It is known that methylmercury poisoning, Minamata disease is very toxic to human body. But, cardiotoxic mechanism of methylmercury is left unknown, Recent study has been reported that the cleavage of methylmercury produce oxygen radicals as well as methyl radicals, and also these radicals induce the release of excitotoxic amino acids(EAAs). So, oxygen radicals and EAA are regarded as a causative factors in the various diseases such as heart disease induced by toxicity of methylmercury. We studied to know the cardiotoxic effect of methylmercury on cultured myocardial cells derived from neonatal rat in order to evaluate the toxic mechanism of methylmercury.

Myocardial cells of neonatal rat were incubated with various concentrations of methylmercuric chloride for 1-96 hours. MTT₉₀ and MTT₅₀ values were measured and cell viability was determined by MTT assay. In addition, morphological study was performed by light microscope after cultured myocardial cells that were exposed to methymercuric chloride.

MTT₉₀ and MTT₅₀ values were 1µM and 15µM of methylmercuric chloride in cultured myocardial cells of neonatal rat respectively. Exposure of cultured rat myocardial cells to methylmercuric chloride resulted in a significant cell death in a time-dependent manner. In the observation of morphological changes, cultured cells treated with methlymercuric chloride showed decrease of cell number and disconnection between cultured myocardial cells.

These observation suggest that methylmercury has a severe myocardiotoxicity on cultured myocardial cells derived from neonatal rat by the decrease of cell viability and morphological changes.