Nitric oxide suppresses aluminum-induced programmed cell death in peanut (Arachis hypoganea L.) root tips by improving mitochondrial physiological properties

文献类型： 外文期刊

第一作者： Huang, Wenjing

作者： Huang, Wenjing;Oo, Thet Lwin;Gu, Minghua;Zhan, Jie;Wang, Aiqin;He, Long-Fei;He, Huyi;He, Long-Fei

作者机构：

关键词： Aluminum;Programmed cell death;Nitric oxide;Mitochondria;Peanut

期刊名称：NITRIC OXIDE-BIOLOGY AND CHEMISTRY （ 影响因子：4.427； 五年影响因子：4.505 ）

ISSN： 1089-8603

年卷期： 2018 年 74 卷

页码：

收录情况： SCI

摘要： Aluminum (Al) stress alters nitric oxide (NO) and induces programmed cell death (PCD) in plants. Recent study has shown that NO inhibits Al-induced PCD. However, the mechanism of NO inhibiting Al-induced PCD has not been revealed yet. Here, we investigated the behavior of mitochondria during Al-induced PCD suppressed by NO in peanut. Seedlings of peanut was grown hydroponically in a controllable growth room. The mitochondrial physiological parameters were determined spectrophotometrically. The expression of AhANT and AhHsp70 was determined by quantitative RT-PCR. Al-induced cell death rapidly in peanut root tips is mitochondria-dependent PCD. There was a significantly negative relationship between PCD and mitochondrial NO/H2O2 level. Compared with Al treatment alone, the addition of NO donor sodium nitroprusside (SNP) increased the ratio of NO/H2O2, down-regulated AhANT expression and inhibited the opening of mitochondrial permeability transition pore (MPTP), up-regulated AhHsp70 expression and increased mitochondrial inner membrane potential (Mini), reduced cytochrome c (Cyt c) release from mitochondria and caspase 3-like protease activity, while the effect of NO specific scavenger cPTIO supplement was opposite. NO suppresses Al-induce PCD in peanut root tips by improving mitochondrial physiological properties.

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