Wounding increased the extracellular Adenosine 5'-triphosphate (eATP) level of kidney bean leaves. Treatment with wounding or exogenous ATP increased the hydrogen peroxide (HO) content, activities of catalase and polyphenol oxidase, and malondialdehyde content in both the treated and systemic leaves. Pre-treatment with ATP-degrading enzyme, apyrase, to the wounded leaves reduced the wound-induced local and systemic increases in HO content, activities of catalase and polyphenol oxidase, and malondialdehyde content. Application of dimethylthiourea (DMTU) and diphenylene iodonium (DPI) to the wounded and ATP-treated leaves, respectively, reduced the wound- and ATP-induced local and systemic increases in HO content, activities of catalase and polyphenol oxidase, and malondialdehyde content. Moreover, the wound- and ATP-induced systemic increases of these physiological parameters were suppressed when DMTU or DPI applied to leaf petiole of the wounded and ATP-treated leaves. These results suggest that eATP at wounded sites could mediate the wound-induced local and systemic responses by HO-dependent signal transduction.
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http://dx.doi.org/10.1080/09168451.2018.1547623 | DOI Listing |
Health Res Policy Syst
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University College London, London, United Kingdom.
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KontinenzZentrum AG Zürich, Witellikerstrasse 40, 8032, Zürich, Schweiz.
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Department of Medicine, Divisions of Geriatric Medicine and Gerontology, the Department of Physiology and Biomedical Engineering, and the Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota. Electronic address:
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School of Medicine and Health, Department of Diagnostic and Interventional Neuroradiology, Technical University of Munich, Munich, Germany; School of Medicine and Health, TUM-NIC Neuroimaging Center, Technical University of Munich, Munich, Germany.
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Affiliated Eye Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Jiangxi Research Institute of Ophthalmology & Visual Science, Jiangxi Provincial Key Laboratory for Ophthalmology, Jiangxi Clinical Research Center for Ophthalmic Disease, Nanchang, China. Electronic address:
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