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Title: THE EFFECT OF DICLOFOP-METHYL AND ITS ANTAGONIST, VITAMIN E, ON MEMBRANE LIPIDS IN OAT (AVENA FATUA L.) AND LEAFY SPURGE EUPHORBIA ESULA L.)

Author
item SHIMABUKURO, RICHARD - FORMER ARS (DECEASED)
item Davis, David
item Hoffer, Barry

Submitted to: Pesticide Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/25/2000
Publication Date: N/A
Citation: N/A

Interpretive Summary: Dichlofop-methyl (DM) was used as a model method of inducing senescence in susceptible oat and tolerant leafy spurge (a perennial weed) to generate additional information on mechanism(s) of the senescence process. DM increased free fatty acid (FFA) content in susceptible oat more than in tolerant leafy spurge. Linolenic acid was the major polyunsaturated fatty acid (PUFA). Both total and unsaturated fatty acids from polar lipids decreased in oat and in leafy spurge. DM treatment increased neutral lipid fatty acids approximately 2-fold in oat, but not in leafy spurge. Vitamin E protected against DM-induced membrane damage in susceptible oat. Enzymes were assayed that are involved in membrane disassembly (phospholipase D; PLD) and in the generation of reactive oxygen species (lipoxygenase; LOX). PLD activity was high in both controls and DM-treated plants of both species. 2,4-D (found by others to protect against DM treatment in the field) decreased LOX activity approximately 50% in oat. The lipid analyses and enzymatic data support a hypotheses that the primary lethal mechanism of DM is to accelerate senescence by disrupting membranes, and inducing oxidative stress via reactive oxygen species. This information will lead to better understanding of the defense mechanisms of plants to combat stress, enabling weed control experts to develop ways to overcome these mechanisms to better control perennial weeds.

Technical Abstract: Diclofop-methyl (DM) increased the free fatty acid content (FFA) in leaves of DM-susceptible oat (Avena sativa L.) and in mature leaves of leafy spurge (Euphorbia esula L.). The total and unsaturated FFAs increased 9.0- and 17.4-fold, respectively, over control levels in oat and 5.7- and 7.2-fold, respectively in leafy spurge. Linolenic acid increased in both plant species. The DM-induced increase in the FFA fraction was accompanied by decreases in total and unsaturated polar lipid fatty acid (PL-FA) fractions to approximately 25% and 60% of control in oat and leafy spurge, respectively. The PL-FA fraction is likely the source of the the FFAs. DM treatment increased total and unsaturated neutral lipid fatty acid fractions 1.9- and 2.2-fold, respectively, in oat; but not in leafy spurge. A protective effect of Vitamin E against membrane deterioration caused by DM was apparent in both oat and leafy spurge. The total and unsaturated FFA levels of oat leaves treated with Vitamin E+DM increased 4.5- and 8.4-fold, respectively, over controls and 4.2- and 5.5-fold in leafy spurge. Vitamin E+DM increased both total and unsaturated PL-FAs of oat to approximately 47% of control. Phospholipase D activity was high in both controls and DM-treated oat and leafy spurge at pH 6.0. Lipoxygenase activity was unaffected by either DM or Vitamin E. However, 2,4-D (which protects against DM damage in the field) decreased LOX activity approximately 50% in etiolated oat leaves in vitro. The data support the hypothesis that the primary lethal mechanism of DM is accelerated senescence via membrane disassembly, membrane lipid catabolism and oxidative stress mediated by active oxygen species.