表明，MeHg 可能会导致血脑屏障（BBB）损伤。MeHg 通过主动转运系统，主要是通过内皮细胞膜上的 l 型氨基酸转运蛋白 1，穿透 BBB 进入脑实质。最近，汞的暴露量显著增加。许多报告表明，长期低水平的 MeHg 暴露会损害内皮功能，增加心血管疾病的风险。最广泛报道的 MeHg 毒性机制是氧化应激和相关途径，如神经炎症。MeHg 中毒的体外和体内模型均提示 BBB 功能障碍。针对维持 BBB 和抑制氧化应激的治疗可能代表治疗 MeHg 中毒的一种有前途的治疗策略。本文综述了 MeHg 暴露与血管功能障碍之间的关系研究，特别强调了 BBB。
