Literature DB >> 15925408

Effects of herbicide chlorimuron-ethyl on physiological mechanisms in wheat (Triticum aestivum).

Meie Wang1, Qixing Zhou.   

Abstract

Changes in the activity of antioxidant enzymes including peroxidases (POD) and superoxide dismutases (SOD) and in the contents of chlorophyll (CHL), malondialdehyde (MDA), and soluble proteins (SP) in wheat (Triticum aestivum) under the stress of chlorimuron-ethyl in soil were examined. Chlorimuron-ethyl induced oxidative stress that was indicated by elevated MDA content in leaves and roots after a 1-day exposure. The 300-microg/kg chlorimuron-ethyl treatment caused significant damage to CHL accumulation. The higher POD activity in roots than in leaves may be the result of the tissue-specific gene expression in the roots. Our data could suggest that the plant has the capacity to counteract the oxidative stress caused by 5-150 microg/kg chlorimuron-ethyl exposure at the first stage, but the capacity would be lost with exposure time. It is indicated that the increase of POD activity in the leaves may have been caused by H(2)O(2) produced from sources other than SOD. The damage to the antioxidative defensive systems in plants is affected by the concentration of chlorimuron-ethyl and exposure time, and the defensive effect of antioxidative enzymes is completely lost with prolonged exposure. When treated with 300 microg/kg of chlorimuron-ethyl, a significant decrease of SP content and SOD activity in the leaves and roots indicated that the decrease of SP content and the activity of SOD can be considered biomarkers of the serious stress of chlorimuron-ethyl in soil. The increase of SP content in leaves after 3-4 days of exposure to 5-150 microg/kg chlorimuron-ethyl suggests that the enhanced POD activity was due to true induction of de novo synthesis rather than reactivation of preexisting apoprotein. It can also be concluded that dose-response relationships exist only between the SP content in roots and leaves and the concentration of chlorimuron-ethyl.

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Year:  2005        PMID: 15925408     DOI: 10.1016/j.ecoenv.2005.03.032

Source DB:  PubMed          Journal:  Ecotoxicol Environ Saf        ISSN: 0147-6513            Impact factor:   6.291


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