Auxin herbicides induce H(2)O(2) overproduction and tissue damage in cleavers (Galium aparine L.).
The phytotoxic effects of auxin herbicides, including the quinoline carboxylic acids quinmerac and quinclorac, the benzoic acid dicamba and the pyridine carboxylic acid picloram, were studied in relation to changes in phytohormonal ethylene and abscisic acid (ABA) levels and the production of H(2)O(2) in cleavers (Galium aparine). When plants were root-treated with 10 microM quinmerac, ethylene synthesis was stimulated in the shoot tissue, accompanied by increases in immunoreactive levels of ABA and its precursor xanthoxal. It has been demonstrated that auxin herbicide-stimulated ethylene triggers ABA biosynthesis. The time-course and dose-response of ABA accumulation closely correlated with reductions in stomatal aperture and CO(2) assimilation and increased levels of hydrogen peroxide (H(2)O(2)), deoxyribonuclease (DNase) activity and chlorophyll loss. The latter parameters were used as sensitive indicators for the progression of tissue damage. On a shoot dry weight basis, DNase activity and H(2)O(2) levels increased up to 3-fold, relative to the control. Corresponding effects were obtained using auxin herbicides from the other chemical classes or when ABA was applied exogenously. It is hypothesized, that auxin herbicides stimulate H(2)O(2) generation which contributes to the induction of cell death in Galium leaves. This overproduction of H(2)O(2) could be triggered by the decline of photosynthetic activity, due to ABA-mediated stomatal closure.[1]References
- Auxin herbicides induce H(2)O(2) overproduction and tissue damage in cleavers (Galium aparine L.). Grossmann, K., Kwiatkowski, J., Tresch, S. J. Exp. Bot. (2001) [Pubmed]
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