Methylmercury induces ectopic expression of complement components and apoptotic cell death in the retina of the zebrafish embryo

Methylmercury (MeHg) isa well-known neurotoxin of humans and wildlife. Visual impairments, including blindness, are frequently present in human patients with MeHg poisoning and in affected animals. It is widely assumed that MeHg-induced damage to the visual cortex is the sole or primary cause of vision loss. MeHg has been shown to accumulate in the outer segments of photoreceptor cells, and to alter the thickness of the inner nuclear layer of the fish retina. However, it is unclear whether the bioaccumulated MeHg has direct deleterious effects on the retina. Herein we report that the genes encoding complement components 5 (c5), c7a, c7b, and c9 were ectopically expressed in the inner nuclear layer of the retinas of zebrafish embryos exposed to MeHg (6-50 & mu;g/L). The numbers of apoptotic cell deaths scored in the retinas of MeHg-treated embryos significantly increased in a concentration-dependent manner. In comparison with cadmium and arsenic, ectopic expression of c5, c7a, c7b, and c9, and the observed apoptotic cell death in the retina were specific to MeHg exposure. Our data provide evidence supporting the hypothesis that MeHg has deleterious impacts on the retinal cells, especially the inner nuclear layer. We propose that MeHginduced retinal cell death may trigger the activation of the complement system.

Automated summary

Methylmercury is a neurotoxin that affects visual abilities and causes damage to retinal cells. Exposure to methylmercury in zebrafish embryos resulted in abnormal expression of complement component genes and increased apoptosis in the retina. These effects were specific to methylmercury exposure, as compared to cadmium and arsenic.