EFFECT OF ELECTRON-TRANSPORT INHIBITORS AND SOME METABOLITES ON [6-C-14] CITRATE CONVERSIONS IN PLANTS

Metabolization of [6-C-14] citrate in the leaves of maize (Zea mays L. ) and wheat (Triticum aestivum L.) was studied in the presence of elec tron transport inhibitors and some metabolites involved in tricarboxyl ic acid cycle, photorespiration pathways, and ascorbate oxidase system . Release of (CO2)-C-14, which was measured after infiltrating leaf se gments with [6-C-14] citrate, was suppressed by KCN and salicylhydroxa mic acid and was stimulated by rotenone. The main route of [6-C-14] ci trate utilization was through the isocitrate dehydrogenase reaction, a s indicated by strong suppression of (CO2)-C-14 release after synergis tic inhibition of isocitrate dehydrogenase with, glyoxylate and oxaloa cetate, and after retroinhibition of the enzyme activity by 2-oxogluta rate. The addition of ascorbate with glutathione stimulated oxidation of [6-C-14] citrate; this phenomenon was caused by activation of NADP- isocitrate dehydrogenase and by coupling of this enzyme activity with operation of NAD(P)H-oxidizing ascorbate oxidase system. Utilization o f [6-C-14] citrate was suppressed by succinate and glyoxylate, presuma bly as a result of activated isocitrate synthesis by extraglyoxysomal isocitrate lyase. Inhibition of cyanide-sensitive and cyanide-resistan t electron transport stimulated utilization of citrate in the reaction s of gamma-aminobutyric pathway shunting, the tricarboxylic acid cycle . It is concluded that intermediates of tricarboxylic acid cycle and p hotorespiration (succinate, glyoxylate, glycine, etc.) play an importa nt role in the regulation of citrate conversion pathways. The coupling of citrate metabolism with essential cellular processes and various e lectron transport chains allows effective control of metabolic convers ions of citrate according to the requirements of the plant organism.