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

Abstract

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 EMD-IT 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 herbicidetreated, 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.

Nature of Photooxidative Events in Leaves Treated with Chlorosis-Inducing Herbicides

“…In aminotriazole-treated tissue an even greater accumulation of the resulting internal H202 is to be expected because of the inactivation of catalase through aminotriazole (10). Nevertheless, Chl was not significantly degraded after application of glycolic acid, as compared to leaf sections floated as controls on a citric acid solution of the same pH as the glycolic acid solution applied.…”

“…In previous work, two groups of chlorosis-inducing herbicides of different potency were discriminated (10,11). A representative of the pyridazinone herbicides, San 6706, and difunon (group 2) induced a severe carotenoid deficiency and very intense photooxidative damage oftreated leaves in light, including the degradation of ChM, 70S ribosomes, chloroplast enzymes, and even the inactivation of many or conceivably all peroxisomal enzymes.…”

The in Vivo and in Vitro Inhibition of Catalase from Leaves of Nicotiana sylvestris by 3-Amino-1,2,4-Triazole

“…The uptake, metabolism, and mode of action of the compound in plants have been studied (4-6, 18, 24), but the in vivo inactivation of the enzyme has seldom been investigated and there are no in vitro studies with a catalase of plant origin. Catalase activity was inhibited 50% in a suspension culture of pear cells after 4 h exposure to 1 mm aminotriazole (6), and was inhibited approximately 85% in rye seedlings soaked and grown in the presence of 0.25 mm inhibitor (5). Also, clones of tobacco have been selected that grow in the presence of 0.19 mM aminotriazole (25), but neither the cells nor the regenerated plants were analyzed for enzymic activities.…”

Chloroplastic Regulation of Apoplastic α-Amylase Activity in Pea Seedlings

“…Photooxidation as a result of NF treatments causes the destruction of plastidic ribosomes (1,13,33) and proteins (14,19,31,35), but does not adversely affect cytosolic ribosomes or proteins (4,33). However, in that the effects of NF on chloroplastic function are so wide ranging, and because we have found that inhibitors ofplastid functions which occur after protein synthesis have little or no effect on apoplastic a-amylase, seedlings were treated with inhibitors of plastid protein synthesis to determine if the effect of NF is through blocking plastid or nuclear genome expression.…”