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Comparative Investigation of the Action of Several Chlorosis-inducing Herbicides on the Biogenesis of Chloroplasts and Leaf Microbodies.

Seedlings of Triticum aestivum L. and Secale cereale L. were grown in the presence of six different (five having different chemical structures) chlorosis-inducing herbicides: aminotriazole and its derivative SDR 5175, haloxidine, Sandoz 6706, fluometuron, and EMD-IT 5914. Concentrations were applied which allowed the leaves to grow normally and to reach normal total amino nitrogen contents but evoked a complete chlorosis (less than 6% chlorophyll). The effects of the herbicides on the accumulation of several chloroplast constituents and on peroxisomal and mitochondrial marker enzyme activities were compared. Wheat and rye, in general, gave very similar results, wheat being more sensitive to unspecific inhibitory effects.In dark-grown plants, the herbicides had no or only minor effects on the rRNA pattern and on enzyme activities of the leaves. In the light, all herbicides applied prevented the accumulation of carotenoids and of chloroplastic rRNA. Consequently, ribulose-1,5-bisphosphate carboxylase activity was virtually absent. After all herbicide treatments in light, the leaves contained only rather low catalase activity. In the presence of aminotriazole and haloxidine, the chloroplast-specific NADP-glyceraldehyde-3-phosphate dehydrogenase and the peroxisomal enzymes glycolate oxidase and hydroxypyruvate reductase had high or even normal activities, as in untreated leaves. In leaves treated with Sandoz 6706, fluometuron, or EMDIT 5914, the activities of the latter three enzymes were, in parallel, only very low. Some herbicides interfered with enzyme activities in vitro, particularly with those of catalase and of glycolate oxidase. Among mitochondrial enzymes, cytochrome c oxidase activity was either unaffected or lower, while fumarase had considerably higher activities in the herbicide-treated, as compared to untreated leaves. The specific effects on peroxisomal enzymes cannot be explained by the hypothesis of herbicide-induced photodestructions in carotene-deficient plastids. Alternative explanations for the genesis of the chlorosis are discussed.