Ascorbic Acid Oxidase in Cell Growth

Abstract

It has been demonstrated by Marre and his associates that ascorbic acid (AA) antagonizes auxin in most of its effects, and that this antagonism is attributed to the rapid oxidation of AA to inhibitory concentrations of dehydroascorbic acid (DHA) wi,thin the tissues (6, 7, 14). In 1957 Marre and Arrigoni (8) postulated a mechanism through which the effect of auxin on ascorbic acid oxidation could be transmitted to metabolic functions of fundamental importance to cell growth. They suggested that an auxin-induced decrease of ascorbic acid oxidation would produce a shift toward the reduced form of glutathione (GSH), possibly through the participation of dehydroascorbic acid reductase. A shift in the reduced-oxidized glutathione (GSH/GSSG) ratio could affect the reduction state of sulfhydryl enzymes and cofactors. They concluded that the GSH/GSSG ratio is closely controlled by growth regulators and that auxin-induced growth favors GSH. More recently Key (2, 3) has presented data that would tend to support the Milan group. While this theory and its supporting data are of considerable interest it does not explain the observation that the highest ascorbic acid oxidase activity in the maize root tip is associated with those cells which are undergoing rapid cell elongation (9). Furthermore, Newcomb (11, 12) has demonstrated that ascorbic acid oxidase activity is increased by auxin in tobacco pith tissue. It was because of these discrepancies that the following study was undertaken to determine what changes occur in asorbic acid oxidase activity in a tissue that has been induced to grow.