Author
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Shimabukuro, Richard |
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Hoffer, Barry |
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Submitted to: Pesticide Biochemistry and Physiology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 2/5/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Diclofop-methyl (DM) is a herbicide believed to kill grasses (monocotyle- dons) but not broadleaf plants (dicotyledons). This property was reported to be due to the inhibition by DM of an enzyme (ACCase) that is involved in the synthesis of fatty acids in plants. Grasses have sensitive whereas dicotyledons have insensitive ACCase. DM was also reported to kill plants through an interaction with the cell membrane of susceptible plants to cause premature senescence which results in the production of free radicals, the most destructive chemical forms in living tissues. Ethylene is evolved in the senescence process as a result of free radical produc- tion. The immature leaves of leafy spurge, a dicotyledon, is resistant to DM but its mature leaves are susceptible. ACCase in both young and old leaves is apparently insensitive to inhibition by DM, but significantly higher increases in ethylene evolution occurs in older than in younger leaves only 7 hours after DM application. DM increases ethylene production in susceptible oat but not in resistant wheat. Phytotoxicity of DM in oat is reversed by the auxinic herbicide, 2,4-D, when applied in combination with DM. Ethylene production caused by DM is prevented by 2,4-D. Therefore, 2,4-D appears to reverse the lethal action of DM by preventing the production of free radicals which leads to increased ethylene evolution due to DM. The origin for this reversal resides at the cell membrane where 2,4-D counters the action of DM. The results indicate that induction of senescence and not inhibition of ACCase may be the primary phytotoxic mechanism of DM. Technical Abstract: Diclofop-methyl (DM) is an effective inducer of ethylene production in leafy spurge (Euphorbia esula), a dicotyledonous weed, and oat (Avena sativa), a susceptible monocotyledon. DM was ineffective against resistant wheat (Triticum aestivum) which metabolizes and detoxifies DM very rapidly. Immature leafy spurge leaves were resistant to DM whereas mature leaves were susceptible and death occurred within 6-7 days following application of 4.5 mM DM. Significant amounts of ethylene were produced by immature and mature leaves 7 h after DM application. Differential response of immature and mature leaves to DM was not due to differences in their metabolism and detoxification of the herbicide nor to a putative ACCase resistant to inhibition by DM. The most likely mechanism of action of DM is the induction of senescence with lipid peroxidation and free radical oxidation as the cause of lethality. Ethylene production in senescence appears to be an indirect consequence of lipid peroxidation and free radical formation. DM and 2,4-D applications induced significant ethylene evolution in oat (232 and 300% of control, respectively) after 7 h of treatment. All concentrations of 2,4-D, except for 0.75 mM, reversed DM phytotoxicity when applied as combinations. The auxinic herbicide, 2,4-D, appeared to reverse DM phytotoxicity when applied simultaneously by preventing lipid peroxida- tion and free radical formation by DM as indicated by the inhibition of ethylene production due to DM. DM phytotoxicity was not reversed when 4.5 mM DM was combined with 0.75 mM 2,4-D. Therefore, ethylene production in oat treated with this combination was approximately equal to the sum of ethylene produced by DM and 2,4-D applied separately. |
