Induction of Rapid Metabolism of Metolachlor in Sorghum (Sorghum bicolor) Shoots by CGA-92194 and Other Antidotes

Abstract

Sorghum [Sorghum bicolor(L.) Moench. ‘G-623 GBR’] bioassays indicated that shoot growth was more susceptible to metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide] and more responsive to the antidote CGA-92194 {α-[(1,3-dioxolan-2-yl-methoxy)-imino] benzeneacetonitrile} than root growth. Seed treatment with CGA-92194 increased seedling shoot tolerance to metolachlor approximately tenfold. CGA-92194 seed treatment enhanced shoot absorption of14C-metolachlor approximately twofold. Metolachlor was initially metabolized to the glutathione conjugate in untreated shoots and those treated with CGA-92194. However, CGA-92194 seed treatment caused accelerated metolachlor metabolism in the shoot, decreasing metolachlor content and increasing formation of the glutathione conjugate. Cyometrinil {(Z)-α[(cyanomethoxy)imino] benzeneacetonitrile}, flurazole [phenylmethyl 2-chloro-4-(trifluoromethyl)-5-thiazolecarboxylate], naphthalic anhydride (1H,3H-naphtho[1,8-cd]-pyran-1,3-dione), and dichlormid (2,2-dichloro-N,N-di-2-propenylacetamide) also protected sorghum from metolachlor injury and enhanced metolachlor absorption and metabolism. The degree of protection conferred by a particular antidote was correlated with its ability to enhance metabolism of metolachlor in shoot tissue. These results are consistent with the hypothesis that the above antidotes protect sorghum from metolachlor injury by inducing rapid detoxification of metolachlor through conjugation with glutathione.