Quinclorac-induced cell death is accompanied by generation of reactive oxygen species in maize root tissue.
The importance of reactive oxygen species for herbicide quinclorac (3,7-dichloro-8-quinolinecarboxylic acid)-induced cell death in roots was investigated. This was in order to understand its mode of action in grass species grown in the dark. Under these dark conditions, quinclorac suppressed the shoot and root growth of maize (Zea mays L. cv. Honey Bantam) in a concentration-dependent manner (50microM), although the inhibition level was less than that observed under growth conditions in the light. Analysis of cell viability using Evans blue or fluorescein diacetate-propidium iodide (FDA-PI) staining showed that the maize root cells significantly lost their viability after 14h root treatment with 10microM quinclorac, but not 10microM 2,4-dichlorophenoxyacetic acid (2,4-D). Determination of reactive oxygen species (ROS) in maize roots using a superoxide anion (O2-)-specific indicator, dihydroethidium (DHE), indicated that 50microM quinclorac induced a high level of O2- production in maize roots after 14h root treatment than that of either the control (non-treated) or with 50microM 2,4-D. Moreover, either cell death or ethane evolution, an indicator of lipid peroxide formation, in maize root segments was significantly enhanced by 50microM quinclorac, but not by 50microM 2,4-D. On the other hand, the 50microM 2,4-D treatment induced much higher ethylene and cyanide production in the root segments than with the 50microM quinclorac. These results suggest that quinclorac-induced cell death in maize roots may be caused by ROS and lipid peroxidation, but not by ethylene and its biosynthetic pathway-related substances including cyanide, which have been thought to be the causative factor of quinclorac-induced phytotoxicity in susceptible grass weeds such as Echinochloa, Digitaria, and Setaria.
Sunohara
Yukari
Y
Doctoral Program in Life Sciences and Bioengineering, Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan. sunohara@sakura.cc.tsukuba.ac.jp
Matsumoto
Hiroshi
H
D015084:2,4-Dichlorophenoxyacetic Acid / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects*; D018517:Plant Roots / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D011804:Quinolines / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D003313:Zea mays / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*
D011804:Quinolines; D017382:Reactive Oxygen Species; D015084:2,4-Dichlorophenoxyacetic Acid; C489048:quinclorac