Abstract

The nitrodiphenyl ether herbicide acifluorfen-methyl and the pyridine derivative LS 82-556 induce porphyrin accumulation in green cucumber cotyledons. When experiments are done with intact plants absorbing the herbicide through the roots, that accumulation is light-dependent. 3-(3,4-Dichlorophenyl)-1,1-dimethylurea (DCMU) which prevents cellular damages under these conditions (M. Matringe and R. Scalla, Pestic. Biochem. Physiol. 26, 150 (1986), also inhibits porphyrin accumulation. In contrast, when detached cotyledons are cut into pieces and floated on herbicide solutions, porphyrins accumulate in the dark. Accordingly, DCMU does not inhibit porphyrin accumulation or protect the tissues against herbicidal effects. Furthermore, 4,6-dioxoheptanoic acid, and inhibitor of tetrapyrrole biosynthesis, prevents both porphyrin accumulation and phytotoxic effects. The same results can be obtained with norflurazon, an inhibitor of carotenoid biosynthesis; in this case, inhibition of porphyrin biosynthesis is probably a secondary consequence of abnormal development of chloroplasts. These results indicate that the herbicidal activity of diphenyl ether-type herbicides probably results from their ability to interfere with the metabolism of tetrapyrroles.

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