Ⅱ型糖尿病肾病和红细胞膜ATP酶活性的关系

目的 探讨Ⅱ型糖尿病患红细胞膜Na^K^ -ATP酶和Ca^2 Mg^2 -ATP酶活性改变参与糖尿病肾病的可能机制。方法 按Reinila制膜法测定了25例无糖尿病肾病和57例糖尿病肾病患红细胞膜Na^ K^ -ATP酶和Ca^2 Mg^2 -ATP酶含量,并与35名正常人作对照。结果 糖尿病无肾病组和肾病组红细胞膜Na^ -K^ -ATP酶和Ca^2 Mg^2 -ATP酶活性均显地低于正常人组（P＜0．01）,糖尿病肾病组与无肾病组比较差异亦有显性（P＜0．05）。结论 Ⅱ型糖尿病肾病的发生和发展与红细胞膜Na^2 K^ -ATP酶和Ca^2 Mg^2 -ATP酶活性有密切的关系。     

自体血液回收技术对红细胞膜ATP酶的影响

目的 探讨血液回收技术对红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性的影响。方法 将24例患者麻醉前静脉血、术野回收原血及回收红细胞血液标本采用沈茂星法测定红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性,并予统计分析。结果 经血液回收技术处理后的红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性与术野回收血值比较均有显著降低（P〈0．05）。结论 自体血液回收技术能使红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性明显降低。     

利多卡因对家兔心肌缺血/再灌注损伤氧自由基及Na+-K+-ATPase、Ca2+-Mg2-ATPase的作用

目的观察利多卡因对心肌缺血再灌注损伤家兔血清GSH—P^2X、MDA及心肌组织Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase的影响。方法24只家兔随机分为3组：假手术组（A组）、缺血／再灌注组（B组）、利多卡因组（c组）,每组8只。B组、C组阻断左冠状动脉前降支40min．再灌注90min．A组仅穿线不结扎。C组于开放冠状动脉再灌注前经颈静脉注射利多卡因5mg／kg,B、C组注射等量生理盐水。于再灌注90min取颈静脉血测定GSH—PX、MDA;再灌注90min后取心肌组织测定Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase。结果血清GSH—PXB组较A、C组降低（P〈0．01）、血清MDAB组较A、C组升高;心肌组织Na^＋ - K^＋ - ATPase、Ca^2＋ - Mg^2＋ - ATPase B组较A、C组降低（P〈0．01）。结论利多卡因对心肌缺血再灌注损伤具有保护作用。     

线粒体及内质网对铅引起的[Ca2+]i升高的作用

目的 研究线粒体、内质网Ca^2 -ATP酶以及Na^ 和K^ -ATP酶活力的改变对铅引起的[Ca^2 ]i升高的调节作用，探讨铅引起的[Ca^2 ]i增高对学习记忆功能的影响。方法 Wistar大鼠神经肉瘤C6细胞培养于含醋酸铅的培养液中，于不同时间终止染铅，检测[ca2’]；及线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力。结果 (1)0．2μmol／L染铅组：[Ca^2 ]i轻度升高，线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力升高，内质网酶活力略增高；(2)1．0μmol／L染铅组：[Ca^2 ]；于染铅后0．5h升至最高，以后逐渐降低，波动于iL60～190nmol／L之间；线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶于染铅后0．5h升至最高(分别为未染铅前酶活力的29．1、39．2、10．8和19．8倍)，2d后降至接近正常水平。结论 (1)铅可使Wistar大鼠神经肉瘤C6细胞Ca^2 浓度及线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高；(2)当[Ca^2 ]i增高不显著时以线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高为主；当[Ca^2 ]i急剧升高时，线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力均明显增高，尤其是线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高更为显著。     

复合离子盐对老年人细胞内Na+、K+、Ca2+的影响及其机制

目的：观察复合离子盐对老年人细胞内Na^＋、K^＋、Ca^2＋及红细胞膜钠泵和钙泵活性的影响。方法：在天津市河东区社区中抽取226例老年人作为研究对象．其中高血压者112例。正常血压者114例。两者再随机分为离子盐组和普通加碘盐组．分别给予复合离子盐和普通加碘盐摄入，6个月后观察研究对象细胞内Na^＋、K^＋、Ca^2＋及钠泵、钙泵活性的变化。结果：6个月时高血压患者中离子盐组细胞内钠、钙离子浓度低于基线水平（P〈0．05），但钾离子无明显变化。离子盐组钠泵、钙泵活性均明显高于基线水平（P〈0．05），但在正常血压者中，2组与基线水平比较差异无统计学意义。结论：复合离子盐可增强钠泵、钙泵活性，使细胞内的钠、钙含量减少。     

肥胖儿童高血压发病因素有机理的研究

目的：探讨儿童肥胖引起高血压的机制。方法：测定104例12－16岁儿童的血脂、胰岛素水平,Na^ -K^ -ATP酶和Ca^2 -ATP酶活性。结果：在正常血压肥胖组（ONT）和高血压肥胖组（OHT）,空腹胰岛素（Ins）显著升高,面NNa^ -K^ -ATP酶和Ca^2 -ATP酶活性显著下降,三者在ONT和OHT组之间也有显著性差异,在OHT组Ins升高,两酶活性下降,Pearson相关和多元回归分析显示,在OHT组,Ins和Ca^2 -ATP酶与收缩压（SBP）显著相关,Na^ -K^ -ATP酶与舒张压9DBP）显著相关。结论：高胰岛素血症、Na^ -K^ -ATP酶和Ca^2 -ATP酶活性降低可能在肥胖儿童高血压的发病机制中起重要作用。     

甲状腺机能减退征患者红细胞膜Ca2+.Mg2+ -ATPase活性测定

目的了解红细胞膜钙-镁三磷酸腺苷酶（Ca^2＋．Mg^2＋ -ATPase）活性在甲状腺功能减退征患者中的变化及该酶活性是否随甲状腺功能的恢复而逆转至正常,以确定该酶活性可否作为甲状腺激素在细胞水平作用的一个指标。方法低温、低渗溶解红细胞,差速离心法制备红细胞膜悬液。酶活性以含酶的红细胞膜悬液水解底物ATP释放出无机磷的量表示,无钙条件下无机磷的产生量为Mg^2＋ -ATPase活性。有钙条件下无机磷的产生量为总ATPase活性,二者之差为Ca^2＋．Mg^2＋ -ATPase活性。结果甲状腺功能减退患者红细胞Ca^2＋．Mg^2＋ -ATPase活性明显低于正常组。但3月后,随着甲状腺功能恢复正常,酶活性也随之恢复正常。结论红细胞膜Ca^2＋．Mg^2＋ -ATPase活性可作为甲状腺激素在细胞水平作用的一个指标,用于甲状腺功能异常的辅助诊断。     

大鼠心肌缺血再灌注损伤对心肌细胞膜钠泵表达的影响

目的：观察心肌缺血再灌注（MIR）损伤大鼠心肌组织内洋地黄素水平、ATP酶活性、线粒体Ca^2＋浓度以及Na^＋-K^＋-ATP酶各亚基基因表达的改变，并观察钙通道阻滞剂维拉帕米对其影响，探讨内洋地黄素在MIR损伤细胞内钙超载中的可能作用及其机制。方法：24只雄性SD大鼠随机分成3组，每组8只。假手术组：丝线穿过左冠状动脉前降支，但不结扎：缺血再灌注组（MIR组）：结扎左冠状动脉前降支30min，再灌注45min；维拉帕米组：MIR模型＋5mg／kg维拉帕米，维拉帕米于再灌注前5min经股静脉注射。取缺血区左室心肌检测心肌匀浆内洋地黄素水平、心肌细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性、线粒体Ca^2＋浓度；免疫组化方法检测心肌Na^＋-K^＋-ATP酶α1、α2、α3和β1亚基蛋白水平表达的改变。结果：MIR损伤时，心肌组织内洋地黄素水平明显升高，心肌细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性显著下降，线粒体Ca^2＋浓度升高，Na^＋-K^＋-ATP酶α1、α2、α3和β1亚基蛋白水平表达均明显下降；维拉帕米除具有降低线粒体Ca^2＋浓度外，对缺血再灌注引起的其它各项异常指标无明显改善作用。结论：MIR促进机体内洋地黄素分泌增加，后者可能通过影响心肌细胞膜上的Na^＋-K^＋-ATP酶α1、α2、α3和β1亚基基因表达，抑制Na^＋-K^＋-ATP酶活性，导致线粒体内Ca^2＋超载。     

辛伐他汀对大鼠骨骼肌线粒体膜流动性及ATP酶活性的影响

目的：观察辛伐他汀（Sim）对大鼠骨骼肌线粒体膜流动性及ATP酶活性的影响.方法：大鼠口服给予3种不同剂量Sim,酶法测定丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）及肌酸激酶（CK）活性.以1-苯氨基萘-8-磺酸（ANS）、1,6-二苯基-1,3,5-己三烯（DPH）为荧光探针标记骨骼肌线粒体膜浅层及深层,测定骨骼肌线粒体膜荧光强度（F）,荧光偏振度（P）及平均微黏度（^-η）.比色法测定Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性.结果：给予Sim 3.6,7.2 mg·kg^-1·d^-1组,血清ALT、AST、CK和骨骼肌线粒体膜Na^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶的活性均无显著变化.而给予Sim 14.4mg·kg^-1·d^-1,血清CK活性显著增高,骨骼肌线粒体膜Na^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶活性则明显降低.给予Sim3.6,7.2,14.4 mg·kg-1·d-1组,ANS标记的线粒体膜浅层和DPH标记的线粒体膜深层F、P、^-η均明显降低,表明Sim可增加线粒体膜浅层及深层流动性.结论：Sim在高剂量时可导致骨骼肌细胞损伤,其机制可能与Sim能增加骨骼肌线粒体膜流动性,降低骨骼肌线粒体膜Ca^2＋-Mg^2＋-ATP酶及Na^＋-K^＋-ATP酶活性有关.     

灯盏花素对缺血再灌注沙土鼠海马ATP含量变化和兴奋性氨基酸释放的影响

目的 研究灯盏花素对缺血再灌注沙土鼠海马ATP含量、ATP酶活性和兴奋性氨基酸释放的影响。方法 脑缺血10min建立沙土鼠缺血再灌注模型。90只沙土鼠分为假手术组、脑缺血组和灯盏花素组。测定脑缺血后和再灌注1、12和24h海马ATP含量、ATP酶活性和兴奋性氨基酸含量。结果 脑缺血组,ATP、Na^＋-K^＋ATP酶和Ca^2＋-ATP酶含量明显下降（P〈0．01）,谷氨酸（Glu）、天冬氨酸（Asp）、γ-氨基丁酸（GABA）含量明显增加（P〈0．01）,谷氨酰胺（Gln）含量在缺血时降低,再灌注后增加（P〈0．01）。灯盏花素组,ATP、Na^＋-K^＋-ATP酶和Ca^2＋-ATP酶含量高于脑缺血组（P〈0．01）。Glu、Asp、GABA含量明显低于脑缺血组（P〈0．01）,Gln含量高于脑缺血组（P〈0．01）。结论 灯盏花素明显增加脑缺血及再灌注后ATP含量和ATP酶活性,降低兴奋性氨基酸释放,可减轻脑缺血再灌注损伤。     

肥胖儿童高血压发病因素和机理的研究

目的探讨儿童肥胖引起高血压的机制。方法测定104例12～16岁中学儿童的血脂、胰岛素水平, Na     

Chloral hydrate inhibition in vitro of ATPase in membrane of rat erythrocytes and in microsomes of dog kidney external medulla

The study of the general anesthetic chloral hydrate and its effects on rat erythrocyte membranes and dog kidney microsomes showed that ATPases were reversibly inhibited in every case. The inhibition was cooperative in the cases of (Mg2+ + Na+ + K+)-ATPase, Mg2+-ATPase and (Na+ + K+)-ATPase of rat erythrocyte membrane, while Ca2+-ATPase and (Mg2+ + Ca2+)-ATPase were non-cooperative. The chloral hydrate concentrations necessary to diminish the activity of the enzyme to half of the Vmax (I50) were 6 mM for Ca2+-ATPase from erythrocyte membranes and 82 mM for Mg2+-ATPase from intact external kidney medulla microsomes. When Ca2+-ATPase was studied in the absence of Mg2+ in these microsomes, the affinity for Ca2+ was very low, but the enzyme was sensitive to chloral hydrate.     

l-Cysteine and glutathione restore the modulation of rat frontal cortex Na, K-ATPase activity induced by aspartame metabolites

BACKGROUND: Studies have suggested that aspartame (ASP) ingestion is implicated in neurological problems. AIM: The aim of this study was to evaluate rat frontal cortex Na+, K+ -ATPase and Mg2+ -ATPase activities after incubation with ASP or each of its metabolites, phenylalanine (Phe), methanol (MeOH) and aspartic acid (asp) separately. METHOD: Suckling rat frontal cortex homogenates or pure Na+, K+ -ATPase were incubated with ASP metabolites. Na+, K+ -ATPase and Mg2+ -ATPase activities were measured spectrophotometrically. RESULTS: Incubation of frontal cortex homogenate or pure Na+, K+ -ATPase with various ASP concentrations as expected in the cerebrospinal fluid (CSF) after ASP consumption of 34, 150 or 200mg/kg, decreased the frontal cortex enzyme activity by 33%, 53% or 57%, respectively, whereas pure enzyme was remarkably stimulated. Moreover, incubation of frontal cortex homogenate with each one of the expected ASP metabolites in the CSF, except MeOH, which are related to the intake of the above mentioned doses of the sweetener, resulted in an activation of the membrane Na+, K+ -ATPase, as well as pure enzyme. Frontal cortex Mg2+-ATPase remained unaltered. Addition of l-cysteine (cys) or reduced glutathione (GSH) to ASP metabolites mixtures, corresponding to 150 or 200mg/kg doses of the sweetener, completely or partially restored to normal the modulated membrane and pure Na+, K+ -ATPase activities. CONCLUSION: CSF concentrations of the sum of ASP metabolites corresponding to the intake of common, abuse or toxic doses (34 or 150 or 200mg/kg, respectively) of the additive significantly increased rat frontal cortex Na+, K+ -ATPase and pure enzyme activities. Cys or GSH completely or partially restored to normal both enzyme activities, possibly due to amelioration of the cellular GSH reduction from the action of MeOH, a metabolite of the sweetener and/or by their scavenging effect.     

The oxidative damage of butenolide to isolated erythrocyte membranes.

Butenolide (CAS No. 16275-44-8), a mycotoxin produced by several Fusarium species, has been shown to be a potential risk factor for animal and human health. This study was undertaken to investigate the potential oxidative damage of butenolide to biomembranes in vitro using the erythrocyte membrane model. Following exposure of isolated rat erythrocyte membranes to butenolide, the extent of oxidative damage was assessed by measuring lipid peroxidation, -SH groups content, Ca2+/Mg2+-ATPase and Na+/K+-ATPase activities, and conformational changes in membrane proteins. It was observed that butenolide resulted in a significant lipid peroxidation, revealed by a concentration-dependent increase in the level of thiobarbituric acid reactive substances (TBARS). Similarly, this toxin induced a concentration-dependent decrease in the content of membrane total -SH groups, as well as free -SH groups. Membrane-bound enzymes were also impaired by the toxin, demonstrated by the marked inhibition of the activities of Na+/K+-ATPase and Ca2+/Mg2+-ATPase. Conformational changes in membrane proteins were determined using electron paramagnetic resonance (EPR) spin labeling. Butenolide caused an increase in the ratio of weakly to strongly immobilized components (W/S ratio) in a manner of concentration-dependent, indicating conformational changes in membrane proteins occurred. In conclusion, these findings indicate that butenolide is capable of inducing significant oxidative damage to membrane lipids and proteins.     

氯喹对烟雾吸入伤大鼠肺细胞膜ATP酶活性和丙二醛含量的影响

目的：探讨氯喹对烟雾吸入伤大鼠肺细胞膜ＡＴＰ酶活性及丙二醛含量的影响,方法：８０只Ｗｉｓｔａｒ大鼠随机分成正常对照组,烟雾吸入伤１,３,６,１２和２４ｈ组以及氯喹治疗６ｈ和１２ｈ组,分别于各时相点活杀动物,取肺制备膜制剂,用生化比色法测定膜上Ｎａ＾＋,Ｋ＾＋－ＡＴＰ酶Ｍｇ＾２＋－ＡＴＰ酶和Ｃａ＾２＋－ＡＴＰ酶活性,用比色法测定膜上丙醛含量,并用定磷法测定膜总磷脂含量,结果：烟雾吸入伤后,肺细胞膜３     

Effect of hydroxychlorodiphenyl ethers (chlorinated pre-and isopredioxins) on erythrocyte membrane adenosinetriphosphatase activity

The effect of hydroxychlorodiphenyl ethers (HO-ClX-DPEs; chlorinated pre- and isopredibenzodioxins), contaminants of technical chlorophenol preparations, on human erythrocyte membrane-bound adenosinetriphosphatases (ATPases) has been investigated. Both 2- and 3-HO-Cl9-DPE inhibited the Na+ + K+-activated, Mg2+-dependent ATPase (Na+, K+, Mg2+-ATPase). The Mg2+-dependent ATPase (Mg2+-ATPase) was stimulated at lower concentration of these compounds, but at higher concentrations there was a gradual decrease in the extent of stimulation, 2-Hydroxy-21, 41, 41-trichlorodiphenyl ether (2-HO-Cl3-DPE; Irgasan DP-300; Triclosan) was not as effective as the nonachloro compounds at inhibiting Na+, K+, Mg2+-ATPase and was inactive at stimulating Mg2+-ATPase. Pure pentachlorophenol (PCP) caused both inhibition of Na+, K+, Mg2+-ATPase and stimulation of Mg2+-ATPase, although each effect required a higher concentration of PCP than was needed for the HO-CL9-DPEs. The possible relationship of the effects of HO-CL x-DPEs on human erythrocyte membrane ATPase activities to the potent hemolytic activity of these compounds is discussed.     

异丙酚、氯胺酮对大鼠突触体Na~ ,K~ -ATP酶活性的影响

目的观察异丙酚、氯胺酮对大鼠不同脑区突触体Na ,K -ATP酶活性的影响。方法SD大鼠 ,随机分为三组 ,每组10只 ,分别ip生理盐水10ml/kg(对照组) ,异丙酚100mg/kg 或氯胺酮100mg/kg。用分光光度法测定大脑皮层、海马和脑干突触体Na ,K -ATP酶活性。结果与对照组比较 ,异丙酚明显抑制大脑皮层、海马和脑干突触体Na ,K -ATP酶活性(P<0.01),氯胺酮明显降低大脑皮层和脑干突触体Na ,K -ATP酶活性(P<0.01) ,但对海马突触体Na ,K -ATP酶活性无明显影响(P<0.01)。结论异丙酚、氯胺酮的全身麻醉作用可能与其抑制脑突触体Na ,K -ATP酶活性有关     

Effects of calcium antagonists on (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities of rat cortical synaptosomes

1. The effects of 11 calcium antagonists on (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities of rat cortical synaptosomes were studied. 2. All the calcium antagonists studied had inhibitory effects on ouabain-sensitive (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities in synaptosomes at high concentrations (10 or 100 microM). 3. Calcium antagonists such as trifluoperazine, flunarizine and cinnarizine had inhibitory effects on Ca2+-ATPase activity at low concentrations (1-10 microM). 4. Trifluoperazine and La3+ had inhibitory effects on Mg2+-ATPase activity at low concentration (1 microM). 5. Our results suggest that most of the calcium antagonists studied have little effects on neuronal (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities at therapeutic dose ranges (1 microM or lower).     

Effect of methacrylonitrile on membrane bound enzymes of rat brain

Methacrylonitrile (MeAN) is a plastic monomer. Its effect on membrane bound enzymes like Na+K+ -ATPase, Ca2+ -ATPase, Mg2+ -ATPase, NADH dehydrogenase, alkaline phosphatase (ALP) and various elements like sodium (Na+), potassium (K+), and calcium (Ca2+) in rat brain were studied. Administration of 50 mg/kg body weight/day (0.25 LD50) and 100 mg/kg body weight/day (0.5 LD50) by gavage to rats for 7 days resulted in a significant decrease in activities of Na+K+ -ATPase, Ca2+ -ATPase, Mg2+ -ATPase, and NADH dehydrogenase. A significant reduction in calcium content, potassium content and a significant increase in sodium content and alkaline phosphatase activity in MeAN treated animals were observed. Inhibition of membrane bound enzymes occurred due to either direct effect of MeAN or indirect effect of changes in ionic homeostasis in MeAN treated animals.