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一氧化氮延缓蝴蝶兰花中黄嘌呤氧化酶介导的超氧阴离子生成:一氧化氮在衰老和氧化应激调节中的作用

Nitric oxide retards xanthine oxidase-mediated superoxide anion generation in Phalaenopsis flower: an implication of NO in the senescence and oxidative stress regulation.

作者信息

Tewari Rajesh Kumar, Kumar Praveen, Kim Soohyun, Hahn Eun-Joo, Paek Kee-Yoeup

机构信息

Research Center for the Development of Advanced Horticultural Technology, Chungbuk National University, Cheongju, Republic of Korea.

出版信息

Plant Cell Rep. 2009 Feb;28(2):267-79. doi: 10.1007/s00299-008-0632-8. Epub 2008 Nov 5.

DOI:10.1007/s00299-008-0632-8
PMID:18985352
Abstract

Senescence is a developmentally regulated and highly ordered sequence of events. Senescence leads to abscission of plant organs and eventually leads to death of a plant or part of it. Present study revealed that Phalaenopsis flower undergo senescence due to over activation of O(2) (.-)generating xanthine oxidase (XO), which consequently increases the concentrations of O(2) (.-) leading to enhanced oxidative damage and disturbed cellular redox environment as indicated by increased lipid peroxidation and DHA/AsA + DHA ratio, respectively. While activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), and non-specific peroxidase (POD) were enhanced in sepals and petals of old flower, activities of catalase (CAT) and glutathione reductase (GR) were decreased. Exogenous application of nitric oxide (NO) retarded H(2)O(2)-induced senescence of Phalaenopsis flower by downregulating activity of XO and concentrations of O(2) (.-), H(2)O(2) and malondialdehyde (MDA, an index of lipid peroxidation). Exogenous application of NO also downregulated SOD activity and upregulated antioxidant enzymes involved in the detoxification of H(2)O(2) (CAT and APX), and in the regulation of redox couples viz, monodehydroascorbate reductase (MDHAR) and GR, together with the modulation in non-protein thiol status and DHA/AsA + DHA ratio.

摘要

衰老过程是一系列受发育调控且高度有序的事件。衰老会导致植物器官脱落,并最终致使整株植物或其部分死亡。目前的研究表明,蝴蝶兰花朵的衰老归因于产生活性氧(O₂⁻)的黄嘌呤氧化酶(XO)过度激活,这会相应地增加O₂⁻的浓度,进而导致氧化损伤加剧以及细胞氧化还原环境紊乱,分别表现为脂质过氧化增加和DHA/AsA + DHA比值升高。虽然在老花的萼片和花瓣中超氧化物歧化酶(SOD)、抗坏血酸过氧化物酶(APX)和非特异性过氧化物酶(POD)的活性增强,但过氧化氢酶(CAT)和谷胱甘肽还原酶(GR)的活性却降低了。外源施加一氧化氮(NO)通过下调XO活性以及O₂⁻、H₂O₂和丙二醛(MDA,脂质过氧化指标)的浓度,延缓了H₂O₂诱导的蝴蝶兰花朵衰老。外源施加NO还下调了SOD活性,并上调了参与H₂O₂解毒(CAT和APX)以及氧化还原对调控(即单脱氢抗坏血酸还原酶(MDHAR)和GR)的抗氧化酶,同时调节了非蛋白硫醇状态和DHA/AsA + DHA比值。

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