EFFECTS OF VICTORIN ON NITROGEN METABOLISM OF AVENA SPECIES.

Abstract

VICTORIA, the specific toxin produced by Helmintho-sporium victoriae M. and M., affects only Avena species and varieties that carry the Victoria gene conditioning susceptibility to the fungus1. This toxin, which has been extensively used to examine the physiology of disease, has been shown to be the disease-inducing agent2. One of the most striking physiological responses to victorin is a sharp respiratory increase in susceptible tissues3. When victorin was added to homogenates of susceptible tissue no effect on cytochrome oxidase, polyphenol oxidase, or catalase occurred, but a 2- to 4-fold increase in ascorbate oxidation was observed. The increase in ascorbate oxidation was accompanied by a marked decrease in ascorbic acid content; therefore it was concluded that increased respiration was mediated through an ascorbic acid pathway of oxidation4. Additional data indicated that although ascorbic acid oxidation influenced respiration, it did not initiate the response because increased ascorbate oxidation occurred only after the respiratory rate had reached its maximum5. More recent data indicate that toxin treatment changes cell permeability which may influence respiration because organic acids and potassium salts leak from the vacuole into the cytoplasm6. Therefore, the pathway of increased respiration in victorin-treated susceptible tissue is not fully understood.