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Relationship between configuration, function, and permeability in calcium-treated mitochondria.

D R Hunter, R A Haworth, J H Southard

The Journal of Biological Chemistry

|August 25, 1976

Summary

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Low levels of calcium trigger mitochondrial changes, increasing inner membrane permeability and uncoupling oxidative phosphorylation. These effects are reversible, highlighting the membrane

Area of Science:

Mitochondrial physiology
Cellular respiration
Membrane transport

Background:

Mitochondria regulate cellular energy production through oxidative phosphorylation.
Mitochondrial membrane permeability is crucial for its function.
Calcium ions are known signaling molecules with diverse cellular roles.

Purpose of the Study:

To investigate the effects of low calcium levels on mitochondrial structure and function.
To elucidate the mechanism by which calcium influences mitochondrial permeability and oxidative phosphorylation.
To compare the effects of calcium with other ions and molecules on mitochondrial transitions.

Main Methods:

Addition of calcium (100 nmol/mg) to beef heart mitochondria.
Monitoring of configurational changes, oxidative phosphorylation, and membrane permeability.

Related Experiment Videos

Use of calcium transport inhibitors (EGTA, ruthenium red, lanthanum) and other agents (phosphate, arsenate, oleic acid, N-ethylmaleimide, strontium, magnesium).

Main Results:

Calcium induced a transition from aggregated to orthodox mitochondrial state and uncoupled oxidative phosphorylation.
Calcium increased inner membrane permeability, allowing sucrose entry, and this effect was reversible.
Phosphate, arsenate, and oleic acid mimicked calcium's transition-inducing effects, requiring endogenous calcium.

Conclusions:

Mitochondrial coupling is dependent on inner membrane permeability, not configurational state.
Calcium, phosphate, and fatty acids activate a common mitochondrial mechanism.
This mechanism involves increased permeability, ATPase induction, uncoupling, and loss of respiratory control.