Effect of Mono-oxygenase Inhibitors on Uptake, Metabolism and Phytotoxicity of Propanil in Resistant Biotypes of Jungle-Rice,Echinochloa Colona

Abstract

: The e †ect of the mono-oxygenase inhibitors tridiphane, piperonyl butoxide and prochloraz on propanil uptake, metabolism and phytotoxicity was measured in a resistant (R) biotype of Echinochloa colona. The uptake of propanil was not signiÐcantly a †ected by any of the three mono-oxygenase inhibitors. The Ðrst metabolite of propanil metabolism, 3,4-dichloroaniline, was found to accumulate to higher levels in E. colona treated with each of the mono-oxygenase inhibitors mixed with formulated propanil, compared to propanil applied alone.Accumulation of further metabolites of propanil (glucosyl-3,4-dichloroaniline and bound products) was reduced in the presence of mono-oxygenase inhibitors, compared with propanil application alone. Leaf damage caused by a single drop of propanil compared to propanil ] mono-oxygenase inhibitor was used to assess the degree of propanil tolerance in E. colona biotypes. Leaf damage was signiÐcantly greater in propanil ] mono-oxygenase inhibitor treatments. No leaf damage was observed in mono-oxygenase inhibitor treatments alone at the concentrations used.Peroxidase activity was measured in crude extracts of the R-biotype of E. colona using 3,4-dichloroaniline as substrate, in the presence and absence of mono-oxygenase inhibitors and the speciÐc peroxidase inhibitor salicylhydroxamic acid. Peroxidase activity was inhibited by all three monooxygenase inhibitors at 10 kM and by salicylhydroxamic acid at 1 kM. Glucosyl-3,4-dichloroaniline was found not to be a substrate for peroxidase activity.These results suggest that the incorporation of 3,4-dichloroaniline into bound residues involves peroxidase activity which can be inhibited by mono-oxygenase inhibitors. When peroxidase activity is inhibited, the precursor metabolite 3,4-dichloroaniline accumulates, and propanil resistance in E. colona is reduced, possibly as a consequence of phytotoxicity of this metabolite and/or product inhibition of the Ðrst step in propanil metabolism, responsible for the formation of 3,4-dichloroaniline. Glasshouse trials have demonstrated that the application of mono-oxygenase inhibitors, (particularly tridiphane which is also known to inhibit glutathione transferase activity) with propanil o †ers a promising approach to the control of propanil resistant biotypes of Jungle-Rice.

Characterization of aryl acylamidase activity from propanil‐resistant barnyardgrass (Echinochloa crus‐galli [L.] Beauv.)

“…Similar results were obtained in propanil-resistant junglerice (Lopez-Martinez et al 2001). Research on two propanil-resistant biotypes of junglerice demonstrated that the resistance mechanism was also elevated aryl acylamidase activity (Leah et al 1994(Leah et al , 1997. In propanil-resistant junglerice, the aryl acylamidase was isolated and some of its properties elucidated (Leah et al 1997).…”

“…Both the total and specific enzyme activity increased with junglerice plant age up to 15 days (4‐leaf stage), then decreased after 20 days to about half of the maximum at 36 days. Biochemical analysis of partially purified aryl acylamidases from junglerice and rice seedlings indicated that these enzymes possessed similar pH optima (pH = 7.5) and native molecular masses, as estimated by gel filtration (Leah et al . 1997).…”

“…2001). Research on two propanil‐resistant biotypes of junglerice demonstrated that the resistance mechanism was also elevated aryl acylamidase activity (Leah et al . 1994, 1997).…”

“…1994, 1997). In propanil‐resistant junglerice, the aryl acylamidase was isolated and some of its properties elucidated (Leah et al . 1997).…”

Resistance mechanism of Leptochloa chinensis Nees to propanil

“…2001). Research on two R‐JR biotypes demonstrated that the resistance mechanism also was due to elevated aryl acylamidase activity (Leah et al . 1994; 1997).…”