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Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
Published on: September 7, 2012
Magnesium-induced inner membrane aggregation in heart mitochondria.
The Journal of Cell Biology
|May 1, 1978
Summary
Divalent cations like Mg(2+) cause bovine heart mitochondria inner membranes to aggregate, increasing optical density. This aggregation is reversible by adenine nucleotide transport inhibitors, suggesting a role for the adenine nucleotide carrier.
Area of Science:
- Mitochondrial biophysics
- Biochemistry
- Cell biology
Background:
- Mitochondria possess a complex inner membrane structure crucial for energy production.
- The surface charge of biological membranes influences their interactions and stability.
- Adenine nucleotide transport is vital for mitochondrial function.
Purpose of the Study:
- To investigate the effect of divalent cations on mitochondrial inner membrane aggregation.
- To explore the role of the adenine nucleotide carrier in cation-induced aggregation.
- To elucidate the mechanisms underlying mitochondrial inner membrane aggregation.
Main Methods:
- Incubation of bovine heart mitochondria under low ionic strength conditions.
- Measurement of optical density changes to quantify aggregation.
- Assessment of cation effectiveness and the impact of inhibitors like carboxyatractyloside and bongkrekic acid.
Main Results:
- Mg(2+) at 2mM induced significant increases in mitochondrial optical density (up to 30%) due to inner membrane aggregation.
- Various polyvalent cations and Ag(+) mimicked Mg(2+)-induced aggregation, with varying effectiveness.
- Inhibitors of adenine nucleotide transport prevented and reversed Mg(2+)-induced aggregation, indicating carrier involvement.
Conclusions:
- Mitochondrial inner membranes aggregate due to cation binding, which reduces the net negative surface charge.
- The adenine nucleotide carrier plays a role in regulating inner membrane aggregation.
- Carboxyatractyloside and bongkrekic acid inhibit aggregation by binding to the outer surface of the membrane, increasing negative charge.
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