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A Proposed Mechanism for Diuron-Induced Phytotoxicity

Published online by Cambridge University Press:  12 June 2017

Charles E. Stanger Jr.  and
Arnold P. Appleby
Charles E. Stanger Jr.
Affiliation:
Dep. of Crop. Sci., Oregon State Univ., Corvallis, Oregon 97331
Arnold P. Appleby
Affiliation:
Dep. of Crop. Sci., Oregon State Univ., Corvallis, Oregon 97331
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Abstract

Chloroplasts isolated from spinach (Spinacia oleracea L.) 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.

Type
Research Article
Information
Weed Science , Volume 20 , Issue 4 , July 1972 , pp. 357 - 363
Copyright
Copyright © Weed Science Society of America 

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