Mitochondrial oxygen consumption in response to complex I and II substrates is reduced by caspase treatment (blue).

Caspases seem to have their hand in everything during apoptosis. They cleave and activate enzymes that degrade DNA, induce cell blebbing, and induce changes in the plasma membrane that make the dying cell attractive to phagocytes. Now, add another to the list—caspases disturb electron transport.

Ricci et al. (page 65) show that, in both isolated mitochondria and living cells, caspase-3 induces a loss of membrane potential in mitochondria that have been permeabilized by proapoptotic proteins. Inhibition of caspase activity prevented this loss in potential, which places membrane potential loss downstream of cytochrome c release and subsequent activation of caspases.

Mitochondria lost membrane potential because complexes I and II were injured. Caspase-treated permeabilized mitochondria did not consume oxygen in response to substrates used by complexes I and...

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