微量元素硒对红细胞老化的保护作用

红细胞老化过程中,释放囊泡,增加脆性以及减少酶活性等等均是细胞衰老的征状。本文在前文的基础上,探讨了微量元素硒对红细胞老化的保护作用。发现在红细胞老化体系中补充适量 Na_2SeO_3(0.04～0.64ppm)后,红细胞延缓释放囊泡,溶血减少以及膜上 AchE 脱落减少,而过量的 Na_2SeO_3(6.4 ppm 以上)对红细胞则有一定的损伤作用。用电子顺磁共振(ESR)波谱仪分别测定了红细胞膜,Na_2SeO_3溶液以及外加硒红细胞膜的 ESR 谱。结果表明,外加硒红细胞膜的 ESR 谱与红细胞膜和 Na_2SeO_3溶液均不相同,其特征峰的 g 值在2.0760左右。这提示了 Na_2SeO_3对红细胞膜的作用可能是以膜结合硒的形式进行的。     

微量元素硒对红细胞老化的保护作用

红细胞老化过程中,释放囊泡,增加脆性以及减少酶活性等等均是细胞衰老的征状.本文在前文的基础上,探讨了微量元素硒对红细胞老化的保护作用.发现在红细胞老化体系中补充适量Na_2SeO_3(0.04～0.64ppm)后,红细胞延缓释放囊泡,溶血减少以及膜上AchE脱落减少,而过量的Na_2SeO_3(6.4 ppm以上)对红细胞则有一定的损伤作用.用电子顺磁共振(ESR)波谱仪分别测定了红细胞膜,Na_2SeO_3溶液以及外加硒红细胞膜的ESR谱.结果表明,外加硒红细胞膜的ESR谱与红细胞膜和Na_2SeO_3溶液均不相同,其特征峰的g值在2.0760左右.这提示了Na_2SeO_3对红细胞膜的作用可能是以膜结合硒的形式进行的.     

大豆磷脂对小鼠红细胞膜和脑组织中脂肪酸含量的影响

采用高效液相色谱法研究了小鼠灌胃大豆磷脂乳液(剂量为w(大豆磷脂/体质量)=2.5、5.0、10.0 g/kg)30 d对小鼠红细胞膜和脑组织中脂肪酸含量的影响.结果表明:(1)w(大豆磷脂/体质量)=10.0 g/kg剂量组小鼠红细胞膜和脑组织中亚油酸、亚麻酸的含量及多不饱和脂肪酸(PUFA)占总脂肪酸(TFA)的比例显著增加(P＜0.05),红细胞膜中油酸的含量显著下降(P＜0.05);(2)w(大豆磷脂/体质量)=5.0 g/kg剂量组小鼠红细胞膜中亚油酸、亚麻酸的含量和w(PUFA/TFA),以及脑组织中亚油酸的含量显著提高(P＜0.05);(3)w(大豆磷脂/体质量)=2.5 g/kg剂量组小鼠红细胞膜和脑组织中各所测脂肪酸的含量无显著差异.说明大豆磷脂可增加小鼠红细胞膜和脑组织中亚油酸、亚麻酸等的含量,改善两者的脂肪酸组成,但两者的变化存在差异.     

小分子团水在鸡血红细胞膜上的转运速率

研究了小分子团水在鸡血红细胞膜上的转运速率.采用低渗水样处理鸡血红细胞悬液、倒置显微镜观察细胞吸胀过程并拍照记录,统计了显微拍摄照片中的细胞胀破率,比较了各水样在鸡血红细胞膜上的转运速率.结果表明,在低渗条件下,小分子团水在鸡血红细胞膜上的转运速率小于普通水.鸡血红细胞悬液和碳酸氢钠水溶液混合后观察细胞胀破率,发现随着p H值增大,水分子在鸡血红细胞膜上的转运速率变慢.小分子团水低渗处理效果与碳酸氢钠水溶液(较高p H值)低渗处理效果类似.在低渗条件下小分子团水在鸡血红细胞膜上的转运速率比普通水更慢,可能与小分子团水的高p H值相关.     

过度训练对红细胞膜结构和功能影响的实验研究

为进一步探讨过度训练的发生机制,采用建立一般训练和过度训练动物模型,应用荧光法和比色法分别测定了过度训练后红细胞膜MDA含量、红细胞变形性、Na~+-K~+-ATPase、Ca~(2+)-ATPase活性以及红细胞膜总磷脂、胆固醇含量及其比值.结果显示:与对照组相比,MDA含量在运动后即刻显著升高(P<0.01);红细胞变形性显著下降(<0.05;P<0.01),Na~+-K~+-ATPase和Ca~(2+)-ATPase活性显著下降(P<0.05),红细胞膜总磷脂显著下降(P<0.05),红细胞膜上胆固醇在运动后即刻显著低于对照组(P<0.01),红细胞膜上胆固醇/磷脂比值在运动后即刻显著低于对照组(P<0.05),相关分析表明,红细胞的变形性与红细胞膜上MDA含量呈显著负相关(P<0.05).结果揭示:过度训练运动引发的自由基产生的脂质过氧化对红细胞膜结构有损害,使Na~+-K~+-ATPase和Ca~(2+)-ATPase活性下降,红细胞膜上的磷脂和胆固醇含量以及其比值降低,致使红细胞变形性下降,可能是造成过度训练后红细胞功能下降的重要原因之一.     

糖尿病患者红细胞膜葡萄糖运输速率的变化

测定了１８例糖尿病患者（其中Ⅰ型５例，Ⅱ型１３例）红细胞膜上葡萄糖跨膜运输速率的变化，结果显示患者的葡萄糖输出速率略有减小，但变化不显著，虽然在１３例Ⅱ型糖尿病患者中的２例显示出最大运输速度（Ｖｍａｘ）和半饱和浓度（Ｋｍ）有变化的趋势．对９例Ⅱ型糖尿病患者红细胞的葡萄地跨膜输入测定表明，患者的葡萄糖跨膜向内运输速率较正常的显著降低．葡萄糖向内和向外运输速率变化的差异表明在糖尿病患者红细胞膜上葡萄糖运输蛋白的外侧葡萄糖结合位点发生了某种变化．     

镧离子跨入红细胞膜的研究

本文采用fura-2荧光指示剂技术研究了在不同条件下镧离子跨红细胞膜的行为,结果发现：在正常条件下无论钙或镧离子都不能跨膜进入红细胞;红细胞ATP耗竭后出现明显的Ca^2 内流现象,而镧离子仍不能观察到跨膜现象,由此可见,稀土镧离子在过膜上与钙子表现出很大的差异性,不能利用钙通道进入细胞内。     

微波（2450MHz）对整体小白鼠红细胞膜的损伤效应及药…

本文采用２４５０ＭＨＺ微波慢性辐射整体昆明小白鼠，从分子水平研究微波对小白鼠红细胞膜的影响。选择功率密度０ｍＷ／ｃｍ＾２、５ｍＷ／ｃｍ＾２、１０ｍＷ／ｃｍ＾２的微波连续辐射小白鼠４０天，每天６小时。发现１０ｍＷ／ｃｍ＾２的微波对小白鼠红细胞膜的损伤较为明显。表现为小白鼠红细胞的渗透脆性增加，膜脂流动性下降，血浆丙二醛（ＭＤＡ）及红细胞膜ＭＤＡ均为明显升高，但红细胞溶血度未增加，红细胞ＳＯＤ、红细胞     

高血脂症患者红细胞膜脂质的研究

分析了高血脂症患者红细胞膜的脂质含量及红细胞膜的胆固醇与磷脂的物质 的量比（ｎＣＨ／ｎＰＬ）。实验表明高血脂症患者红细胞膜的脂质含量比正常人的低１６％，而 ｎＣＨ／ｎＰＬ值却显著地（Ｐ＜０．０５）高于正常人的值。这个研究对于病因及发病机理，药 物疗效及基础研究具有一定的价值。     

超重女性有氧运动对红细胞代谢的影响作用

有氧运动是人体在氧气充分供应的情况下进行的体育锻炼,红细胞代谢时可运输氧气,研究超重女性有氧运动对红细胞代谢产生的影响作用具有十分重要的意义。对64名超重女性进行为期三周的有氧运动。通过流式细胞检测法检测超重女性体内红细胞膜的PS外翻量,对有氧运动前后的血脂、PS外翻及Na+K+-ATPase和Ca2+Mg2+-ATPase酶三维活性进行检验。实验结果表明:有氧运动干预之前,轻度超重组女性体内的PS外翻量与其余两组有明显的差别(P≤0.05),HDL在轻度超重组和重度超重组之间有明显的区别;有氧运动干预后,Na+K+-ATPase的活性有显著提高(P≤0.05),红细胞膜的PS外翻量虽然有降低的趋势,但差异不显著。说明在红细胞脂质代谢紊乱的初期,红细胞膜PS外翻量比血脂指标更能体现超重女性的体重发展情况。有氧运动能够有效提高红细胞膜膜Na+K+-ATPase酶的活性,提高红细胞膜PS的外翻量,同时加快红细胞的代谢速度。     

The membrane attachment protein for spectrin is associated with band 3 in human erythrocyte membranes.

Ankyrin, the membrane attachment protein for human erythrocyte spectrin, is tightly linked in a 1:1 molar ratio with band 3 in detergent extracts of spectrin-depleted membranes. Ankyrin-linked band 3, which represents 10--15% of the total band 3, spans the membrane, and is nearly identical to the major band 3 by peptide analysis. Spectrin binds to solubilised ankyrin-linked band 3, but not to free band 3. A portion of band 3 remains firmly associated with detergent-extracted cytoskeletal proteins. It is concluded that a fraction of band 3 is attached to the erythrocyte cytoskeleton through association with ankyrin, which in turn is bound to spectrin.     

Hereditary spherocytosis associated with deletion of human erythrocyte ankyrin gene on chromosome 8

Hereditary spherocytosis (HS) is one of the most common hereditary haemolytic anaemias. HS red cells from both autosound dominant and recessive variants are spectrin-deficient, which correlates with the severity of the disease. Some patients with recessive HS have a mutation in the spectrin alpha-2 domain (S.L.M. et al., unpublished observations), and a few dominant HS patients have an unstable beta-spectrin that is easily oxidized, which damages the protein 4.1 binding site and weakens spectrin-actin interactions. In most patients, however, the cause of spectrin deficiency is unknown. The alpha- and beta-spectrin loci are on chromosomes 1 and 14 respectively. The only other genetic locus for HS is SPH2, on the short arm of chromosome 8 (8p11). This does not correspond to any of the known loci of genes for red cell membrane proteins including protein 4.1 (1p36.2-p34), the anion exchange protein (AE1, band 3; 17q21-qter), glycophorin C (2q14-q21), and beta-actin (7pter-q22). Human erythrocyte ankyrin, which links beta-spectrin to the anion exchange protein, has recently been cloned. We now show that the ankyrin gene maps to chromosome 8p11.2, and that one copy is missing from DNA of two unrelated children with severe HS and heterozygous deletions of chromosome 8 (del(8)(p11-p21.1)). Affected red cells are also ankyrin-deficient. The data suggest that defects or deficiency or ankyrin are responsible for HS at the SPH2 locus.     

再生障碍性贫血病人红细胞膜骨架蛋白的研究

十二烷基磺酸钠—聚丙烯酰胺凝胶电泳(简称为SDS-PAGE)方法分离12例再生障碍性贫血(简称再障)病人红细胞膜蛋白,发现其中有6例红细胞骨架蛋白带1、带2和带4有不同程度减少或缺损。同时用扫描电子显微镜观察其红细胞形态,发现亦有不同程度异常,表现为棘状、刺状及波浪状。提示红细胞骨架蛋白的含量与红细胞的形态有密切关系。     

Primary structure and transmembrane orientation of the murine anion exchange protein

The amino-acid sequence of murine band 3, deduced from the nucleotide sequence of a complementary DNA clone, confirms that this integral membrane glycoprotein is composed of two major structural domains which correlate with its dual functions as the anchor for the erythrocyte cytoskeleton and as a plasma membrane anion antiporter. This latter activity resides within a highly hydrophobic domain that crosses the plasma membrane at least 12 times.     

Partial deficiency of erythrocyte spectrin in hereditary spherocytosis

Hereditary spherocytosis (HS) is a common, clinically heterogeneous haemolytic anaemia in which the primary erythrocyte defect is believed to be some abnormality in the spectrin-actin membrane skeleton, leading to loss of surface membrane. Recessively inherited spectrin deficiency with extreme erythrocyte fragility and spherocytosis has been identified in certain mutant mice and two severely anaemic humans. Although suspected, deficiency of spectrin has not been demonstrated in less severe forms of human HS. We not report the quantitation of erythrocytes spectrin by radioimmunoassay. We found that normal erythrocytes contained 240,000 copies of spectrin heterodimer, whereas erythrocytes from 14 patients with a variety of types of HS were all partially deficient in spectrin (range 74,000-200,000 copies), the magnitude of the deficiency correlating with the severity of the disease. Spectrin deficiency of varying degrees is common in HS and probably represents the principal structural defect leading to loss of surface membrane.     

Immunoreactive forms of human erythrocyte ankyrin are present in diverse cells and tissues.

Ankyrin is a polypeptide of molecular weight (MW) 200,000 which is tightly bound to the cytoplasmic surface of the human erythrocyte membrane and has been identified as the high-affinity membrane attachment protein for spectrin. This protein has also been shown to be associated with band 3 (ref. 4), the major transmembrane protein which links a cytoplasmic structural protein to an integral membrane protein. A water-soluble, 72,000-MW, proteolytic fragment of ankyrin has been purified which retains the ability to bind to spectrin, and competitively inhibits reassociation of spectrin with membranes. Monospecific antibodies directed against this fragment have been prepared and demonstrated to cross-react only with ankyrin among the erythrocyte membrane proteins. The present study reports the use of these antibodies to develop a radioimmunoassay capable of detecting femtomolar quantities of ankyrin, and demonstrates the presence of small but significant amounts of immunoreactivity in a variety of types of cells and tissues.     

红细胞沉降速率Ⅲ—红细胞可变形性的实验研究

介绍了一种利用红细胞沉降过程测量评价红细胞可变形性的新方法，并用它考查了猪红细胞在生理盐水溶液及ＳＦ６０溶液中的可变形性，实验得到的可变形性参数分别为０．８６２和０．９７１。     

Regulation of glutamate receptor binding by the cytoskeletal protein fodrin

The erythrocyte cytoskeleton, which consists primarily of a meshwork of spectrin and actin, controls cell shape and the disposition of proteins within the membrane. Proteins similar to spectrin have recently been found in diverse cells and tissues, and it is possible that they mediate the capping of cell-surface receptors, although this has not been demonstrated directly. In neurones, the spectrin-like protein fodrin lines the cortical cytoplasm and may link actin filaments to the membrane. Fodrin has been hypothesized to regulate the number of receptor binding sites on neuronal membranes for the putative neurotransmitter L-glutamate. Micromolar calcium concentrations activate the thiol protease calpain I, induce fodrin degradation and more than double the density of glutamate binding sites; these effects are all blocked by thiol protease inhibitors. We have now used specific antibodies to examine further the role of fodrin proteolysis in regulating glutamate receptors. We report that fodrin antibodies block the fodrin degradation and increase in glutamate binding normally induced by calcium, and so provide direct evidence for control of membrane receptors by a non-erythroid spectrin.