Alcohol stimulates Na sup + /Ca sup 2+ exchange in brain mitochondria
- Hahnemann Univ., Philadelphia, PA (USA)
Ethanol, at low concentrations, specifically stimulates the Na{sup +}-dependent Ca{sup 2+}-efflux in brain mitochondria. In addition, at higher concentrations, ethanol inhibits the Na{sup +}-independent Ca{sup 2+}-efflux. The electrogenic Ca{sup 2+}-uptake system is not affected by ethanol. The specific stimulation of Na{sup +}/Ca{sup 2+} exchange reaches a maximum of 60% stimulation, with half-maximal stimulation at 130 mM ethanol. The inhibition of the Na{sup +}-independent efflux is proportional to the ethanol concentration, becoming significant only above 200 mM, with 50% inhibition at 0.5 M. The inhibition of the Na{sup +}-independent efflux is, in large part, due to an inhibition of the activation of the Cyclosporin-sensitive pore. Long-term ethanol-feeding had no effect on the Ca{sup 2+} transport systems and their sensitivity to acute ethanol treatment. It is suggested that the stimulation of the Na{sup +}-dependent Ca{sup 2+}-efflux, which is the dominant Ca{sup 2+} efflux pathway in brain mitochondria, contributes to the intoxicating effects of ethanol.
- OSTI ID:
- 5923480
- Journal Information:
- Life Sciences; (USA), Vol. 48:10; ISSN 0024-3205
- Country of Publication:
- United States
- Language:
- English
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CALCIUM COMPOUNDS
MEMBRANE TRANSPORT
ETHANOL
METABOLISM
SODIUM COMPOUNDS
BIOLOGICAL PATHWAYS
BRAIN
MITOCHONDRIA
RATS
ALCOHOLS
ALKALI METAL COMPOUNDS
ALKALINE EARTH METAL COMPOUNDS
ANIMALS
BODY
CELL CONSTITUENTS
CENTRAL NERVOUS SYSTEM
HYDROXY COMPOUNDS
MAMMALS
NERVOUS SYSTEM
ORGANIC COMPOUNDS
ORGANOIDS
ORGANS
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560300* - Chemicals Metabolism & Toxicology