Reduced coenzyme Q10 supplementation decelerates senescence
in SAMP1 mice
The SAMP1 strain is a mouse model for accelerated senescence
and severe senile amyloidosis. We determined whether supplementation with
coenzyme Q10 (CoQ10) could decelerate aging in SAMP1 mice and its potential role
in aging. Plasma concentrations of CoQ10 and CoQ9 decreased with age in SAMP1
but not in SAMR1 mice. Supplementation with reduced CoQ10 (CoQH(2),
250mg/kg/day) for one week increased plasma CoQ10 concentrations, with an
accompanying decrease in plasma CoQ9 concentrations. In two series of
experiments, lifelong supplementation with CoQH(2) decreased the senescence
grading scores from 10 to 14 months, 7 to 15 months, and at 17 months of age.
The body weight of female mice increased from 2 to 10 months of age versus
controls in the second series of experiments. Lifelong CoQH(2) supplementation
did not prolong or shorten the lifespan, nor did it alter the murine senile
amyloid (AApoAII) deposition rate or cancer incidence. In the second series of
experiments, urinary levels of 8-hydroxydeoxyguanosine did not change with age
or long-term supplementation with CoQH(2).Urinary levels of acrolein (ACR)-lysine
adduct increased significantly with age in SAMP1 mice; however, CoQH(2) had no
effect. Thus, lifelong dietary supplementation with CoQH(2) decreased the degree
of senescence in middle-aged SAMP1 mice. Yan J, Fujii K, Yao J, et al. Exp Gerontol. 2006 Feb;41(2):130-40.
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