Kumar Praveen, Tewari Rajesh Kumar, Sharma Parma Nand
Department of Botany, University of Lucknow, Lucknow 226007, India.
Plant Cell Rep. 2008 Feb;27(2):399-409. doi: 10.1007/s00299-007-0453-1. Epub 2007 Sep 27.
In this study, we examined the modulation of Cu toxicity-induced oxidative stress by excess supply of iron in Zea mays L. plants. Plants receiving excess of Cu (100 microM) showed decreased water potential and simultaneously showed wilting in the leaves. Later, the young leaves exhibited chlorosis and necrotic scorching of lamina. Excess of Cu suppressed growth, decreased concentration of chloroplastic pigments and fresh and dry weight of plants. The activities of peroxidase (EC 1.11.1.7; POD), ascorbate peroxidase (EC 1.11.1.11; APX) and superoxide dismutase (EC 1.15.1.1; SOD) were increased in plants supplied excess of Cu. However, activity of catalase (EC 1.11.1.6; CAT), was depressed in these plants. In gel activities of isoforms of POD, APX and SOD also revealed upregulation of these enzymes. Excess (500 microM)-Fe-supplemented Cu-stressed plants, however, looked better in their phenotypic appearance, had increased concentration of chloroplastic pigments, dry weight, and improved leaf tissue water status in comparison to the plants supplied excess of Cu. Moreover, activities of antioxidant enzymes including CAT were further enhanced and thiobarbituric acid reactive substance (TBARS) and H(2)O(2) concentrations decreased in excess-Fe-supplemented Cu-stressed plants. In situ accumulation of H(2)O(2), contrary to that of O(2)(-) radical, increased in both leaf and roots of excess-Cu-stressed plants, but Cu-excess plants supplied with excess-Fe showed reduced accumulation H(2)O(2) and little higher of O(2)(-) in comparison to excess-Cu plants. It is, therefore, concluded that excess-Cu (100 microM) induces oxidative stress by increasing production of H(2)O(2) despite of increased antioxidant protection and that the excess-Cu-induced oxidative damage is minimized by excess supply of Fe.
在本研究中，我们检测了过量供应铁对玉米植株中铜毒性诱导的氧化应激的调节作用。接受过量铜（100微摩尔）的植株水势降低，同时叶片出现萎蔫。随后，幼叶出现黄化和叶片坏死焦枯。过量的铜抑制生长，降低叶绿体色素浓度以及植株的鲜重和干重。在供应过量铜的植株中，过氧化物酶（EC 1.11.1.7；POD）、抗坏血酸过氧化物酶（EC 1.11.1.11；APX）和超氧化物歧化酶（EC 1.15.1.1；SOD）的活性增加。然而，这些植株中过氧化氢酶（EC 1.11.1.6；CAT）的活性受到抑制。POD、APX和SOD同工酶的凝胶活性也显示这些酶上调。然而，与供应过量铜的植株相比，补充过量铁（500微摩尔）的铜胁迫植株在表型外观上更好，叶绿体色素浓度增加、干重增加，叶片组织水分状况改善。此外，补充过量铁的铜胁迫植株中，包括CAT在内的抗氧化酶活性进一步增强，硫代巴比妥酸反应性物质（TBARS）和H₂O₂浓度降低。与O₂⁻自由基相反，过量铜胁迫植株的叶片和根中H₂O₂的原位积累增加，但与过量铜植株相比，供应过量铁的过量铜植株H₂O₂积累减少，O₂⁻略高。因此，得出结论：尽管抗氧化保护增加，但过量的铜（100微摩尔）通过增加H₂O₂的产生诱导氧化应激，并且过量供应铁可使过量铜诱导的氧化损伤最小化。
