The influence of the safener, CGA 185072 (5-chloro-8-quinolinoxy-acetic acid-1-methylhexyl-ester), on the metabolism of the aryloxyphenoxypropanoate herbicide, CGA 184927 (2-propynyl-R-2-[4-(5-chloro-3-fluoro-2-pyridinyloxy)-phenoxy]-propionate), was studied in excised leaves of wheat, barley, and maize. In wheat and barley, CGA 184927 readily under­went ester hydrolysis followed by hydroxylation at the pyridinyl moiety as well as ether cleav­age between the pyridinyl and the phenyl ring. Ether cleavage constituted the minor pathway in both species. All metabolites were subject to glycosyl conjugation. Tetcyclacis strongly in­hibited pyridinyl-ring hydroxylation in wheat. Metabolism by hydroxylation and ether cleav­age was more rapid in wheat than in barley, and was found to be accelerated in the presence of the safener CGA 185072 in both wheat and, to a lesser degree, in barley. Moreover, the safener increased the capacity for O-glycoside formation in wheat as suggested from studies using the ,4C-labelled pyridinyl-ring hydroxylated metabolite as a precursor. In maize, which is highly susceptible to CGA 184927, rapid ester hydrolysis of CGA 184927 and partial conversion of the corresponding carboxylic acid to glycosyl ester conjugate(s) occurred. However, no further transformation of the herbicide was found in maize, both in the absence or presence of CGA 185072. It is concluded that the ability of CGA 185072 to protect wheat from injury by the herbicide, CGA 184927, and to confer partial protection to barley, is related to the ability of the safener to stimulate herbicide metabolism in these crop species.

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