Inability of aflatoxin B1 to stimulate arachidonic acid metabolism in human polymorphonuclear and mononuclear leukocytes

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Abstract
Previous reports have suggested that aflatoxin B 1 (AFB 1 ) is a membrane-active compound capable of mediating chromosomal damage through release of toxic oxygen radicals and arachidonic acid metabolites by human leukocytes. Thus, the ability of AFB 1 to stimulate directly arachidonic acid metabolism and generate a respiratory burst in human neutrophils and monocytes was examined. AFB 1 (10 −8 – 10 −6 M) failed to induce [ 3 H]arachidonate release from prelabeled human neutrophils or mononuclear leukocytes. Similarly AFB 1 exposure at these concentrations failed to stimulate the production of either thromboxane (TX)B 2 or leukotriene (LT)B 4 from adherent monocytes. AFB 1 was also ineffective in stimulating respiratory burst activity as measured by superoxide anion (O 2− ) formation in both neutrophil and mononuclear leukocytes. We conclude that AFB 1 is unable to stimulate either arachidonic acid metabolism or initiate a respiratory burst of human leukocytes. Therefore, it appears that these pathways are not involved in the genotoxic mechanisms of AFB 1 as previously suggested.