Related Experiment Videos
Uncoupling of mitochondrial oxidative phosphorylation by hexetidine
Biochemical and Biophysical Research Communications
|September 15, 1987
Summary
The antibacterial hexetidine disrupts mitochondrial function by causing pyridine nucleotide oxidation and stimulating oxygen uptake. It also inhibits ATP synthesis and promotes hydrolysis, revealing its uncoupling properties.
Area of Science:
- Biochemistry
- Mitochondrial Bioenergetics
Background:
- Hexetidine is an antibacterial agent.
- Its effects on cellular energy production are not fully understood.
Purpose of the Study:
- To investigate the biochemical effects of hexetidine on mitochondrial bioenergetics.
- To determine if hexetidine impacts oxidative phosphorylation.
Main Methods:
- Isolated rat liver mitochondria were treated with hexetidine.
- Oxygen uptake, ATP synthesis/hydrolysis, and membrane potential (delta psi) were measured.
Main Results:
- Hexetidine caused oxidation of intramitochondrial pyridine nucleotides.
- It stimulated oxygen uptake with various respiratory substrates.
- Hexetidine inhibited ATP synthesis, promoted ATP hydrolysis, acidified the extramitochondrial medium, and collapsed delta psi.
Conclusions:
- Hexetidine exhibits uncoupling properties in mitochondria.
- These findings suggest a mechanism for hexetidine's antibacterial action involving mitochondrial dysfunction.