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Related Experiment Video

Updated: Jul 9, 2026

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry

Published on: November 23, 2011

Mitochondrial dysfunction in mammalian ageing.

Mügen Terzioglu¹, Nils-Göran Larsson

¹Department of Laboratory Medicine, Karolinska Institutet, S-14186 Stockholm, Sweden.

Novartis Foundation Symposium

|December 14, 2007

Summary

Ageing involves accumulated cellular damage, particularly mitochondrial DNA (mtDNA) mutations, leading to impaired respiratory function. While mitochondrial dysfunction is linked to ageing, its role in increased reactive oxygen species (ROS) production remains unclear.

Area of Science:

Gerontology
Cellular Biology
Mitochondrial Medicine

Background:

Ageing is a complex process linked to accumulating cellular damage.
Mammalian ageing correlates with increased mitochondrial DNA (mtDNA) mutations and declining respiratory chain function.
Mosaic respiratory chain deficiency is observed in various tissues of aged humans.

Purpose of the Study:

To investigate the link between somatic mtDNA mutations and age-associated phenotypes in mice.
To explore the role of mitochondrial dysfunction and reactive oxygen species (ROS) in mammalian ageing.

Main Methods:

Analysis of age-associated phenotypes in mice with experimentally induced respiratory chain deficiency.
Assessment of oxidative stress levels in mouse models with mtDNA depletion or increased mtDNA point mutations.

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Last Updated: Jul 9, 2026

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry

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Published on: November 23, 2011

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

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Published on: May 5, 2022

Main Results:

Somatic mtDNA mutations in mice are associated with ageing phenotypes like osteoporosis, hair loss, and reduced fertility.
Mouse models with induced respiratory chain deficiency show minimal or no increase in oxidative stress.
Respiratory chain-deficient cells are more susceptible to apoptosis, contributing to cell loss.

Conclusions:

Mitochondrial dysfunction, evidenced by mtDNA mutations and respiratory chain defects, is a significant factor in mammalian ageing.
The direct link between mitochondrial dysfunction and increased ROS production in ageing requires further investigation.
Future research should clarify the relative contributions of mitochondrial dysfunction and ROS to the ageing process.