Hydrogen sulfide alleviates cadmium toxicity through regulations of cadmium transport across the plasma and vacuolar membranes in Populus euphratica cells.
Hydrogen sulfide alleviates cadmium toxicity through regulations of cadmium transport across the plasma and vacuolar membranes in Populus euphratica cells.
复制标题
DOI：
10.1016/j.plaphy.2013.01.003
复制
发表时间：
2013-04
期刊：
影响因子：
--
通讯作者：
Jian Sun;Rui-gang Wang;Xuan Zhang;Yicheng Yu;R. Zhao;Zongyun Li;Shaoliang Chen
中科院分区：
文献类型：
--
作者：
Jian Sun;Rui-gang Wang;Xuan Zhang;Yicheng Yu;R. Zhao;Zongyun Li;Shaoliang Chen
硫化氢（H2S）作为一种新的信号分子参与植物的生长和对非生物胁迫的反应。然而，关于其在镉（Cd）解毒中的作用知之甚少。本研究采用荧光成像技术和非侵入性振动离子选择微电极研究了H2S对胡杨细胞Cd毒性的影响。H2S供体氢硫化钠（NaHS）预处理可显著减轻cd诱导的胡杨细胞程序性死亡。与低剂量（25 μM）和高剂量（200 μM）相比，50 ~ 100 μM NaHS的缓解作用更为明显。Cd胁迫下，nahs处理细胞抗坏血酸过氧化物酶、过氧化氢酶和谷胱甘肽还原酶等抗氧化酶的总活性显著增强，导致h2o2积累和脂质过氧化降低。此外，NaHS降低了细胞质中Cd的积累，但增加了液泡中Cd的比例。Cd通量谱显示H2S抑制Cd通过H2O2激活的质膜钙通道内流。NaHS增强Cd内流进入液泡，Cd内流依赖于细胞质内的pH梯度。综上所述，这些结果表明H2S通过改善抗氧化系统和细胞Cd稳态来减轻Cd毒性。H2S对抗氧化酶的上调减少了H2O2的积累，从而减少了Cd通过H2O2激活的PM钙通道的内流。h2s模拟的液泡Cd隔离可能是由于细胞质Cd2+/H+反转运蛋白的激活。
Hydrogen sulfide (H2S) is emerging as a novel signalling molecule involved in plant growth and responses against abiotic stresses. However, little information is known about its role in cadmium (Cd) detoxification. In the present study, the effects of H2S on Cd toxicity were investigated in Populus euphratica cells using fluorescence imaging technique and a non-invasive vibrating ion-selective microelectrode. Pretreatment with a H2S donor, sodium hydrosulfide (NaHS), significantly mitigated the Cd-induced programmed cell death in P. euphratica cells. The alleviation effect of NaHS was more pronounced at 50–100 μM as compared to low (25 μM) and high doses (200 μM). Under Cd stress, total activities of antioxidant enzymes, such as ascorbate peroxidase, catalase and glutathione reductase, were significantly enhanced in NaHS-treated cells, leading to a decline of H2O2accumulation and lipid peroxidation. Moreover, NaHS reduced Cd accumulation in the cytoplasm but increased the fraction of Cd in the vacuole. Cd flux profiles revealed that H2S inhibited the Cd influx through the plasma membrane (PM) calcium channels that activated by H2O2. NaHS enhanced Cd influx into the vacuole, and the Cd influx was dependent on the pH gradients across the tonoplast. Taken together, these results suggest that H2S alleviates Cd toxicity via the improvement of antioxidant system and cellular Cd homeostasis. The up-regulation of antioxidant enzymes by H2S reduced the accumulation of H2O2, and thus decreased Cd influx through the H2O2-activated PM calcium channels. The H2S-simulated vacuolar Cd sequestration was presumably due to the activation of tonoplast Cd2+/H+antiporters.