胞外三磷酸腺苷通过一氧化氮调节镉诱导的氧化压力和细胞死亡

采用液体悬浮培养方法,研究胞外三磷酸腺苷(ATP)通过一氧化碳(NO)调节镉诱导对烟草(Nicotiana tabacum L.)悬浮细胞氧化压力和死亡水平的影响。结果显示,镉离子(Cd^2+)可以以剂量依赖的模式引起烟草悬浮细胞氧化压力和死亡水平的上升,而施加外源ATP可有效缓解Cd^2+诱导的氧化压力和细胞死亡。进一步研究发现,和外源ATP的缓解作用相似,NO的供体硝普钠(SNP)同样可以缓解Cd^2+诱导的氧化压力和细胞死亡水平的上升;且NO合成抑制剂(L-NAME)可部分解除外源ATP的缓解作用。研究结果表明外源ATP可通过NO调节镉诱导的氧化压力和细胞死亡。

Extracellular adenosine 5'-triphosphate mediates oxidative stress and cell death under cadmium stress by nitric oxide

Cadmium (Cd) is one of the most bio-toxic heavy metals. Extracellular adenosine 5'-triphosphate (ex ATP) is an important signaling molecule involved in regulating physio-logical processes in cells. This study showed that Cd ions (Cd²⁺) increased oxidative stress and death level of Nicotiana tabacum L. suspension cells in a concentration-dependent manner. Conversely, application of exogenous ATP effectively alleviated the increase in Cd²⁺-induced oxidative stress and cell death. Furthermore, similar to the above-mentioned mitigation effects of exogenous ATP, SNP (a nitric oxide donor) also alleviated the increase in Cd²⁺-induced oxidative stress and cell death levels. Moreover, NO synthesis inhibitor (L-NAME) partially relieved the alleviating effects of exogenous ATP. These results indicate that ex ATP regulates Cd-induced oxidative stress and cell death by NO.