Improvement of the anoxia-induced mitochondrial dysfunction by membrane modulation.
The mitochondrial dysfunction induced by anoxia in vitro was improved with chlorpromazine, cepharanthine, bromophenacyl bromide, and mepacrine without affecting phospholipid or adenine nucleotide metabolisms. The drugs inhibited lipid peroxidation by Fe2+, mitochondrial disruption by Ca2+, and membrane perturbation by lysolecithin, and retained the activity to control H+ permeability across mitochondrial membranes. The drugs appeared to preserve the functions by acting to suppress the development of membrane deterioration which may have resided in the deenergization of mitochondria in the absence of oxygen.
D000098:Acetophenones / Q000494:pharmacology; D000227:Adenine Nucleotides / Q000378:metabolism; D000470:Alkaloids / Q000494:pharmacology; D000818:Animals; D044182:Benzylisoquinolines; D002746:Chlorpromazine / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D000860:Hypoxia / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism*; D008933:Mitochondrial Swelling; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption / Q000187:drug effects; D010743:Phospholipids / Q000378:metabolism; D011796:Quinacrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D052117:Benzodioxoles
D000098:Acetophenones; D000227:Adenine Nucleotides; D000470:Alkaloids; D044182:Benzylisoquinolines; D002746:Chlorpromazine; D004533:Egtazic Acid; D010743:Phospholipids; D011796:Quinacrine; C006947:cepharanthine; D052117:Benzodioxoles; C006821:4-bromophenacyl bromide