Toxicology of the 8-aminoquinolines and genetic factors associated with their toxicity in man

P. E. Carson, Raymond Hohl, M. V. Nora, G. W. Parkhurst, T. Ahmad, S. Scanlan, H. Frischer

Research output: Contribution to journalArticle

43 Scopus citations

Abstract

In vitro studies on primaquine have been carried out to examine its ability to stimulate the oxidative pathway of glucose metabolism in human erythrocytes and in vivo studies were carried out after ingestion of the drug to determine plasma levels and to investigate the formation of metabolites and the effects of the drug on human erythrocytes. These investigations showed that: Two mechanisms are involved in the stimulation of the oxidative pathway. This was demonstrated by comparing the effects of methylene blue, ascorbic acid, primaquine, and other drugs on normal, glutathione-reductase-deficient, and G6PD-deficient erythrocytes. A start was made toward classifying drugs according to the mechanism by which they stimulate CO 2 production. Following oral ingestion of primaquine, three as yet unidentified metabolites were present, two in the plasma and one in the urine. The rapid disappearance of primaquine from the plasma (within 24 hours) was confirmed. Two factors that stimulate glucose oxidation in human erythrocytes were found in plasma; one occurred only in fresh plasma, when EDTA was present, and the other occurred in all plasma and serum samples studied. The erythrocytes of blood drawn 24 hours after the ingestion of primaquine (after primaquine had disappeared from the plasma) showed increased ability to oxidize glucose. It is not yet known whether serum or plasma prepared from blood drawn 24 hours after ingestion of primaquine has the ability to increase the oxidation of glucose.

Original languageEnglish (US)
Pages (from-to)427-437
Number of pages11
JournalBulletin of the World Health Organization
Volume59
Issue number3
StatePublished - 1981

All Science Journal Classification (ASJC) codes

  • Public Health, Environmental and Occupational Health

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