Although mostly epidemiological studies suggested that carbon disulfide produces cardiovascular effects in occupationally exposed workers, little is known about its cellular mechanism. The purpose of the present study was to evaluate the functional and histological effects on cardiac myocytes cultured under the condition of carbon disulfide exposure. Cardiac myocytes were isolated from neonatal rat ventricles by trypsin dispersion and cultured for 3 days in a full (Dulbecco's modified eagle medium) medium containing 2% calf serum. Thereafter the myocytes (10(6) myocytes/culture flask) were incubated with carbon disulfide at (CS(2)) the concentrations of 0, 20, 40, and 80 micromol/mL) for 24h. The beating arrest rate of myocytes for each group was examined and succinodehydrogenase (SDH) activity in the myocardial cells was also assessed by cytochemical method, and morphological examination was also performed. We found that the beating arrest rate of cardiac myocytes increased with increasing exposure levels. Vacuolization and pseudopodia may be seen in the cytoplasm of exposure group. SDH activity decreased with increasing exposure levels. The results suggested that CS(2) has a direct cytotoxic effect which is dose dependent. The biochemical mechanism may be a reduction of the availability of energy of the cardiac cytocyte in the form of ATP, resulting in a decrease of contractility by lacking of energy.