PHYSIOLOGICAL RESPONSE OF LIPID COMPONENTS TO THIOCARBAMATES AND ANTIDOTES

Abstract

Thiocarbamate herbicide symptomology is consistent with a chronic loss of vital metabolic components on increasing toxicant concentration but not with acute blockage of a central reaction. S -Ethyl dipropylthiocarbamate (EPTC) activity is representative of the thiocarbamate herbicides. EPTC inhibits epicuticular wax synthesis, chloroplast fatty acid synthesis (FAS), “aged” tissue FAS and olelyl desaturase (DE) activity. These EPTC inhibitions of FAS and DE are reversed by 1, 8-naphthalic anhydride (N) and N , N -diallyl-2, 2-dichloroacetamide (R). Protein synthesis is not involved. EPTC-induced betacyanin efflux from “aged” red beet discs is time, temperature and concentration dependent and is reversed by N and R. Wheat root phospholipid content is decreased by EPTC and soybean leaf complex lipid class fatty acid contents are quantitatively and qualitatively altered by μM EPTC. The major response is a drastic decrease in linolenic acid (18:3) content. At high light intensities, wheat and corn growth is inhibited by EPTC. In darkness, neither crop is susceptible to EPTC at the same concentrations which induce growth reductions in the light. Differential penetration is not involved. EPTC inhibits wheat growth more than chlorophyll and carote-noid synthesis. Variation in wheat chloroplast electron carrier ratios indicates inhibition of epoxidation. Inhibition of polyphenol oxidase by EPTC is reversed by N and R. Thus, only the FAS portion of the total plant lipid synthesis is inhibited by the thiocarbamate herbicides. Mitochondrial phospholipid requirements for respiratory control and oxidative phosphorylation indicate that FAS inhibition is sufficient to explain thiocarbamate herbicide toxicity. However, the light intensity influence on plant responses to EPTC indicates the existence of more than one thiocarbamate herbicide mode of activity.