Hirooka Takashi, Yoshida Eiko, Eto Komyo, Kaji Toshiyuki
Department of Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science.
Kanagawa Academy of Science and Technology, KSP.
J Toxicol Sci. 2017;42(3):329-333. doi: 10.2131/jts.42.329.
In a cerebrum damaged by methylmercury, where neuropathological lesions tend to localize along deep sulci and fissures, edematous changes in white matter have been proposed as the cause of such localization. Since hyaluronan has a high water-retention capability and can contribute to the progression of edematous changes, we hypothesize that methylmercury increases hyaluronan in brain microvascular cells. Our experimental results indicate that methylmercury induces the expression of hyaluronan in cultured human microvascular endothelial cells and pericytes through the induction of expressed UDP-glucose dehydrogenase and hyaluronan synthase 2, respectively. After exposure to methylmercury, hyaluronan largely accumulates in perivascular space, where it contributes to the progression of edematous changes.
在因甲基汞而受损的大脑中，神经病理损伤往往沿深部脑沟和脑裂定位，白质中的水肿变化被认为是这种定位的原因。由于透明质酸具有高保水能力并可促进水肿变化的进展，我们推测甲基汞会增加脑微血管细胞中的透明质酸。我们的实验结果表明，甲基汞分别通过诱导表达的UDP-葡萄糖脱氢酶和透明质酸合酶2，诱导培养的人微血管内皮细胞和周细胞中透明质酸的表达。暴露于甲基汞后，透明质酸大量积聚在血管周围间隙，在那里它促进了水肿变化的进展。
