One hypothesis put forward to explain species-related differences in rate
of cell aging is the "oxygen radical" hypothesis. The rate of oxygen con-
sumption roughly correlates with life span. One thought in this area is that
molecular oxygen is reduced to free radical forms which are highly reactive, and
can participate in numerous reactions, the most biologically significant of
which are probably damage to DNA (adduct formation and strand scission) and
lipid peroxidation. One likely site for this activity is the mitochondria.
One article which I have come across (although this must be somewhat out of
date by now) is "Theoretical and experimental support for an `oxygen radical
-- mitochondrial injury' hypothesis of cell aging" by Jaime Miquel and James
Fleming, pp. 51-74 of Free Radicals, Aging, and Degenerative Diseases (1986,
Alan R Liss, Inc).
Most people reading this message base are probably aware that not all
human cells continue to divide after reaching a terminal stage of differ-
entiation (eg muscle, nerve...). However, consider that mitochondria within
these cells _do_ continue to turnover. I do not believe that there has ever
been a study demonstrating intraindividual variation in human mitochondrial DNA
(aside from those mitochondriopathies inwhich degeneration of mtDNA is known
to occur, eg Kearns-Sayre syndrome) correlated with aging or age-related
loss of function. Some have suggested that mitochondrial membrane might be
an alternative site of damage with correlation to aging. Turnover of mito
chondrial membrane and biogenesis of mitochondria remain fuzzy areas. All
this mitochondria stuff is just food for thought.
-- JJW
