This study was undertaken to determine whether necrosis or apoptosis was the predominant mechanism responsible for gastric mucosal cellular death using the cell line known as AGS cells. Cells were exposed to various concentrations of DC (50 µM to 500 µM) for periods ranging from 30 minutes to 24 hours. Lactic dehydrogenase (LDH) activity was used as a marker for necrotic cell death, while apoptosis was characterized by DAPI staining, DNA gel electrophoresis, TUNEL assay and DNA-histone associated complex formation. When cells were bathed in Hank's balanced salt solution, DC-induced necrosis was the predominant mechanism of cell death. In contrast, when cells were bathed in Ham's F-12 solution (a more physiologically relevant medium), no evidence of cytotoxicity (by LDH assay) was discernible when cells were exposed to DC (50 µM to 300 µM) for periods as long as 8 hours; instead, clear evidence of apoptosis was noted that was time and dose dependent. When cells were exposed for 24 hours to these DC concentrations, cytotoxicity was also present, indicating necrosis as well. Further, acidification of the ambient environment also evoked a necrotic response when exposed to DC. We demonstrated that apoptosis induced by DC shows early activation of caspase-3 that is dependent on both receptor and mitochondrial pathways. Our results indicate that physiologic concentrations of DC (50 µM to 300 µM) primarily induce cellular death through an apoptotic process. Only after prolonged exposure to DC or acidification of the bathing solution does necrosis also occur.