4.4 Article

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

期刊

NITRIC OXIDE-BIOLOGY AND CHEMISTRY
卷 74, 期 -, 页码 47-55

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2018.01.003

关键词

Aluminum; Programmed cell death; Nitric oxide; Mitochondria; Peanut

资金

  1. National Natural Science Foundation of China [31660350, 31660352, 31560346, 31260296, 31301249]
  2. Guangxi Natural Science Foundation of China [2014GXNSFAA118074]
  3. Science AMP
  4. Technology Development Fund of Guangxi Academy of Agricultural Sciences [Guinongke2017JZ11]

向作者/读者索取更多资源

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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