1. Recovery of Indicators of Mitochondrial Biogenesis, Oxidative Stress, and Aging With (-)-Epicatechin in Senile Mice.
- Author
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Moreno-Ulloa, Aldo, Nogueira, Leonardo, Rodriguez, Alonso, Barboza, Jonathan, Hogan, Michael C., Ceballos, Guillermo, Villarreal, Francisco, and Ramirez-Sanchez, Israel
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MITOCHONDRIA formation , *OXIDATIVE stress , *EPICATECHIN , *PHYSIOLOGICAL aspects of aging , *GLUTATHIONE , *BIOMARKERS , *HEART metabolism , *PROTEIN metabolism , *AGE distribution , *AGING , *ANIMAL experimentation , *BRAIN , *FLAVONOIDS , *GLYCOSIDASES , *KIDNEYS , *MICE , *MYOCARDIUM , *OXIDOREDUCTASES , *RESEARCH funding , *TRANSFERASES , *SKELETAL muscle ,BRAIN metabolism - Abstract
There is evidence implicating oxidative stress (OS) as the cause of the deleterious effects of aging. In this study, we evaluated the capacity of the flavanol (-)-epicatechin (Epi) to reduce aging-induced OS and restore mitochondrial biogenesis, as well as, structural and functional endpoints in aged mice. Senile (S; 26-month-old) C57BL/6 male mice were randomly assigned to receive either water (vehicle) or 1mg/kg of Epi via oral gavage (twice daily) for 15 days. Young (Y; 6-month-old) mice were used as controls. In S brain, kidney, heart, and skeletal muscle (compared with Y animals) an increase in OS was observed as evidenced by increased protein-free carbonyls and decreased reduced glutathione levels as well as sirtuin 3, superoxide dismutase 2, catalase, thioredoxin and glutathione peroxidase protein levels. Well-recognized factors (eg, sirtuin 1) that regulate mitochondrial biogenesis and mitochondrial structure- and/or function-related endpoints (eg, mitofilin and citrate synthase) protein levels were also reduced in S organs. In contrast, the aging biomarker senescence-associated β-galactosidase was increased in S compared with Y animals, and Epi administration reduced levels towards those observed in Y animals. Altogether, these data suggest that Epi is capable of shifting the biology of S mice towards that of Y animals. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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