Reactive oxygen species, nitric oxide, and their interactions play different roles in Cupressus lusitanica cell death and phytoalexin biosynthesis
Reactive oxygen species, nitric oxide, and their interactions play different roles in Cupressus lusitanica cell death and phytoalexin biosynthesis
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DOI：
10.1111/j.1469-8137.2007.02109.x
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发表时间：
2007-01-01
期刊：
影响因子：
9.4
通讯作者：
Sakai, Kokki
中科院分区：
文献类型：
--
作者：
Zhao, Jian;Fujita, Koki;Sakai, Kokki
β-崖柏素是一种天然的肌钙蛋白，具有很强的抗真菌、抗病毒和抗癌活性。研究了酵母激发子诱导墨西哥柏细胞产生β-崖柏素及其与活性氧（ROS）和一氧化氮（NO）的关系，结果表明：超氧阴离子自由基（O-2）诱导细胞死亡，抑制β-崖柏素的积累，而过氧化氢（H2 O2）诱导β-崖柏素的积累，但对细胞死亡无明显影响。激发子和O-2（中心点-）均诱导细胞程序性死亡，此过程可被蛋白酶抑制剂、蛋白激酶抑制剂和Ca ~（2+）螯合剂阻断，激发子诱导的NO生成依赖于一氧化氮合酶（NOS）。NO、H_2O_2和O_2 ~-（中点-）之间的相互作用表明，NO的产生和H_2O_2的产生是相互依赖的，而NO和O_2 ~-（中点-）的积累由于NO和O_2 ~-（中点-）的共同消耗而呈负相关。NO-和O-2（中心点）诱导的细胞死亡相互需要，两者都需要激发子诱导的细胞死亡。NO和O-2（中心点-）之间的直接相互作用涉及一种有效的氧化剂过氧亚硝酸盐的产生，这可能介导激发子诱导的细胞死亡。
beta-Thujaplicin is a natural troponoid with strong antifungal, antiviral, and anticancer activities. beta-Thujaplicin production in yeast elicitor-treated Cupressus lusitanica cell culture and its relationships with reactive oxygen species (ROS) and nitric oxide (NO) production and hypersensitive cell death were investigated.Superoxide anion radical (O-2(center dot-)) induced cell death and inhibited beta-thujaplicin accumulation, whereas hydrogen peroxide (H2O2) induced beta-thujaplicin accumulation but did not significantly affect cell death. Both elicitor and O-2(center dot-) induced programmed cell death, which can be blocked by protease inhibitors, protein kinase inhibitors, and Ca2+ chelators.Elicitor-induced NO generation was nitric oxide synthase (NOS)-dependent. Inhibition of NO generation by NOS inhibitors and NO scavenger partly blocked the elicitor-induced beta-thujaplicin accumulation and cell death, and NO donors strongly induced cell death.Interaction among NO, H2O2, and O-2(center dot-) shows that NO production and H2O2 production are interdependent, but NO and O-2(center dot-) accumulation were negatively related because of coconsumption of NO and O-2(center dot-). NO- and O-2(center dot-)-induced cell death required each other, and both were required for elicitor-induced cell death. A direct interaction between NO and O-2(center dot-) was implicated in the production of a potent oxidant peroxynitrite, which might mediate the elicitor-induced cell death.