Cardiomyocyte apoptosis contributes to cell death during myocardial infarctions. One of the factors that regulates the degree of apoptosis during ischemia is the amino acid, taurine. To study the mechanism underlying the beneficial effect of taurine, the interaction between taurine and mitochondria-mediated apoptosis was examined using a simulated ischemia model with cultured rat neonatal cardiomyocytes sealed in closed flasks. Exposing the cells to medium containing 20 mM taurine reduced the degree of apoptosis following periods of ischemia varying from 24-72 h. In the untreated group, simulated ischemia for 24 h led to mitochondrial depolarization accompanied by cytochrome c release. It also activated the apoptotic cascade, as evidenced by the activation of caspases 9 and 3. Taurine treatment had no effect on mitochondrial membrane potential and cytochrome c release, however, it inhibited ischemia-induced cleavage of caspases 9 and 3. Taurine loading also suppressed the formation of the Apaf-1/caspase-9 apoptosome and the interaction of caspase-9 with Apaf-1. These findings demonstrate that taurine effectively prevents myocardial ischemia-induced apoptosis by inhibiting the assembly of the Apaf-1/caspase-9 apoptosome.