College of Environmental Science and Engineering, Hunan University, Changsha, 410082, China.
Environ Sci Pollut Res Int. 2015 Mar;22(5):3489-97. doi: 10.1007/s11356-014-3581-5. Epub 2014 Sep 23.
Cadmium (Cd)-induced growth inhibition is one of the primary factors limiting phytoremediation effect of Boehmeria nivea (L.) Gaud in contaminated soil. Sodium nitroprusside (SNP), a donor of nitric oxide (NO), has been evidenced to alleviate Cd toxicity in many plants. However, as an important mechanism of NO in orchestrating cellular functions, S-nitrosylation is still poorly understood in its relation with Cd tolerance of plants. In this study, higher exogenous NO levels were found to coincide with higher S-nitrosylation level expressed as content of S-nitrosothiols (SNO). The addition of low concentration (100 μM) SNP increased the SNO content, and it simultaneously induced an alleviating effect against Cd toxicity by enhancing the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), and glutathione reductase (GR) and reduced the accumulation of H2O2 as compared with Cd alone. Application of S-nitrosoglutathione reductase (GSNOR) inhibitors dodecanoic acid (DA) in 100 μM SNP group brought in an extra elevation in S-nitrosylation level and further reinforced the effect of SNP. While the additions of 400 μM SNP and 400 μM SNP + 50 μM DA further elevated the S-nitrosylation level, it markedly weakened the alleviating effect against Cd toxicity as compared with the addition of 100 μM SNP. This phenomenon could be owing to excess consumption of glutathione (GSH) to form SNO under high S-nitrosylation level. Therefore, the present study indicates that S-nitrosylation is involved in the ameliorating effect of SNP against Cd toxicity. This involvement exhibited a concentration-dependent property.
镉（Cd）诱导的生长抑制是限制苎麻（Boehmeria nivea（L.）Gaud）在污染土壤中修复效果的主要因素之一。硝普钠（SNP），一氧化氮（NO）的供体，已被证明可以减轻许多植物中的 Cd 毒性。然而，作为 NO 调节细胞功能的重要机制之一，S-亚硝基化在与植物 Cd 耐受性的关系方面仍知之甚少。本研究发现，较高的外源性 NO 水平与较高的 S-亚硝基化水平（以 S-亚硝基硫醇（SNO）的含量表示）相一致。添加低浓度（100μM）SNP 可增加 SNO 含量，并通过增强超氧化物歧化酶（SOD）、抗坏血酸过氧化物酶（APX）和谷胱甘肽还原酶（GR）的活性，同时减轻 Cd 单独作用引起的毒性，减少 H2O2 的积累。与单独 Cd 相比，在 100μM SNP 组中应用 S-亚硝基谷胱甘肽还原酶（GSNOR）抑制剂十二烷酸（DA）会导致 S-亚硝基化水平进一步升高，并进一步增强 SNP 的作用。而添加 400μM SNP 和 400μM SNP+50μM DA 会进一步提高 S-亚硝基化水平，但与添加 100μM SNP 相比，明显减弱了对 Cd 毒性的缓解作用。这种现象可能是由于高 S-亚硝基化水平下谷胱甘肽（GSH）的消耗过多而形成 SNO。因此，本研究表明 S-亚硝基化参与了 SNP 对 Cd 毒性的缓解作用。这种参与表现出浓度依赖性。
