首页> 外文期刊>Frontiers in Physiology >Nitric Oxide Inhibits Al-Induced Programmed Cell Death in Root Tips of Peanut ( Arachis hypogaea L.) by Affecting Physiological Properties of Antioxidants Systems and Cell Wall
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Nitric Oxide Inhibits Al-Induced Programmed Cell Death in Root Tips of Peanut ( Arachis hypogaea L.) by Affecting Physiological Properties of Antioxidants Systems and Cell Wall

机译:通过影响抗氧化剂系统和细胞壁的生理特性

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It has been reported that nitric oxide (NO) is a negative regulator of aluminum (Al)-induced programmed cell death (PCD) in peanut root tips. However, the inhibiting mechanism of NO on Al-induced PCD is unclear. In order to investigate the mechanism by which NO inhibits Al-induced PCD, the effects of co-treatment Al with the exogenous NO donor or the NO-specific scavenger on peanut root tips, the physiological properties of antioxidants systems and cell wall (CW) in root tip cells of NO inhibiting Al-induced PCD were studied with two peanut cultivars. The results showed that Al exposure induced endogenous NO accumulation, and endogenous NO burst increased antioxidant enzyme activity in response to Al stress. The addition of NO donor sodium nitroprusside (SNP) relieved Al-induced root elongation inhibition, cell death and Al adsorption in CW, as well as oxidative damage and ROS accumulation. Furthermore, co-treatment with the exogenous NO donor decreased MDA content, LOX activity and pectin methylesterase (PME) activity, increased xyloglucan endotransglucosylase (XET) activity and relative expression of the xyloglucan endotransglucosylase/hydrolase ( XTH-32 ) gene. Taken together, exogenous NO alleviated Al-induced PCD by inhibiting Al adsorption in CW, enhancing antioxidant defense and reducing peroxidation of membrane lipids, alleviating the inhibition of Al on root elongation by maintaining the extensibility of CW, decreasing PME activity, and increasing XET activity and relative XTH-32 expression of CW.
机译:据报道,一氧化氮(NO)是铝(Al)诱导的程序化细胞死亡(PCD)的负调节剂,在花生根提示中。然而,否在Al-诱导的PCD上的抑制机制尚不清楚。为了探讨不抑制Al-诱导的PCD的机制,共治疗Al与外源没有供体或花生根尖的特异性清除剂的影响,抗氧化剂系统和细胞壁(CW)的生理性质用两种花生品种研究了抑制Al诱导的PCD的根尖细胞中。结果表明,Al曝光诱导内源性没有积聚,并且内源性响应于Al胁迫的抗氧化酶活性增加。添加没有供体硝普钠(SNP)可缓解Al诱导的根伸长率抑制,细胞死亡和CW中的Al吸附,以及氧化损伤和ROS积累。此外,与外源没有供体的共处理降低了MDA含量,LOX活性和果胶甲基酯酶(PME)活性,增加的木葡聚糖内凝血糖基酶(XET)活性和XELoglucan内甘油糖苷基酶/水解酶(XTH-32)基因的相对表达。通过抑制CW中的Al吸附,增强抗氧化防御和减少膜脂质的过氧化,通过维持CW,降低PME活性的伸展性,增加PME活性和增加XET活性,增强抗氧化防御和减少抗氧化防御和减少过氧化的抗氧化防御和减少过氧化。和相对Xth-32 CW的表达。

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