DIPHENYL ETHER HERBICIDE-DECREASED HEME CONTENTS STIMULATE 5-AMINOLEVULINIC ACID SYNTHESIS

Our previous reports showed that diphenyl ether herbicides stimulate 5-aminolevulinic acid (ALA)-synthesizing system activity in vivo. Based on this result, we investigated diphenyl ether herbicides (mainly acifluorfen-methyl [methyl 5-(2-chloro-4-trifluoromethylphenoxy)-2-nitrobenzoate]) treated tissue. The activity of cell-free 5-aminolevulinic acid-synthesizing enzymes in nonchlorophyllous tobacco cells (Nicotiana tabacum L. cv. samsun) and the activity controlled by the addition of heme were not affected by the diphenyl ether herbicides in vitro. The pattern of accumulated tetrapyrroles in etiolated cucumber (Cucumis sativus L. cv. okuji) cotyledons was apparently different between the treatment with acifluorfen-methyl and 5-aminolevulinic acid-treated tissue. The addition of heme greatly inhibits both the light-dependent O2 consumption activity and ALA synthesis in tobacco cells induced by the treatment of acifluorfen-methyl. Heme contents in both nonchlorophyllous tobacco cells and etiolated cucumber cotyledons were apparently decreased by the treatment with acifluorfen-methyl. The ferrochelatase activity in the green spinach leaves was not affected by the foliar treatment with acifluorfen-methyl. Sn protoporphyrin IX, a potent inhibitor of heme oxygenase, had no significant effect on the action of acifluorfen-methyl on ALA synthesis in tobacco cells. These results suggested that diphenyl ether herbicides indirectly inhibit the accumulation of heme, which conducts feedback regulation on 5-aminolevulinic acid synthesis, and stimulates 5-aminolevulinic acid-synthesizing enzymes. © 1990.