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Oxidative damage and cellular defense mechanisms in sea urchin models of aging.
Free Radic Biol Med. 2013 Oct; 63:254-63.FR

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 because of 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 life span. Levels of protein carbonyls and 4-hydroxynonenal measured in tissues (muscle, nerve, esophagus, gonad, coelomocytes, ampullae) and 8-hydroxy-2'-deoxyguanosine 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.

Authors+Show Affiliations

Bermuda Institute of Ocean Sciences, St. George's GE 01, Bermuda.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23707327

Citation

Du, Colin, et al. "Oxidative Damage and Cellular Defense Mechanisms in Sea Urchin Models of Aging." Free Radical Biology & Medicine, vol. 63, 2013, pp. 254-63.
Du C, Anderson A, Lortie M, et al. Oxidative damage and cellular defense mechanisms in sea urchin models of aging. Free Radic Biol Med. 2013;63:254-63.
Du, C., Anderson, A., Lortie, M., Parsons, R., & Bodnar, A. (2013). Oxidative damage and cellular defense mechanisms in sea urchin models of aging. Free Radical Biology & Medicine, 63, 254-63. https://doi.org/10.1016/j.freeradbiomed.2013.05.023
Du C, et al. Oxidative Damage and Cellular Defense Mechanisms in Sea Urchin Models of Aging. Free Radic Biol Med. 2013;63:254-63. PubMed PMID: 23707327.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative damage and cellular defense mechanisms in sea urchin models of aging. AU - Du,Colin, AU - Anderson,Arielle, AU - Lortie,Mae, AU - Parsons,Rachel, AU - Bodnar,Andrea, Y1 - 2013/05/23/ PY - 2013/01/03/received PY - 2013/05/06/revised PY - 2013/05/16/accepted PY - 2013/5/28/entrez PY - 2013/5/28/pubmed PY - 2013/11/2/medline KW - 4-hydroxynonenal KW - 8-OHdG KW - 8-hydroxy-2′-deoxyguanosine KW - Aging KW - Antioxidants KW - Free radicals KW - HNE KW - Lipofuscin KW - Negligible senescence KW - Oxidative damage KW - Proteasome KW - ROS KW - Reactive oxygen species KW - SOD KW - Sea urchin KW - TAC KW - reactive oxygen species KW - superoxide dismutase KW - total antioxidant capacity SP - 254 EP - 63 JF - Free radical biology & medicine JO - Free Radic. Biol. Med. VL - 63 N2 - 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 because of 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 life span. Levels of protein carbonyls and 4-hydroxynonenal measured in tissues (muscle, nerve, esophagus, gonad, coelomocytes, ampullae) and 8-hydroxy-2'-deoxyguanosine 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. SN - 1873-4596 UR - https://www.unboundmedicine.com/medline/citation/23707327/Oxidative_damage_and_cellular_defense_mechanisms_in_sea_urchin_models_of_aging_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(13)00233-5 DB - PRIME DP - Unbound Medicine ER -