title: Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice.
abstract: 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 (CoQH2, 250 mg/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 CoQH2 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 CoQH2 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 CoQH2. Urinary levels of acrolein (ACR)-lysine adduct increased significantly with age in SAMP1 mice; however, CoQH2 had no effect. Thus, lifelong dietary supplementation with CoQH2 decreased the degree of senescence in middle-aged SAMP1 mice.
authors.affiliation: Department of Aging Biology, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, 3-1-1, Asahi, Matsumoto 390-8621, Japan.
authors.forename: Jingmin
authors.initials: J
authors.lastname: Yan
authors.forename: Kenji
authors.initials: K
authors.lastname: Fujii
authors.forename: Junjie
authors.initials: J
authors.lastname: Yao
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Kishida
authors.forename: Kazunori
authors.initials: K
authors.lastname: Hosoe
authors.forename: Jinko
authors.initials: J
authors.lastname: Sawashita
authors.forename: Toshio
authors.initials: T
authors.lastname: Takeda
authors.forename: Masayuki
authors.initials: M
authors.lastname: Mori
authors.forename: Keiichi
authors.initials: K
authors.lastname: Higuchi
mesh_terms: D019588:Aging, Premature / Q000188:drug therapy*; D000686:Amyloidosis / Q000378:metabolism / Q000517:prevention & control; D000818:Animals; D016633:Apolipoprotein A-II / Q000032:analysis; D015415:Biomarkers / Q000652:urine; D003067:Coenzymes; D019587:Dietary Supplements; D005260:Female; D008136:Longevity / Q000187:drug effects; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D023421:Models, Animal; D018384:Oxidative Stress; D011897:Random Allocation; D014451:Ubiquinone / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000097:blood
chemical_list: D016633:Apolipoprotein A-II; D015415:Biomarkers; D003067:Coenzymes; D014451:Ubiquinone; C024989:coenzyme Q10; C030571:ubiquinone 9