College of Life Sciences, Nanjing Agricultural University, Nanjing 210095, China.
J Exp Bot. 2012 Sep;63(15):5521-34. doi: 10.1093/jxb/ers201. Epub 2012 Aug 21.
This work examines the involvement of haem oxygenase-1 (HO-1) in salicylic acid (SA)-induced alleviation of oxidative stress as a result of cadmium (Cd) stress in alfalfa (Medicago sativa L.) seedling roots. CdCl(2) exposure caused severe growth inhibition and Cd accumulation, which were potentiated by pre-treatment with zinc protoporphyrin (ZnPPIX), a potent HO-1 inhibitor. Pre-treatment of plants with the HO-1 inducer haemin or SA, both of which could induce MsHO1 gene expression, significantly reduced the inhibition of growth and Cd accumulation. The alleviation effects were also evidenced by a decreased content of thiobarbituric acid-reactive substances (TBARS). The antioxidant behaviour was confirmed by histochemical staining for the detection of lipid peroxidation and the loss of plasma membrane integrity. Furthermore, haemin and SA pre-treatment modulated the activities of ascorbate peroxidase (APX), superoxide dismutase (SOD), and guaiacol peroxidase (POD), or their corresponding transcripts. Significant enhancement of the ratios of reduced/oxidized homoglutathione (hGSH), ascorbic acid (ASA)/dehydroascorbate (DHA), and NAD(P)H/NAD(P)(+), and expression of their metabolism genes was observed, consistent with a decreased reactive oxygen species (ROS) distribution in the root tips. These effects are specific for HO-1, since ZnPPIX blocked the above actions, and the aggravated effects triggered by SA plus ZnPPIX were differentially reversed when carbon monoxide (CO) or bilirubin (BR), two catalytic by-products of HO-1, was added. Together, the results suggest that HO-1 is involved in the SA-induced alleviation of Cd-triggered oxidative stress by re-establishing redox homeostasis.
这项工作研究了血红素加氧酶-1(HO-1)在水杨酸(SA)诱导的缓解苜蓿(Medicago sativa L.)幼苗根中镉(Cd)胁迫引起的氧化应激中的作用。CdCl2 暴露导致严重的生长抑制和 Cd 积累,而用 HO-1 抑制剂锌原卟啉(ZnPPIX)预处理则增强了这种作用。用 HO-1 诱导剂血红素或 SA 预处理植物,均可诱导 MsHO1 基因表达,显著降低了生长抑制和 Cd 积累。通过降低丙二醛(TBARS)含量也证实了缓解作用。抗氧化行为通过脂质过氧化和质膜完整性丧失的组织化学染色得到证实。此外,血红素和 SA 预处理调节了抗坏血酸过氧化物酶(APX)、超氧化物歧化酶(SOD)和愈创木酚过氧化物酶(POD)或其相应转录本的活性。观察到还原/氧化同型谷胱甘肽(hGSH)、抗坏血酸(ASA)/脱氢抗坏血酸(DHA)和 NAD(P)H/NAD(P)(+)的比值显著增强,以及它们的代谢基因表达增强,与根尖活性氧(ROS)分布减少一致。这些作用是 HO-1 特异性的,因为 ZnPPIX 阻断了上述作用,并且当添加 HO-1 的两种催化副产物一氧化碳(CO)或胆红素(BR)时,SA 加 ZnPPIX 引发的加重作用会得到不同程度的逆转。总之,结果表明 HO-1 通过重新建立氧化还原稳态参与了 SA 诱导的缓解 Cd 引发的氧化应激。