A Proposed Mechanism for Diuron-Induced Phytotoxicity

Abstract

Chloroplasts isolated from spinach(Spinacia oleraceaL.) leaves were used to study mechanisms of toxicity from 3-(3,4-dichlorophenyl)-1,1-dimethylurea (diuron). Light was needed to initiate diuron injury. The addition of ascorbate plus 2,6-dichlorophenylindolephenol (DPIP) as an electron donor system completely protected the chloroplasts from diuron-induced toxicity. The protective effect from the electron donor system occurred only in functional chloroplasts. Diuron caused rapid and extensive chlorophyll degradation at chlorophyll: diuron ratios of 200:1 and lower. At higher ratios the effect was much less measurable. The electron donor system gave complete protection in the presence of methylamine HCl, a known inhibitor of photophosphorylation, indicating that a deficiency of ATP was not the primary cause of diuron toxicity. Time-course studies showed that carotenoid pigments began to degrade before initiation of chlorophyll degradation. These results are interpreted as supporting a hypothesis that diuron induces phytotoxicity by catalyzing lethal photosensitized oxidations in the cell. This may occur as a result of (a) a greater concentration of oxidized chlorophyll caused by an interruption of electron flow and (b) an inhibition of NADPH formation which is necessary to maintain a functional carotenoid protective mechanism.