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Cadmium Disrupts the Balance between Hydrogen Peroxide and Superoxide Radical by Regulating Endogenous Hydrogen Sulfide in the Root Tip of Brassica rapa

机译:镉调节甘蓝型油菜根尖内源性硫化氢破坏了过氧化氢和超氧自由基之间的平衡

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摘要

Cd (cadmium) stress always alters the homeostasis of ROS (reactive oxygen species) including H2O2 (hydrogen sulfide) and O2•– (superoxide radical), leading to the oxidative injury and growth inhibition in plants. In addition to triggering oxidative injury, ROS has been suggested as important regulators modulating root elongation. However, whether and how Cd stress induces the inhibition of root elongation by differentially regulating endogenous H2O2 and O2•–, rather than by inducing oxidative injury, remains elusive. To address these gaps, histochemical, physiological, and biochemical approaches were applied to investigate the mechanism for Cd to fine-tune the balance between H2O2 and O2•– in the root tip of Brassica rapa. Treatment with Cd at 4 and 16 μM significantly inhibited root elongation, while only 16 μM but not 4 μM of Cd induced oxidative injury and cell death in root tip. Fluorescent and pharmaceutical tests suggested that H2O2 and O2•– played negative and positive roles, respectively, in the regulation of root elongation in the presence of Cd (4 μM) or not. Treatment with Cd at 4 μM led to the increase in H2O2 and the decrease in O2•– in root tip, which may be attributed to the up-regulation of Br_UPB1s and the down-regulation of their predicted targets (four peroxidase genes). Cd at 4 μM resulted in the increase in endogenous H2S in root tip by inducing the up-regulation of LCDs and DCDs. Treatment with H2S biosynthesis inhibitor or H2S scavenger significantly blocked Cd (4 μM)-induced increase in endogenous H2S level, coinciding with the recovery of root elongation, the altered balance between H2O2 and O2•–, and the expression of Br_UPB1s and two peroxidase genes. Taken together, it can be proposed that endogenous H2S mediated the phytotoxicity of Cd at low concentration by regulating Br_UPB1s-modulated balance between H2O2 and O2•– in root tip. Such findings shed new light on the regulatory role of endogenous H2S in plant adaptions to Cd stress.
机译:Cd(镉)应力总是会改变ROS(活性氧)的稳态,包括H2O2(硫化氢)和 O 2 •- (超氧化物自由基),导致植物的氧化损伤和生长抑制。除引发氧化损伤外,ROS被认为是调节根伸长的重要调节剂。但是,镉胁迫是否以及如何通过差异调节内源性H2O2和 O 2 •– 仍然无法实现,而不是通过诱发氧化损伤来实现。为了解决这些差距,采用了组织化学,生理和生化方法来研究Cd调节H2O2和 O 2 •– 。用4和16μM的Cd处理可显着抑制根伸长,而仅16μM而不是4μM的Cd会引起根尖的氧化损伤和细胞死亡。荧光和药物测试表明H2O2和 O 2 •– 在是否存在Cd(4μM)的情况下,在调节根伸长方面分别发挥了负作用和正作用。用4μM的Cd处理导致H2O2的增加和 O 2 •– 可能是由于Br_UPB1s的上调和其预测靶标(四个过氧化物酶基因)的下调所致。 4μM的镉通过诱导LCD和DCD的上调而导致根尖内源性H2S的增加。用H2S生物合成抑制剂或H2S清除剂处理可显着阻止Cd(4μM)诱导的内源性H2S水平增加,这与根伸长的恢复,H2O2和 O 2 •– ,以及Br_UPB1s和两个过氧化物酶基因的表达。两者合计,可以认为内源性H 2 S通过调节H 2 O 2 之间的Br_UPB1s调节平衡来介导低浓度Cd的植物毒性。 sub>和 O 2 •– < / math>在根尖。这些发现为内源性H 2 S在植物对Cd胁迫的适应中的调控作用提供了新的思路。

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