作者: Kevin L. Quick , Sameh S. Ali , Robert Arch , Chengjie Xiong , David Wozniak
DOI: 10.1016/J.NEUROBIOLAGING.2006.09.014
关键词: Genetically modified mouse 、 Oxidative stress 、 Cell biology 、 Biology 、 Superoxide dismutase 、 Caenorhabditis elegans 、 Morris water navigation task 、 Biochemistry 、 Mitochondrion 、 Reactive oxygen species 、 Oxidative phosphorylation
摘要: In lower organisms, such as Caenorhabditis elegans and Drosophila, many genes identified key regulators of aging are involved in either detoxification reactive oxygen species or the cellular response to oxidatively-damaged macromolecules. Transgenic mice have been generated study these mammalian aging, but not general exhibited expected lifespan extension beneficial behavioral effects, possibly reflecting compensatory changes during development. We administered a small-molecule synthetic enzyme superoxide dismutase (SOD) mimetic wild-type (i.e. non-transgenic, non-senescence accelerated) starting at middle age. Chronic treatment only reduced age-associated oxidative stress mitochondrial radical production, significantly extended lifespan. Treated also improved performance on Morris water maze learning memory task. This is our knowledge first demonstration that an antioxidant with activity nervous system penetration increases lifespan, rescues age-related cognitive impairment mammals. SOD mimetics characteristics may provide unique complements genetic strategies contribution processes aging.