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白血病中血红蛋白和红细胞膜氧化损伤的进一步证据。

Further evidence for oxidative damage to hemoglobin and red cell membrane in leukemia.

作者信息

Pavri R S, Gupta A D, Baxi A J, Advani S H

出版信息

Leuk Res. 1983;7(6):729-33. doi: 10.1016/0145-2126(83)90066-8.

Abstract

The presence of significant methemoglobinemia in a large number (79%) of cases of leukemia prompted us to look into the evidence for oxidative injury to the other red cell constituents, e.g. the cell membrane. Forty-five per cent of cases showed increased malonyldialdehyde (MDA) levels indicating in vivo peroxidation of membrane lipids in leukemia patients. Red cell superoxide dismutase (SOD) activity was reduced in 25% of cases while plasma alpha-tocopherol levels were markedly low in 68% of patients. The presence of an inverse correlation between MDA levels and SOD and tocopherol levels in a large number of cases suggested that the red cells in leukemia lack the ability to counter increased oxidative stress. Low hemoglobin content of the red cells in these patients seemed to contribute to the oxidative injury to the membrane by rendering the latter more accessible to the oxidants. While methemoglobinemia may enhance tissue hypoxia, membrane lipid peroxidation could explain the shortened erythrocyte life-span and anemia in leukemia.

摘要

大量(79%)白血病病例中存在显著的高铁血红蛋白血症,这促使我们研究其他红细胞成分(如细胞膜)受到氧化损伤的证据。45%的病例显示丙二醛(MDA)水平升高,表明白血病患者体内膜脂质发生过氧化。25%的病例红细胞超氧化物歧化酶(SOD)活性降低,而68%的患者血浆α-生育酚水平明显较低。大量病例中MDA水平与SOD及生育酚水平呈负相关,这表明白血病患者的红细胞缺乏应对氧化应激增加的能力。这些患者红细胞中血红蛋白含量低,似乎使细胞膜更容易受到氧化剂的影响,从而导致对膜的氧化损伤。虽然高铁血红蛋白血症可能会加重组织缺氧,但膜脂质过氧化可以解释白血病患者红细胞寿命缩短和贫血的原因。

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