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Cited by 45Coenzyme Q10 studies and effectsGenetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and Senescence

Reduced Coenzyme Q10 Supplementation Decelerates Senescence in SAMP1 Mice

Yan, Jingmin, Fujii, Kenji, Yao, Junjie, Kishida, Hideyuki, Hosoe, Kazunori, Sawashita, Jinko, Takeda, Toshio, Mori, Masayuki +1 more·2006·Experimental Gerontology
DOI 10.1016/j.exger.2005.11.007
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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.

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Crossref · 10.1016/j.exger.2005.11.007

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  • No lifespan improvement was detected with ubiquinol administration in SAMP1 mice.

    “However, no lifespan improvement was detected [68].”

    From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [68]

  • In SAMP1 mice, ubiquinol administration at 250-300 mg/kg/day for at least 10 months can reduce senescence grading scores and ROS production, while enhancing antioxidant defences.

    “In vivo, experiments conducted on SAMP1 mice reported that ubiquinol administration at relatively high doses (250–300 mg/kg/day) for at least 10 months can reduce senescence grading scores and ROS production, while enhancing antioxidant defences [68,70].”

    From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [68]

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Authors
Yan, J., Fujii, K., Yao, J., Kishida, H., Hosoe, K., Sawashita, J., Takeda, T., Mori, M., & Higuchi, K.
Affiliations
  • Shinshu University (JP)
  • Kaneka (Japan) (JP)
Corresponding author
Higuchi, Keiichi
ORCID
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
2006-02
Volume
41
Issue
2
Pages
130-140
ISSN
0531-5565 (ISSN-L)
DOI
10.1016/j.exger.2005.11.007
OpenAlex
W2143126116
Cited by
45
References
59
Citations by year
2026: 1 · 2025: 2 · 2023: 1 · 2022: 2 · 2021: 5 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 4 · 2015: 2 · 2014: 3 · 2013: 2 · 2012: 2
FWCI
0.81
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Experimental Gerontology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ministry of Education, Culture, Sports, Science and Technology
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Keywords
coenzyme Q10, SAMP1 mice, accelerated senescence, aging, senile amyloidosis, CoQ9, lifespan, 8-hydroxy-2'-deoxyguanosine, oxidative DNA damage, dietary supplementation
MeSH terms
Amyloidosis, Animals, Coenzymes, Female, Longevity, Male, Mice, Mutant Strains, Random Allocation, Ubiquinone, Biomarkers, Apolipoprotein A-II, Oxidative Stress, Dietary Supplements, Aging, Premature, Models, Animal, Mice

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