Apoptosis research is a rapidly developing area, but the role of apoptosis
is still unclear and controversial. For example, several studies document a
significant loss of cardiac and skeletal myocytes during normal aging, pos
sibly by apoptotic mechanisms. This loss in cells may be directly mediated
by mitochondrial dysfunction caused by chronic exposure to oxidants and inc
reased activation of mitochondrial permeability transition pores. This revi
ew will discuss apoptosis in the context of normal aging of T cells, cardia
c myocytes, skeletal muscle, and brain cortex. Particular attention is paid
to the role of the mitochondria, because they have been implicated as a ma
jor control center regulating apoptosis. Mitochondrial oxidative stress and
a decline in mitochondrial energy production in vitro often leads to activ
ation of apoptotic pathways, but whether this occurs in vivo is unclear.