cellular
• inactivation of aconitase in response to H2O2 treatment in mitochondria from heart and the liver is attenuated compared to wild-type mitochondria
• 93%, 98%, 98%, and 71% of redox altered cysteines are switched to a more reductive state in mitochondria from the heart, skeletal muscle, liver, and brain, respectively
• augmented Ca2+ retention capacity in mitochondria from the heart, liver, and skeletal muscle indicating delayed permeability transition pore opening
• in older mice the majority of oxidized cysteines are reversed to a more reductive state
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homeostasis/metabolism
• decreased low density lipoprotein levels in aged mice
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• in aged mice
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• in aged mice
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• increase in both ATP-coupled and maximal respiratory rates in mitochondria from the heart and liver
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behavior/neurological
• attenuation of age-related decrease in grip strength
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cardiovascular system
• reversal of age-associated decline in cardiac contractile function as indexed by ejection fraction and fractional shortening with no sign of cardiac hypertrophy at old versus young age
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hematopoietic system
• in aged mice indicating a decrease in age related inflammation
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• in aged mice indicating a decrease in age related inflammation
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liver/biliary system
• markers of liver damage are largely repressed in aged mice compared to age-matched wild-type controls
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immune system
• in aged mice indicating a decrease in age related inflammation
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• in aged mice indicating a decrease in age related inflammation
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muscle
• reversal of age-associated decline in cardiac contractile function as indexed by ejection fraction and fractional shortening with no sign of cardiac hypertrophy at old versus young age
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• attenuation of age-related muscle atrophy
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