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Age-related increase in mitochondrial proton leak and decrease in ATP turnover reactions in mouse hepatocytes

M E Harper¹, S Monemdjou, J J Ramsey

¹Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5.

The American Journal of Physiology

|August 4, 1998

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Mitochondrial function declines with age, showing reduced oxygen consumption and altered control of oxidative phosphorylation in older mice. This age-related shift impacts cellular energy production efficiency.

Area of Science:

Mitochondrial biology
Cellular metabolism
Aging research

Background:

Mitochondria undergo age-related changes affecting cellular respiration.
Previous studies noted decreased respiratory control and altered lipid composition in aging mitochondria.

Purpose of the Study:

To investigate age-related alterations in oxidative phosphorylation control and regulation.
To compare metabolic control in hepatocytes from young and old mice.

Main Methods:

Utilized top-down metabolic control analysis and elasticity analysis.
Examined hepatocytes from young (3 mo) and old (30 mo) male C57BL/J mice.
Assessed oxygen consumption, mitochondrial membrane potential, and metabolic control coefficients.

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Main Results:

Older mice exhibited 15% lower resting oxygen consumption, primarily due to decreased ATP turnover.
A greater proportion of oxygen consumption balanced mitochondrial proton leak in old cells.
Metabolic control shifted from substrate oxidation towards leak and ATP turnover reactions in aged cells.

Conclusions:

Aging alters the control and regulation of mitochondrial oxidative phosphorylation.
Older cells show increased sensitivity of ATP synthesis efficiency to changes in leak and ATP turnover.
These findings highlight age-dependent changes in cellular energy metabolism regulation.