Carbon disulfide cytotoxicity on cultured cardiac myocytes of rats.

Although epidemiological studies have 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 a condition of carbon disulfide exposure. Cardiac myocytes were isolated from neonatal rat ventricles by trypsin, dispersed and cultured for 3 days in a full Dulbecco's Modified Eagle Medium containing 2% calf serum. Then the myocytes (10(6) myocytes/mL) were incubated with carbon disulfide at concentrations of 0, 20, 40, and 80 micromol/mL for 24 h. The beating arrest rate of myocytes for each group was examined, succinodehydrogenase (SDH) activity in the myocardial cells was assessed using a cytochemical method, and a morphological examination was performed. We found that the beating arrest rate of cardiac myocytes increased with increasing exposure levels. Vacuolization and pseudopodia could be seen in the cytoplasm of the exposed group. SDH activity decreased with increasing exposure levels. The results suggest that CS2 has a direct and dose-dependent cytotoxic effect. The biochemical mechanism may be a reduction of the availability of energy (adenosine triphosphate) to cardiac myocytes, resulting in a decrease of contractility by lack of energy.