Oxidative stress, originating from reactive oxygen species and free radical
s provides a constant challenge to eukaryotic cell survival. While implicat
ed in a number of degenerative diseases, some associated with aging and wit
h aging itself, the manner and extent to which oxidative stress contributes
to the initiation or implementation of programmed-cell death is problemati
c. If oxidative stress is an important modulator of programmed-cell death,
any ability intentionally to augment or inhibit it might ameliorate disease
s in which the process is abnormally underactive or overactive.