Oxidative damage and cellular defense mechanisms in sea urchin models of aging

Abstract

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.

Sea urchin immune cells as sentinels of environmental stress

“…In fact, echinoderms do not show variations in metabolic functions and fertility over time, and no cases of cancer, immune and age-related diseases have been reported (Bodnar, 2009). In accordance, recent analysis of oxidative damage and proteomic studies in three sea urchin species with different lifespans revealed that the sea urchin is a promising tool for investigations of oxidative cell damage, senescence, and longevity (Bodnar, 2013;Du et al, 2013).…”

Review of Major Theories of Skin Aging

“…In a study that investigated the aging species of sea urchin short life and extraordinary longevity, found that levels were lower oxidative damage and antioxidant activity was higher in cells or tissues of long-lived species compared with short-lived species [7]. Consistent with the predictions of the oxidative stress theory of aging, the results suggest that the negligible senescence is accompanied by a decrease in cellular accumulation of oxidative damage with age, and maintenance of antioxidant status and the activities of enzymes of proteasome may be important mechanisms to mitigate the damage [7].…”

“…There is substantial evidence showing that aging is associated with damage from free radicals represented by various reactive oxygen species (ROS) [7]- [9].…”

The fine line between lifespan extension and shortening in response to caloric restriction

“…Oxidative stress in an organism is largely due to the accumulation of reactive oxygen species (ROS). By damaging nucleic acids, proteins, and other molecules, ROS decrease the lifespan of many organisms 106 , 107 . CR can promote lifespan by both lowering the production of ROS as well as promoting the function of antioxidants that can repair ROS-induced damage.…”