Caspases (cysteine-containing aspartate-specific proteases) are at the core of 
the cell's suicide machinery. These enzymes, once activated, dismantle the cell 
by selectively cleaving key proteins after aspartate residues. The events 
culminating in caspase activation are the subject of intense study because of 
their role in cancer, and neurodegenerative and autoimmune disorders. Here we 
present a mechanistic mathematical model, formulated on the basis of newly 
emerging information, describing key elements of receptor-mediated and 
stress-induced caspase activation. We have used mass-conservation principles in 
conjunction with kinetic rate laws to formulate ordinary differential equations 
that describe the temporal evolution of caspase activation. Qualitative 
strategies for the prevention of caspase activation are simulated and compared 
with experimental data. We show that model predictions are consistent with 
available information. Thus, the model could aid in better understanding caspase 
activation and identifying therapeutic approaches promoting or retarding 
apoptotic cell death.