The role of glycolysis in aflatoxin biosynthesis.
In resting mycelia of Aspergillus parasiticus NRRL 3240, all the glycolytic intermediates with the exception of glucose and phosphoenolpyruvate stimulated the de novo synthesis of aflatoxin from exogenous acetate. Intracellular levels of glycolytic intermediates were measured in the toxigenic strain, A. parasiticus NRRL 3240, and the nontoxigenic strain, A. flavus NRRL 3537. In 48-h cultures, the concentrations of the intermediates beyond the phosphofructokinase reaction were higher in toxigenic mycelial extracts than in nontoxigenic cultures. There was a marked reduction in the specific activity of phosphofructokinase with increasing age in the toxigenic strain. The specific activity of this enzyme was two- to four-fold lower in zinc-deficient mycelia of A. parasiticus. In resting cultures, the uptake rate of labeled glucose was considerably lower in zinc-deficient mycelia than in zinc-replete or nontoxigenic cultures. On the basis of the results obtained, it can be said that intense formation of aflatoxin is associated with a sharp fall in the level of phosphoenolpyruvic and pyruvic acids. This was accompanied by a significantly higher pyruvate kinase activity.
D000348:Aflatoxins / Q000096:biosynthesis*; D001230:Aspergillus / Q000378:metabolism*; D001231:Aspergillus flavus / Q000378:metabolism*; D006019:Glycolysis; D010728:Phosphoenolpyruvate / Q000378:metabolism; D010732:Phosphofructokinase-1 / Q000378:metabolism; D011770:Pyruvate Kinase / Q000378:metabolism; D011773:Pyruvates / Q000378:metabolism; D019289:Pyruvic Acid; D013431:Sulfates / Q000494:pharmacology; D015032:Zinc / Q000494:pharmacology; D019287:Zinc Sulfate
D000348:Aflatoxins; D011773:Pyruvates; D013431:Sulfates; D010728:Phosphoenolpyruvate; D019287:Zinc Sulfate; D019289:Pyruvic Acid; D010732:Phosphofructokinase-1; D011770:Pyruvate Kinase; D015032:Zinc