Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle. / Hütter, Eveline; Skovbro, Mette; Lener, Barbara; Prats, Clara; Rabøl, Rasmus; Dela, Flemming; Jansen-Dürr, Pidder.

In: Aging Cell, Vol. 6, No. 2, 2007, p. 245-56.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Hütter, E, Skovbro, M, Lener, B, Prats, C, Rabøl, R, Dela, F & Jansen-Dürr, P 2007, 'Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle', Aging Cell, vol. 6, no. 2, pp. 245-56. https://doi.org/10.1111/j.1474-9726.2007.00282.x

APA

Hütter, E., Skovbro, M., Lener, B., Prats, C., Rabøl, R., Dela, F., & Jansen-Dürr, P. (2007). Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle. Aging Cell, 6(2), 245-56. https://doi.org/10.1111/j.1474-9726.2007.00282.x

Vancouver

Hütter E, Skovbro M, Lener B, Prats C, Rabøl R, Dela F et al. Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle. Aging Cell. 2007;6(2):245-56. https://doi.org/10.1111/j.1474-9726.2007.00282.x

Author

Hütter, Eveline ; Skovbro, Mette ; Lener, Barbara ; Prats, Clara ; Rabøl, Rasmus ; Dela, Flemming ; Jansen-Dürr, Pidder. / Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle. In: Aging Cell. 2007 ; Vol. 6, No. 2. pp. 245-56.

Bibtex

@article{bc30c230b4d511df825b000ea68e967b,
title = "Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle",
abstract = "According to the free radical theory of aging, reactive oxygen species (ROS) act as a driving force of the aging process, and it is generally believed that mitochondrial dysfunction is a major source of increased oxidative stress in tissues with high content of mitochondria, such as muscle or brain. However, recent experiments in mouse models of premature aging have questioned the role of mitochondrial ROS production in premature aging. To address the role of mitochondrial impairment and ROS production for aging in human muscles, we have analyzed mitochondrial properties in muscle fibres isolated from the vastus lateralis of young and elderly donors. Mitochondrial respiratory functions were addressed by high-resolution respirometry, and ROS production was analyzed by in situ staining with the redox-sensitive dye dihydroethidium. We found that aged human skeletal muscles contain fully functional mitochondria and that the level of ROS production is higher in young compared to aged muscle. Accordingly, we could not find any increase in oxidative modification of proteins in muscle from elderly donors. However, the accumulation of lipofuscin was identified as a robust marker of human muscle aging. The data support a model, where ROS-induced molecular damage is continuously removed, preventing the accumulation of dysfunctional mitochondria despite ongoing ROS production.",
author = "Eveline H{\"u}tter and Mette Skovbro and Barbara Lener and Clara Prats and Rasmus Rab{\o}l and Flemming Dela and Pidder Jansen-D{\"u}rr",
note = "Keywords: Adult; Aged; Aging; Biopsy; Cell Respiration; Female; Humans; Lipofuscin; Male; Mitochondria; Muscle, Skeletal; Oxidative Stress; Oxygen Consumption; Reactive Oxygen Species",
year = "2007",
doi = "10.1111/j.1474-9726.2007.00282.x",
language = "English",
volume = "6",
pages = "245--56",
journal = "Aging Cell",
issn = "1474-9718",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

TY - JOUR

T1 - Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle

AU - Hütter, Eveline

AU - Skovbro, Mette

AU - Lener, Barbara

AU - Prats, Clara

AU - Rabøl, Rasmus

AU - Dela, Flemming

AU - Jansen-Dürr, Pidder

N1 - Keywords: Adult; Aged; Aging; Biopsy; Cell Respiration; Female; Humans; Lipofuscin; Male; Mitochondria; Muscle, Skeletal; Oxidative Stress; Oxygen Consumption; Reactive Oxygen Species

PY - 2007

Y1 - 2007

N2 - According to the free radical theory of aging, reactive oxygen species (ROS) act as a driving force of the aging process, and it is generally believed that mitochondrial dysfunction is a major source of increased oxidative stress in tissues with high content of mitochondria, such as muscle or brain. However, recent experiments in mouse models of premature aging have questioned the role of mitochondrial ROS production in premature aging. To address the role of mitochondrial impairment and ROS production for aging in human muscles, we have analyzed mitochondrial properties in muscle fibres isolated from the vastus lateralis of young and elderly donors. Mitochondrial respiratory functions were addressed by high-resolution respirometry, and ROS production was analyzed by in situ staining with the redox-sensitive dye dihydroethidium. We found that aged human skeletal muscles contain fully functional mitochondria and that the level of ROS production is higher in young compared to aged muscle. Accordingly, we could not find any increase in oxidative modification of proteins in muscle from elderly donors. However, the accumulation of lipofuscin was identified as a robust marker of human muscle aging. The data support a model, where ROS-induced molecular damage is continuously removed, preventing the accumulation of dysfunctional mitochondria despite ongoing ROS production.

AB - According to the free radical theory of aging, reactive oxygen species (ROS) act as a driving force of the aging process, and it is generally believed that mitochondrial dysfunction is a major source of increased oxidative stress in tissues with high content of mitochondria, such as muscle or brain. However, recent experiments in mouse models of premature aging have questioned the role of mitochondrial ROS production in premature aging. To address the role of mitochondrial impairment and ROS production for aging in human muscles, we have analyzed mitochondrial properties in muscle fibres isolated from the vastus lateralis of young and elderly donors. Mitochondrial respiratory functions were addressed by high-resolution respirometry, and ROS production was analyzed by in situ staining with the redox-sensitive dye dihydroethidium. We found that aged human skeletal muscles contain fully functional mitochondria and that the level of ROS production is higher in young compared to aged muscle. Accordingly, we could not find any increase in oxidative modification of proteins in muscle from elderly donors. However, the accumulation of lipofuscin was identified as a robust marker of human muscle aging. The data support a model, where ROS-induced molecular damage is continuously removed, preventing the accumulation of dysfunctional mitochondria despite ongoing ROS production.

U2 - 10.1111/j.1474-9726.2007.00282.x

DO - 10.1111/j.1474-9726.2007.00282.x

M3 - Journal article

C2 - 17376148

VL - 6

SP - 245

EP - 256

JO - Aging Cell

JF - Aging Cell

SN - 1474-9718

IS - 2

ER -

ID: 21693585