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Mitochondrial permeability transition induced by 1-hydroxyethyl radical.
K Sakurai1, D A Stoyanovsky, Y Fujimoto
1Department of Biochemistry, Hokkaido College of Pharmacy, Otaru Hokkaido, Japan.
Free Radical Biology & Medicine
|April 3, 2001
Summary
1-hydroxyethyl radical (HER) causes mitochondrial swelling and permeability transition, contributing to ethanol-induced liver injury. Glutathione and vitamin E protect against HER-induced mitochondrial damage.
Area of Science:
- Biochemistry
- Hepatology
- Mitochondrial Biology
Background:
- Mitochondrial dysfunction is implicated in ethanol-induced liver injury.
- Ethanol metabolism generates reactive radicals, including 1-hydroxyethyl radical (HER).
Purpose of the Study:
- To investigate the role of HER in inducing mitochondrial swelling and permeability transition.
- To explore the protective mechanisms against HER-induced mitochondrial damage.
Main Methods:
- Electron spin resonance (ESR) spectroscopy to detect HER and its interaction with mitochondria.
- Measurement of mitochondrial swelling via absorbance changes.
- Assessment of membrane potential collapse and protein thiol levels.
Main Results:
- HER interacts with mitochondria, causing concentration-dependent swelling sensitive to cyclosporin A.
- HER induces mitochondrial swelling, thiol depletion, and membrane potential collapse.
- Glutathione and vitamin E prevented HER-induced swelling, while catalase showed mixed effects.
Conclusions:
- HER, similar to hydroxyl radical, can induce mitochondrial permeability transition.
- HER-induced collapse of membrane potential may contribute to mitochondrial dysfunction in ethanol-induced liver injury.