Comparison of biomarkers of oxidative stress and cardiovascular disease in humans and chimpanzees (Pan troglodytes).

Bibliographic Collection: 
MOCA Reference, APE
Publication Type: Journal Article
Authors: Videan, E. N.; Heward, C. B.; Chowdhury, K.; Plummer, J.; Su, Y.; Cutler, R. G.
Year of Publication: 2009
Journal: Comp Med
Volume: 59
Issue: 3
Pagination: 287-96
Date Published: 06/2009
Publication Language: eng
ISSN: 1532-0820
Keywords: Adult, Aging, Animals, Biomarkers, Cardiovascular Diseases, Humans, Life Expectancy, Lipid Peroxidation, Longevity, Male, Oxidative Stress, Pan troglodytes, Reference Values, Risk Factors, Species Specificity, Young Adult

In the oxidative stress hypothesis of aging, the aging process is the result of cumulative damage by reactive oxygen species. Humans and chimpanzees are remarkably similar; but humans live twice as long as chimpanzees and therefore are believed to age at a slower rate. The purpose of this study was to compare biomarkers for cardiovascular disease, oxidative stress, and aging between male chimpanzees and humans. Compared with men, male chimpanzees were at increased risk for cardiovascular disease because of their significantly higher levels of fibrinogen, IGF1, insulin, lipoprotein a, and large high-density lipoproteins. Chimpanzees showed increased oxidative stress, measured as significantly higher levels of 5-hydroxymethyl-2-deoxyuridine and 8-iso-prostaglandin F(2alpha), a higher peroxidizability index, and higher levels of the prooxidants ceruloplasmin and copper. In addition, chimpanzees had decreased levels of antioxidants, including alpha- and beta-carotene, beta-cryptoxanthin, lycopene, and tocopherols, as well as decreased levels of the cardiovascular protection factors albumin and bilirubin. As predicted by the oxidative stress hypothesis of aging, male chimpanzees exhibit higher levels of oxidative stress and a much higher risk for cardiovascular disease, particularly cardiomyopathy, compared with men of equivalent age. Given these results, we hypothesize that the longer lifespan of humans is at least in part the result of greater antioxidant capacity and lower risk of cardiovascular disease associated with lower oxidative stress.

Alternate Journal: Comp. Med.
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