Srigiridhar K, Nair K M
Department of Biophysics, National Institute of Nutrition (ICMR), Hyderabad, India.
Free Radic Biol Med. 1998 Oct;25(6):660-5. doi: 10.1016/s0891-5849(98)00086-0.
Redox-active forms of iron are known to catalyze free radical mediated peroxidative reactions. There is scanty information on such effects at the sites of iron absorption. This was tested in iron-deficient WKY female rats supplemented for 15 days with FeSO4 equivalent to 8 mg of iron (D+) and compared with iron deficient (D) and iron adequate (C) rats. The levels of intestinal MDA and protein carbonyls and the activities of various antioxidant enzymes were estimated. As markers of functional integrity, the activities of alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were evaluated. In addition, we measured the concentrations of ferritin, transferrin, and ceruloplasmin levels in serum and in intestinal mucosa. It was observed that correction of iron deficiency resulted in significant increase in MDA and protein carbonyl formation. Activities of both alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were significantly decreased in D+ compared to C. The increase in catalase and decrease in Gpx was found to be sensitive to iron administration. Neither iron deficiency nor its correction had any effect on the activity of SOD and GSH levels. Iron supplementation has resulted in decreased mobilization of stored iron as reflected by increased mucosal ferritin level and decreased serum ceruloplasmin ferroxidase activity contributing to greater peroxidative stress in the intestine. These results suggest that iron-deficient intestine of rat is more susceptible to iron-mediated peroxidative damage and functional impairment during correction of deficiency with iron.
已知具有氧化还原活性的铁形式可催化自由基介导的过氧化反应。关于铁吸收部位的此类影响的信息很少。在缺铁的WKY雌性大鼠中进行了测试，这些大鼠用相当于8毫克铁的硫酸亚铁补充15天（D +），并与缺铁（D）和铁充足（C）的大鼠进行比较。估计了肠道丙二醛和蛋白质羰基的水平以及各种抗氧化酶的活性。作为功能完整性的标志物，评估了碱性磷酸酶和Lys-Ala-二肽基氨基肽酶的活性。此外，我们测量了血清和肠黏膜中铁蛋白、转铁蛋白和铜蓝蛋白的浓度。观察到缺铁的纠正导致丙二醛和蛋白质羰基形成显著增加。与C组相比，D +组中碱性磷酸酶和Lys-Ala-二肽基氨基肽酶的活性均显著降低。发现过氧化氢酶的增加和谷胱甘肽过氧化物酶的降低对铁的给药敏感。缺铁及其纠正对超氧化物歧化酶的活性和谷胱甘肽水平均无任何影响。铁补充导致储存铁的动员减少，这表现为黏膜铁蛋白水平升高和血清铜蓝蛋白亚铁氧化酶活性降低，从而导致肠道中更大的过氧化应激。这些结果表明，大鼠缺铁的肠道在缺铁纠正过程中更容易受到铁介导的过氧化损伤和功能损害。
