ON THE MODE OF ACTION OF KUWAITIMYCIN

Kuwaitimycin influences the translocation of alkali metal cations in liver mitochondria.In presence of valinomycin, which stimulates uptake of potassium ions by the mitochondria, the addition of kuwaitimycin could augment the loss of these ions when the source of energy was mainly an oxidizable subs...

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Bibliographic Details
Published in:Journal of antibiotics 1974, Vol.27(5), pp.316-320
Main Author: SHIMI, IBRAHIM R.
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Animals
Anti-Bacterial Agents - pharmacology
Cesium - pharmacology
Hydrolysis
Kuwait
Lithium - pharmacology
Mitochondria, Liver - drug effects
Potassium - metabolism
Rats
Rubidium - pharmacology
Sodium - pharmacology
Valinomycin - pharmacology
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Summary:Kuwaitimycin influences the translocation of alkali metal cations in liver mitochondria.In presence of valinomycin, which stimulates uptake of potassium ions by the mitochondria, the addition of kuwaitimycin could augment the loss of these ions when the source of energy was mainly an oxidizable substrate. However, kuwaitimycin fail ed to cause loss of K+ from mitochondria in presence of appropriate amounts of ATP. A relation between the ionic size of the alkali metal cations and the inhibiting effect of the antibiotic on glutamate oxidation could be demonstrated. The ability of kuwaitimycin to restrain ATP supported oscillatory swelling associated with alkali metal cations transport induced by monazomycin was also demonstrated. The more voluminous the cation the more pronounced the effect on cation transport. The effect of kuwaitimycin on ATP hydrolysis in presence of different alkali metal cations was found to be weak and independent or the cationic size.In light of the results obtained it is suggested that the antibiotic is exerting its effect on ion transport by inducing pores in the mitochondrial membrane and that the addition of appropriate amounts of ATP might alter the conformation of the mitochondrial membrane in such a way as to nullify the effect of the antibiotic.
ISSN:0021-8820
1881-1469
DOI:10.7164/antibiotics.27.316