Noriega Guillermo O, Yannarelli Gustavo G, Balestrasse Karina B, Batlle Alcira, Tomaro Maria L
Centro de Investigaciones sobre Porfirinas y Porfirias (CIPYP), CONICET, Buenos Aires, Argentina.
Planta. 2007 Oct;226(5):1155-63. doi: 10.1007/s00425-007-0561-8. Epub 2007 Jun 14.
Heme oxygenase (HO, EC 1.14.99.3) catalyzes the oxidative conversion of heme to biliverdin IXalpha with the concomitant release of carbon monoxide and iron. Recently, HO has been involved in the protection against oxidative stress in plants. The fact that nitric oxide (NO), an endogenous signaling molecule in animals and plants mediates responses to abiotic and biotic stresses, prompted us to study whether this molecule could modulate HO-1 gene transcription. To fulfill this objective leaves of soybean (Glycine max L.) plants were stimulated with Cd, employing an acute intoxication model. Cadmium caused dehydration, chlorophyll loss and ion leakage. Semi-quantitative RT-PCR analysis showed no augmentation of HO-1 transcript levels with respect to controls. Pretreatment with 100 microM sodium nitroprussiate (SNP), a well-known NO donor, prevented the effects caused by Cd. When the HO-1 mRNA levels were analyzed, a significant augmentation (54%) was observed with respect to Cd-treated plants. On the other hand, 50 or 300 microM SNP did not fully prevent the effects elicited by Cd. When HO-1 transcript levels were analyzed, no significant enhancement or a down-regulation was observed. The potassium salt of 2-(4-carboxylphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a specific NO scavenger, arrested NO-mediated protective effects against to Cd-induced oxidative damage. These data provide an understanding of one of the possible roles that NO can play against an oxidative insult. NO is cytoprotective depending on its concentration, and it was further demonstrated that this protection could be, at least in part, mediated by an enhancement of HO-1 mRNA, as it happens with genes associated with the antioxidant defense system.
血红素加氧酶（HO，EC 1.14.99.3）催化血红素氧化转化为胆绿素IXα，同时释放一氧化碳和铁。最近，HO参与了植物对氧化应激的保护作用。一氧化氮（NO）作为动植物体内的一种内源性信号分子，可介导对非生物和生物胁迫的反应，这促使我们研究该分子是否能调节HO-1基因转录。为实现这一目标，我们采用急性中毒模型，用镉刺激大豆（Glycine max L.）植株的叶片。镉导致脱水、叶绿素损失和离子渗漏。半定量RT-PCR分析表明，与对照相比，HO-1转录水平没有增加。用100 microM硝普钠（SNP，一种著名的NO供体）预处理可防止镉造成的影响。当分析HO-1 mRNA水平时，相对于镉处理的植株，观察到显著增加（54%）。另一方面，50或300 microM SNP不能完全防止镉引起的影响。当分析HO-1转录水平时，未观察到显著增强或下调。2-（4-羧基苯基）-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物（cPTIO）的钾盐，一种特异性NO清除剂，可阻止NO介导的对镉诱导的氧化损伤的保护作用。这些数据有助于理解NO在应对氧化损伤时可能发挥的作用之一。NO具有细胞保护作用，这取决于其浓度，并且进一步证明这种保护作用至少部分是由HO-1 mRNA的增强介导的，就像与抗氧化防御系统相关的基因一样。
