Abstract

Root application of the quinolinecarboxylic acid herbicide quinclorac to barnyard grass ((Echinochloa crus-galli (L.) P. Beauv.) caused inhibition of shoot growth accompanied by chlorosis and necrosis. After 1 day of exposure, cyanide levels in the shoot tissue increased according to the concentration of the herbicide and the time of its application and closely correlated with the reduction in shoot fresh weight. Four days after the application of 10 and 100 μM quinclorac, the respective cyanide levels in the shoot tissue were approximately two and three times higher than controls and reached a maximum of 40 μM. Increases in β-cyanoalanine synthase activity, the main HCN detoxifying enzyme, ethylene production, and in the endogenous levels of 1-aminocyclopropane-1-carboxylic acid (ACC) preceded cyanide accumulation, When ACC was exogenously supplied to detached shoots of barnyard grass via the vascular system, its accumulation within the tissue coincided with increases in ethylene formation and cyanide content. Both metabolites of ACC appeared to be formed in stoichiometrically equivalent amounts. Root treatment of intact plants with KCN caused concentration-dependent increases in the levels of cyanide found in the shoot tissue which inversely correlated with the changes in fresh weight. The concentrations of quinclorac or KCN applied via the roots which led to twofold increases in the cyanide levels of the shoots had similar effects on the shoot fresh weight, causing reductions of nearly 30%. The phytotoxic symptoms, chlorosis and necrosis, were also similar. In contrast, phytotoxic tissue sensitivity to ethylene released by applied 2-chloroethylphosphonic acid (ethephon) was only very low. It is concluded that cyanide, derived ultimately from quinchlorac-stimulated ACC synthesis, is a causative factor in the herbicidal effects observed in the shoots of barnyard grass.

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