Testing the rate-of-living/oxidative damage theory of aging in the nematode model Caenorhabditis elegans.
The integration of the rate-of-living and oxidative damage theory of aging predicts that lifespan extension is linked to low energy metabolism, low ROS production rates, low molecular damage and a slow aging rate. In the long-lived Caenorhabditis elegans Ins/IGF-1 mutant daf-2(e1370), low carbonylation levels and postponed morphological decline comply with the latter two of these predictions. However, metabolic rates in daf-2(e1370) refute the rate-of-living theory. The apparent contradiction between increased ROS generation and long lifespan in daf-2(e1370) is reconciled by an enhanced stress defense, acknowledging oxidative damage as a probable cause of aging.
Brys
Kristel
K
Biology Department, Ghent University, K.L.Ledeganckstraat 35, B-9000 Ghent, Belgium.
Vanfleteren
Jacques R
JR
Braeckman
Bart P
BP
D000375:Aging / Q000502:physiology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001481:Basal Metabolism; D017173:Caenorhabditis elegans / Q000235:genetics / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism; D008136:Longevity / Q000235:genetics*; D023421:Models, Animal; D009154:Mutation; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism
D000975:Antioxidants; D029742:Caenorhabditis elegans Proteins; D017382:Reactive Oxygen Species; C107483:DAF-2 protein, C elegans; D011972:Receptor, Insulin