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为了探讨缺铁性贫血（ＩＤＡ）红细胞膜阴离子交换蛋白（带３蛋白）的阴离子转运功能下降病变机理，运用生物膜离子通透研究方法，测定经Ｐｅｒｃｏｌｌ密度梯度分离的ＩＤＡ幼大鼠不同年龄红细胞的阴离子（ＮＯ２、Ｃ１-）通透速率；采用阴离子转运特异抑制剂ＤＩＤＳ和带３膜外侧阴离子转运肽段特异抗体作“探针”，观察其对缺铁红细胞的阴离子通透抑制效应。实验显示，ＤＩＤＳ抗体对ＩＤＡ红细胞的ＣＩ-通透抑制低于对照。进一步分析发现，分布于Ｐｅｒｃｏｌｌ上层的年青缺铁红细胞ＮＯ２一通透时间（Ｔｓ）明显延长，ＤＩＤＳ对该层红细胞的通透抑制率显著下降；中、老年红细胞各参数变化无统计学显著意义。结果提示，缺铁红细胞膜外侧带３蛋白的阴离子结合位点发生病变；病变以新生红细胞表现严重；导致铁红细胞阴离子通透功能改变的带３分子结构变化可能发生在骨髓缺铁红细胞合成期。
To investigate the mechanism of the decline of anion transport function of ion exchange protein (band 3 protein) of iron deficiency anemia (IDA) erythrocyte membrane, the red blood cells of different age in IDA rats isolated by Percoll density gradient (NO2, C1-) permeation rate. The specific anti-DIDS and anion-transporting peptide-specific antibody with 3-membrane was used as probe to observe the anion-permeable inhibitory effect on anion-deficient erythrocytes. Experiments show that DIDS antibodies inhibit CI-permeability of IDA erythrocytes lower than the control. Further analysis showed that the diffusion time of NO2 (Ts) was significantly prolonged in the upper layer of Percoll, and the inhibitory rate of DIDS on the permeation of erythrocytes in this layer was significantly decreased. There was no significant difference in the parameters of middle and old erythrocytes. The results suggest that the negative ion-binding site of 3-protein on the outer side of iron-deficient erythrocyte membrane is diseased; the pathological changes of erythrocytes are severe; the change of 3-membered structure that leads to the change of anion permeability of erythrocytes may occur during the synthesis of bone marrow-deficient erythrocytes.