Methylmercury – the organic form of mercury found in fish – is a potent neurotoxin that accumulates in astrocytes, brain cells that surround and support neurons. How methylmercury exerts its toxic effects is not fully understood.
Michael Aschner and colleagues explored mechanisms of methylmercury neurotoxicity, with a focus on oxidative stress pathways. They exposed cultured rat neonatal astrocytes to methylmercury, with or without pretreatment with the antioxidant compound ebselen.
They report in the journal NeuroToxicology that methylmercury inhibited astrocyte uptake of glutamine, an energy substrate, and depleted the mitochondrial inner membrane potential, an indicator of cell viability. Methylmercury also increased activation of the proteins ERK and caspase-3, signaling molecules that participate in the process of cell death. The selenium-containing compound ebselen blocked each of these methylmercury-induced effects. The findings suggest that selenium-containing compounds may represent promising pharmacological options for treating methylmercury poisoning.
The research was funded by the National Institute of Environmental Health Sciences.