抄録
Methylmercury (MeHg) is an environmental pollutant that causes severe neuropathy in the brain of exposed humans and animals. It is possible that MeHg induces functional damage of the brain microvessels and neuropathy occurs secondarily. Thus, the effects of MeHg on the maintenance of vascular endothelial cell monolayer were investigated using a culture system of human brain microvascular endothelial cells. MeHg did not damage the morphology of the monolayer; however, it retarded the repair of the wounded monolayer. The proliferation of endothelial cells was observed to be inhibited by MeHg when assessed by the cell number, [3H]thymidine incorporation, and lactate dehydrogenase (LDH) leakage in sparsely growing cells. Cadmium also decreased the [3H]thymidine incorporation but failed to decrease the cell number; inorganic mercury and lead did not exhibit any inhibitory effect under the same conditions. Considering these results together, it is suggested that MeHg exhibits toxicity in the brain microvessels when the endothelial monolayer is damaged. MeHg specifically inhibits the proliferation of endothelial cells during the repair process of the damaged monolayers. The present data support the hypothesis that the mechanism of MeHg-induced neuropathy in the brain includes changes in the microenvironment of the neurons caused by functional damage to the microvessels.
