Activated oxygen and iron deficiency in pea plants Activated oxygen and antioxidant defenses in iron-deficient pea plants
Activated oxygen and iron deficiency in pea plants Activated oxygen and antioxidant defenses in iron-deficient pea plants
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豌豆植物中的活性氧和铁缺乏 缺铁豌豆植物中的活性氧和抗氧化防御
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发表时间：
2015
期刊：
影响因子：
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通讯作者：
M. Becana
中科院分区：
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作者：
I..;ITURBE;J.;F.;Morán;C.;ARRESE;Y.;Gogorcena;R. Klucas;M. Becana
缺铁处理导致豌豆叶片叶绿素a、叶绿素B和类胡萝卜素含量大幅度下降（44 - 62%），可溶性蛋白含量下降（18%），净光合速率下降（28%）。过氧化氢酶，非特异性过氧化物酶和抗坏血酸过氧化物酶活性下降了51%，在年轻的铁缺乏的叶子，而单脱氢抗坏血酸还原酶，脱氢抗坏血酸还原酶和谷胱甘肽还原酶的活动保持不受影响。抗坏血酸过氧化物酶活性与叶片铁含量高度相关（r~2 = 0.99，P <0.001），可作为植物铁营养状况的一个指标。铁缺乏导致铜锌超氧化物歧化酶的增加，但没有锰超氧化物歧化酶。抗坏血酸的含量仅下降了24%，还原型和氧化型谷胱甘肽和维生素E的含量没有变化。缺铁叶片的低分子量组分含量为30-65 μ g.（g干重）-1 Mn。该浓度比同一组分中Fe和Cu的浓度高15 - 60倍，并且通过Fe缺乏进一步增强（1.5至2.5倍）而不引起Mn毒性。催化铁的浓度，也就是说，铁活性的自由基的产生，几乎为零，催化铜没有变化与严重的铁缺乏。由于催化金属介导体内脂质和蛋白质氧化，上述发现将解释为什么氧化损伤的脂质和蛋白质不积累在缺铁叶片。
Iron (Fe) deficiency in pea leaves caused a large decrease (44-62%) in chlorophyll a, chlorophyll b and carotenoids, and smaller decreases in soluble protein (18%) and net photosynthesis (28%). Catalase, nonspecific peroxidase and ascorbate peroxidase activities declined by 51% in young Fe-deficient leaves, whereas monodehydroascorbate reductase, dehydroascorbate reductase and glutathione reductase activities remained unaffected. Ascorbate peroxidase activity was highly correlated (r2=0.99, P<0.001) with the Fe content of leaves, which allows its use as an indicator of the Fe nutritional status of the plant. Fe deficiency resulted in an increase of CuZn-superoxide dismutase but not of Mn-superoxide dismutase. The content of ascorbate decreased only by 24% and those of reduced and oxidized glutathione and vitamin E did not vary. The low-molecular-mass fraction of Fesufficient leaves contained 30-65 μg.(g dry weight)-1 Mn. This concentration was 15-60 times greater than that of Fe and Cu in the same fraction, and was further enhanced (1.5 to 2.5 fold) by Fe deficiency without causing Mn toxicity. The concentration of catalytic Fe, that is, of Fe active for free radical generation, was virtually zero and that of catalytic Cu did not change with severe Fe deficiency. Because catalytic metals mediate lipid and protein oxidation in vivo, the above findings would explain why oxidatively-damaged lipids and proteins do not accumulate in Fe-deficient leaves.