The free radical or oxidative stress theory of aging proposes that the
accumulation of oxidative cellular damage is a major contributor to the aging
process and a key determinant of species longevity. This study investigates the
oxidative stress theory in a novel model for aging research, the sea urchin. Sea
urchins present a unique model for the study of aging due to the existence of
species with tremendously different natural life spans including some species
with extraordinary longevity and negligible senescence. Cellular oxidative
damage, antioxidant capacity and proteasome enzyme activities were measured in
the tissues of three sea urchin species: short-lived Lytechinus
variegatus, long-lived Strongylocentrotus
franciscanus and Strongylocentrotus purpuratus
which has an intermediate lifespan. Levels of protein carbonyls and
4-hydroxynonenal (HNE) measured in tissues (muscle, nerve, esophagus, gonad,
coelomocytes, ampullae) and 8-hydroxy-2’-deoxyguanosine (8-OHdG)
measured in cell-free coelomic fluid showed no general increase with age. The
fluorescent age-pigment lipofuscin measured in muscle, nerve and esophagus,
increased with age however it appeared to be predominantly extracellular.
Antioxidant mechanisms (total antioxidant capacity, superoxide dismutase) and
proteasome enzyme activities were maintained with age. In some instances, levels
of oxidative damage were lower and antioxidant activity higher in cells or
tissues of the long-lived species compared to the short-lived species, however
further studies are required to determine the relationship between oxidative
damage and longevity in these animals. Consistent with the predictions of the
oxidative stress theory of aging, the results suggest that negligible senescence
is accompanied by a lack of accumulation of cellular oxidative damage with age
and maintenance of antioxidant capacity and proteasome enzyme activities may be
important mechanisms to mitigate damage.