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Cited by 227Mitochondrial Function and PathologyGenetics, Aging, and Longevity in Model OrganismsExercise and Physiological Responses

Alterations in mitochondrial function, hydrogen peroxide release and oxidative damage in mouse hind-limb skeletal muscle during aging

Mansouri, Abdellah, Muller, Florian L., Liu, Yuhong, Ng, Rainer, Faulkner, John, Hamilton, Michelle, Richardson, Arlan, Huang, Ting-Ting +2 more·2006·Mechanisms of Ageing and Development
DOI 10.1016/j.mad.2005.11.004
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Abstract

Mitochondrial function, hydrogen peroxide generation and oxidative damage were measured in hind-limb skeletal muscle from young (6-8 month) and old (27-29 month) wildtype and heterozygous Mn-superoxide dismutase (MnSOD) knockout mice (Sod2(+/-)). The reduction in MnSOD activity in the Sod2(+/-) mice makes these mice a good model to examine the implications of life-long elevated endogenous mitochondrial oxidative stress on mitochondrial function. ATP production was reduced approximately 30% with age in skeletal muscle mitochondria isolated from wildtype mice, and reduced 40-45% in mitochondria from both young and old Sod2(+/-) mice compared to the young wildtype mice. Release of hydrogen peroxide from skeletal muscle mitochondria increased 40-50% with age in both wildtype and Sod2(+/-) but was not higher in mitochondria from Sod2(+/-) mice. Activities of electron transport Complexes I and V were decreased 25-30% in both young and old Sod2(+/-) mice compared to wildtype mice, and were 25-30% lower in mitochondria from old wildtype and old Sod2(+/-) mice. DNA oxidative damage (oxo8dG levels) increased more than 45% with age and over 130% in the young Sod2(+/-) mice compared to the wildtype mice. These data show that mitochondrial oxidative stress in mouse skeletal muscle is increased with age, leading to alterations in mitochondrial function. In addition, increased oxidative stress generated by reduced activity of MnSOD does not exacerbate these alterations during aging.

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  • SOD knock-out mice (Sod2−/−) die within the first 10 days of life, while heterozygous mice (Sod2+/−) are viable with longevity and OXPHOS activity comparable to WT mice.

    “Similarly, while SOD knock-out mice (Sod2−/−) die within the first 10 days of life (Li et al., 1995), heterozygous mice (Sod2+/−) are viable with longevity and OXPHOS activity comparable to WT mice (Mansouri et al., 2006).”

    From Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases (2017) · cites this paper as Mansouri et al., 2006

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Authors
Mansouri, A., Muller, F. L., Liu, Y., Ng, R., Faulkner, J., Hamilton, M., Richardson, A., Huang, T.-T., Epstein, C. J., & Van Remmen, H.
Affiliations
  • The University of Texas at San Antonio Health Science Center (US)
  • University of Michigan (US)
  • Stanford University (US)
  • University of California, San Francisco (US)
ORCID
Venue
Mechanisms of Ageing and Development
Publisher
Elsevier BV
Published
2006-03
Volume
127
Issue
3
Pages
298-306
ISSN
0047-6374 (ISSN-L)
DOI
10.1016/j.mad.2005.11.004
OpenAlex
W2004643937
Cited by
227
References
45
Citations by year
2026: 1 · 2025: 4 · 2024: 9 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 13 · 2019: 10 · 2018: 9 · 2017: 9 · 2016: 8 · 2015: 9 · 2014: 15 · 2013: 11 · 2012: 19
FWCI
7.79
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Mechanisms of Ageing and Development (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Department of Veterans Affairs
  • National Institutes of Health
  • National Institute on Aging (5T3 AG 021890 02, P01AG020591, AG-08938, P01AG008938, T32AG021890)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
Keywords
mitochondrial oxidative stress, aging, skeletal muscle, manganese superoxide dismutase, Sod2 knockout mice, hydrogen peroxide release, mitochondrial function, ATP production, respiratory chain complexes, oxidative DNA damage, hindlimb muscles
MeSH terms
Superoxide Dismutase 2, Aging, Animals, DNA Damage, Electron Transport, Female, Hindlimb, Hydrogen Peroxide, Mitochondria, Muscle, Oxidation-Reduction, Superoxide Dismutase, Mice, Knockout, Oxidative Stress, Muscle, Skeletal, Mice

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