bFGF对慢性酒精中毒大鼠脑和肝组织ATP酶活力的影响

[目的]观察碱性成纤维细胞生长因子(bFGF)对慢性酒精中毒大鼠脑组织及肝组织Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力,探讨bFGF对慢性酒精中毒所致的脑损伤、肝损伤的保护作用。[方法]选择成年Wistar雄性大鼠,采用白酒灌胃建立慢性酒精中毒模型,慢性酒精中毒模型建立成功的大鼠随机抽签法分为酒精中毒对照组、生理盐水(NS)对照组和bFGF治疗组,每组10只。另10只不灌白酒作为正常对照组。bFGF治疗组大鼠白酒灌胃的同时,1 h后按12μg/kg剂量肌肉注射,共14 d。各组大鼠到相对应的时间点取出各组大鼠脑组织、肝组织制成匀浆,测定脑组织、肝组织匀浆中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力。[结果]与正常对照组相比,慢性酒精中毒后大鼠脑组织及肝组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显降低(P﹤0.01);经bFGF治疗后脑组织及肝组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于酒精中毒对照组及NS对照组(P﹤0.05)。[结论bFGF能提高慢性酒精中毒脑组织和肝组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,提示bFGF对慢性酒精中毒所致的脑损伤和和肝损伤具有保护作用。     

Chronic maternal ethanol consumption results in decreased serotonergic 5-HT1 sites in cerebral cortical regions from offspring

This laboratory previously demonstrated that chronic maternal ethanol consumption results in a marked deficiency of cortical serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) and of 5-HT uptake sites in the 19- and 35-day-old offspring. In order to determine whether in utero exposure to ethanol similarly affects other components of the serotonergic system we examined the influence of chronic maternal ethanol consumption on cortical, serotonergic 5-HT1 binding sites in developing offspring. Female Sprague-Dawley rats were pair-fed, using control or 6.6% (v/v) ethanol liquid diets on a chronic basis prior to parturition. Serotonergic 5-HT1 sites were measured in synaptosomal membranes from whole cortex and cortical regions from developing offspring. Serotonergic 5-HT1 sites were assessed by measuring the binding of [3H]-5-HT to synaptosomal membranes in the presence and absence of nonradioactive 5-HT. Serotonergic 5-HT2 sites were blocked by including 100 nM spiperone in the assay buffer. The results demonstrated that the 19- and 37-day-old offspring of ethanol-fed rats had a significant (approximately 10-40%) reduction in the Bmax for serotonergic 5-HT1 binding sites on synaptosomal membranes from whole cortex (p less than 0.025), motor cortex (p less than 0.01), and somatosensory cortex (p less than 0.025). However, the binding affinity (Kd) for serotonin was not significantly altered (p greater than 0.05). These results emphasize the sensitivity of the developing cortical serotonergic system to prenatal ethanol exposure.     

Characteristics of a (Na+-K+)-ATPase inhibitor in extracts of tea

Extracts of tea were examined for inhibitors of the sodium-potassium pump by investigating the effect of the extracts on 1) isolated preparations of (Na+-K+)-ATPase from hog brain and human blood cells; 2) the displacement of radioactive ouabain from its specific receptor on red blood cells, and 3) the uptake of radioactive rubidium in intact red blood cells. It has been found that extracts of tea were potent inhibitors of the purified hog brain (Na+-K+)-ATPase. However, the inhibition was not specific for the (Na+-K+)-ATPase and the extract of tea did not displace 3H-ouabain in a specific ouabain-receptor assay. Additionally, the tea extracts displayed only a small inhibitory effect on the uptake of 86Rb in intact red blood cells. These observations suggest that the material is not like digitalis and that, unlike cardiac glycosides, it may inhibit the activity of the (Na+-K+)-ATPase by interacting with the enzyme at intracellular sites.     

Effects of in utero ethanol exposure on serotonin uptake in cortical regions

Previously, this laboratory found that the 19- and 35- to 37-day-old offspring of rats that consumed ethanol on a chronic basis prior to parturition had a decreased cortical content of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) as well as a decreased number of cortical 5-HT1 binding sites. These results emphasized the sensitivity of the developing cortical serotonergic nerves to the effects of in utero ethanol exposure. In the present study, we examined the effects of in utero ethanol exposure on an additional component of the developing cortical serotonergic systems. Specifically, we examined the uptake of [3H]-5-HT by synaptosomes which were isolated from the motor or somatosensory regions of the cerebral cortex. The results demonstrated that the Vmax for serotonin uptake was significantly decreased (p less than 0.025) by approximately 15-20% in the motor cortices of the 19- and 35-day-old offspring of rats that consumed ethanol on a chronic basis prior to parturition. In addition, there was a significantly (p less than 0.025) approximately 30% decrease in the Km for serotonin uptake in the motor cortex of 35-day-old offspring of ethanol-fed rats. In contrast, neither the (Km) nor the Vmax for serotonin uptake were significantly altered (p greater than 0.05) in the somatosensory cortices in 19- or 35-day-old offspring of ethanol-fed rats. These results emphasize the selective sensitivity of developing cortical projections of the serotonergic system.     

Effects of manganese on rat brain microsomal Mg2+-Na+-K+-ATPase: in vivo and in vitro studies

The effect of manganese on brain microsomal Mg2+-Na+K+-ATPase was examined both in vitro and in vivo. Daily intraperitoneal administration of MnCl2 . 4H2O (Mn2+, 6 mg/kg) to the rats for a period of 90 days produced 10% (P less than 0.05) inhibition in the activity of Mg2+-ATPase, and 72 and 63% increases in the contents of manganese and copper, respectively, in the microsomal fraction of brain. In in vitro studies, lower concentrations of Mn2+ activated while higher concentrations inhibited the activity of brain microsomal ATPase. Addition of equal concentrations of Mn2+ + Cu2+ (8 mM) in vitro produced 8% inhibition in the activity of Mg2+-ATPase and 83% inhibition in Na+-K+-ATPase. Free Cu2+ ions were able to antagonize the effect of Mn2+ on ATPase in vitro and inhibited the activity of Mg2+-Na+-K+-ATPase with more pronounced effect of Na+-K+-ATPase. The lack of change in the activity of Na+-K+-ATPase in the brain microsomes of rats administered manganese, in spite of a significant increase in copper, could not be explained. It is, however, evident that a manganese-induced elevation in brain copper was not responsible for initiating biochemical changes in manganese neurotoxicity.     

地卓西平对甲基汞致大鼠脑皮质细胞内钙稳态失调的影响

目的研究地卓西平对甲基汞致大鼠脑皮质细胞内钙稳态失调的影响。方法 Wistar大鼠32只,按体重随机分成4组,每组8只。第1组为对照组,腹腔注射0.9%氯化钠;第2组为低剂量甲基汞染毒组,腹腔注射4μmol/kg的甲基汞溶液;第3组为高剂量甲基汞染毒组,腹腔注射12μmol/kg的甲基汞溶液;第4组为地卓西平预处理组,隔日皮下注射0.3μmol/kg地卓西平,2 h后腹腔注射12μmol/kg的甲基汞溶液;注射容量均为5 ml/kg,染毒4周,每周5次。观察神经细胞内Ca2＋浓度及其凋亡情况,同时测定脑皮质Hg含量和与维持钙稳态相关的酶Na＋-K＋-ATPase和Ca2＋-ATPase活性。结果染毒4周后,随着染毒剂量的增加,脑皮质Hg含量和细胞内Ca2＋浓度均明显升高（P〈0.01）;细胞凋亡率明显高于对照组（P〈0.01）;脑皮质Na＋-K＋-ATPase和Ca2＋-ATPase活性均不同程度的受到抑制。地卓西平预处理可以明显缓解神经细胞凋亡和细胞内Ca2＋超载,对Na＋-K＋-ATPase和Ca2＋-ATPase活性也有一定程度的恢复作用。结论甲基汞通过抑制与维持钙稳态相关的酶Na＋-K＋-ATPase和Ca2＋-ATPase活性,干扰神经细胞内钙稳态,进而造成神经细胞凋亡。地卓西平可以阻断Ca2＋通道对钙稳态失调引起的细胞损伤有拮抗作用。     

铅对家兔脑组织血管内皮物质及ATP酶活力的影响

目的探讨铅对家兔脑组织一氧化氮含量及ATP酶活力的影响及其机制。方法将32只家兔随机分为1个对照组和高、中、低3个染铅剂量组。经不同剂量醋酸铅灌胃染毒5d后,测定各组脑组织中内皮素（ET）、一氧化氮（NO）的含量及Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶的活力。结果高、中剂量染毒组ET浓度较对照组显著升高（P〈0.05,P〈0.01）,3个剂量染毒组NO浓度均较对照组显著降低（P〈0.05,P〈0.01）;高、中剂量染毒组Na^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶活力均较对照组显著降低（P〈0.05,P〈0.01）。结论铅可造成家兔脑组织血管内皮活力物质及ATP酶活力的异常,这种改变可能与铅所致中枢神经系统功能损害有关。     

氟对大鼠红细胞膜Na~＋－K~＋－ATPase、Ca~（2＋）－ATPase活性的影响及“抗氟灵”的拮抗作用研究

选择健康雄性Ｗｉｓｔａｒ大鼠４０只,随机分为５组,观察氟对大鼠红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ、Ｃａ２＋－ＡＴＰａｓｅ活性的影响及“抗氟灵”的拮抗作用。染毒及给药方式为自由饮式,染毒剂量为１８０ｍｇＦ－／Ｌ“抗氟灵浓度为２４ｇ％;染毒时间为２个月,“抗氟灵”治疗时间为１个半月。结果显示,染氟组动物红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ、Ｃａ２＋－ＡＴＰａｓｅ活性均有显著升高,给予氟＋“抗氟灵”组比染氟组显著降低;氟中毒后给予“抗氟灵”治疗组明显低于治疗对照组。提示氟对红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ、Ｃａ２＋－ＡＴＰａｓｅ活性有促进作用,而“抗氟灵”具有拮抗氟的作用     

嗜热链球菌grx02发酵乳对大鼠酒精性肝损伤保护作用的实验研究

目的研究嗜热链球菌grx02对酒精性肝损伤大鼠肝细胞线粒体功能的保护作用,探讨其可能的作用机制。方法以56%酒精灌胃,复制大鼠酒精性肝损伤模型。Wistar大鼠随机分为对照组、模型组、东宝肝泰干预组、样品组、阳性对照组,每组10只。grx02发酵乳(高、中、低剂量)分别灌胃含乳酸菌数为108、107、106cfu/ml的脱脂乳发酵液14 ml/kg bw,连续6w。末次灌胃前晚禁食不禁水,灌胃1h后,对照组灌胃蒸馏水,其它各组灌胃50%酒精14ml/kg bw。12h后处死大鼠,检测血清中的谷氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、和甘油三酯(TG);提取肝细胞线粒体,测定丙二醛(MDA)含量,超氧化物歧化酶(SOD)、Na+-K+-ATPase,Ca2+-ATPase活力。结果与模型组比较,嗜热链球菌grx02可降低血清ALT、AST、TG水平,提高线粒体Na+-K+-ATPase,Ca2+-ATPase酶活性(P<0.05);且高剂量下各项指标优于其他组。结论嗜热链球菌grx02可改善酒精诱导急性肝损伤模型大鼠的肝功能,其可明显抑制酒精引发的肝细胞线粒体脂质过氧化反应,减轻自由基对线粒体的氧化损伤,并且它还可增强线粒体Na+-K+-ATPase、Ca2+-ATPase等ATP依赖酶的活性。     

鱼藤酮染毒大鼠纹状体某些生化指标的变化

目的观察鱼藤酮染毒对大鼠纹状体某些生化指标的影响。方法采用微量渗透泵背部埋植法观察不同剂量鱼藤酮对大鼠纹状体的影响,利用Fluoro-JadeB复合荧光尼氏染色观察染毒大鼠纹状体神经细胞的改变情况,高效液相色谱法(HPLC)检测纹状体ATP、ADP和AMP含量,采用生化实验分析Na+-K+-ATP酶和Ca2+-ATP酶的活性。结果染毒大鼠纹状体内出现大量的阳性变性神经细胞,而溶剂对照组未出现类似改变。与溶剂对照组比较,2.0和4.0mg/kg鱼藤酮组大鼠纹状体ATP含量出现显著性降低(P0.01),ADP和AMP含量则相对升高;Na+-K+-ATP酶与Ca2+-ATP酶的活性随染毒剂量的增大出现不同程度的抑制,差异具有统计学意义。结论鱼藤酮可导致纹状体ATP含量降低及Na+-K+-ATP酶与Ca2+-ATP酶活性被抑制。     

REGIONAL DISTRIBUTION OF ZINC, COPPER AND LEAD IN BRAIN: (Na+-K+)-ADENOSINE TRIPHOSPHATASE CORRELATES OF ETHANOL ADMINISTRATIONPERIPHERAL NEUROPATHY AND MYOPATHY IN CHRONIC ALCOHOLISM

Zinc, copper and lead are known as inhibitory trace metals againstbrain (Na⁺-K⁺)-ATPase. Alcohol (4 g/kg intraperitoneally for10 days, to rats) induced an elevated level of lead in the cerebralcortex and cerebellum, whereas that of zinc was elevated onlyin the latter region. Copper levels were found to be decreasedin the hippocampus, amygdala and hypothalamus, but increasedin the spinal cord. Zinc and lead contents were decreased inthe amygdala and hypothalamus. The activity of (Na⁺-K⁺)-ATPasewas enhanced in the hippocampus, amygdala and hypothalamus,but inhibited in the cerebral cortex and cerebellum. It is suggestedthat alcohol acts differentially on brain zinc, copper and leadconcentrations and (Na⁺-K⁺)-ATPase activity.     

右美沙芬和利鲁唑对甲基汞染毒大鼠神经毒性的影响

目的研究右美沙芬(dextromethorphan,DM)和利鲁唑(riluzole)对甲基汞染毒大鼠神经毒性的影响。方法将健康清洁级Wistar大鼠28只按体重随机分为对照组、氯化甲基汞组、右美沙芬+氯化甲基汞组、利鲁唑+氯化甲基汞组,每组7只。对照组和氯化甲基汞组皮下注射生理盐水溶液,右美沙芬+氯化甲基汞组和利鲁唑+氯化甲基汞组分别皮下注射13.5μmol/kg右美沙芬、21.35μmol/kg利鲁唑。注射2h后,对照组腹腔注射生理盐水,氯化甲基汞组、右美沙芬+氯化甲基汞组、利鲁唑+氯化甲基汞组腹腔注射氯化甲基汞溶液12.0μmol/kg,注射容量均为5ml/kg。连续进行4周,每周5天,每天染毒氯化甲基汞1次,每周一、三、五染毒右美沙芬、利鲁唑。测定大脑皮质中汞(Hg)、谷氨酰胺(Gln)、谷氨酸(Glu)含量以及小脑中琥珀酸脱氢酶(SDH)、Na+-K+-ATP酶、Ca2+-ATP酶活力。结果与对照组相比,氯化甲基汞组大脑皮质中Hg、Glu含量上升,Gln含量降低,小脑中SDH和Na+-K+-ATP酶、Ca2+-ATP酶活力降低,差异均有统计学意义(P0.05或P0.01)。与氯化甲基汞组相比,右美沙芬+氯化甲基汞组和利鲁唑+氯化甲基汞组大脑皮质Hg、Glu含量降低,Gln含量升高,SDH、Na+-K+-ATP酶和Ca2+-ATP酶活力升高,差异均有统计学意义(P0.05或P0.01)。结论甲基汞可扰乱谷氨酸-谷氨酰胺循环,右美沙芬和利鲁唑对甲基汞神经毒性具有一定的拮抗作用。     

类毒素-A对PC12细胞内ATP酶活力的影响

目的 研究类毒素-A（ANTX-A）对PC12细胞内ATP酶活力的影响.方法 用不同浓度（0、10^-9、10^-8、10^-7mol/L）ANTX-A刺激PC12细胞1 h,或10^-7mol/L ANTX-A刺激PC12细胞不同时间（0、30、60、90min）后,诱导PC12细胞激活;2相刺激方法（用ANTX-A 2次处理PC12细胞）诱导PC12细胞脱敏;用比色法测定这2种状态下胞内Na^＋-K^＋-ATP酶和Ca^2＋-ATP酶活力.结果 10^-9、10^-8、10^-7mol/L ANTX-A激活PC12细胞1 h和10-7 mol/L ANTX-A激活PC12细胞30、60、120 min时,胞内Na^＋-K^＋-ATP酶活力均有下降趋势,Ca^2＋-ATP酶活力在不同激活状态均比对照组显著降低（P＜0.05,P＜0.01）,有明显的剂量-反应关系和时间-效应关系.在2相脱敏试验中,当第1相ANTX-A浓度为10^-8、10^-7mol/L时,所对应脱敏状态胞内Na^＋-K^＋-ATP酶活力也均有减少趋势,Ca^2＋-ATP酶活力比相应激活状态明显降低（P＜0.01）.结论 Ca^2＋-ATP酶在ANTX-A激活和脱敏PC12细胞过程中可能有重要调节作用.     

铅对心肌酶、钠钾泵、钙镁泵活性以及肾素、血管紧张素Ⅱ活性影响探讨

本研究同时测定了铅作业组、非铅作业组两组对象红细胞钠-钾泵、钙-镁泵活性、血浆肾素活性、血管紧张素Ⅱ以及血清心肌酶CMB、CPK、LDH活性。结果发现两组间钠-钾汞、钙-镁泵活性以及血浆肾素活性、血管紧张素Ⅱ均无显著差异,但铅作业组CMB水平与血铅水平呈正相关,提示铅负荷增加情况下可能导致心肌细胞损伤。心肌细胞受损是铅作业工人心功能受损的可能机制之一。     

魔芋多糖对小鼠肠道吸收功能的抑制作用与机制

目的探讨魔芋多糖(konjac polysaccharide,KP)对小鼠肠道吸收功能的抑制作用与机制。方法将实验动物分为正常对照(N)、高脂(HF)和KP高、中、低剂量(KPH、KPM、KPL)共5个组,连续喂饲20d。紫外分光光度法测定小肠粘膜Na+-K+-ATP酶活性,血糖仪测定血糖并称量体重和粪便湿、干重等。结果HF组和KPH组的Na+-K+-ATP酶活性分别为16.2±1.48和11.2±1.10μmolPi/(mgpro·h),体重和餐后血糖分别为34.3±2.07g、7.5±1.15mmol/L和28.1±1.95g、4.8±0.73mmol/L。两组间各项指标的差别均有显著性意义(P<0.05)。结论KP降低小鼠餐后血糖和血清胆固醇水平,抑制体重增长、降低小肠粘膜Na+-K+-ATP酶活性,对肠道吸收功能有抑制作用。     

大豆硒蛋白对糖尿病大鼠心肌损伤的保护作用

目的探讨大豆硒蛋白对糖尿病大鼠心肌损伤的保护作用。方法 Wistar大鼠50只,,随机分为正常对照组(NC)、糖尿病对照组(DM)、低剂量Se治疗组(L-Se)、中剂量Se治疗组(M-Se)、高剂量Se治疗组(H-Se)。后4组腹腔注射链脲佐菌素55 mg/kg制备DM模型。第7w起,NC、DM组予0.5%CMC-Na 10ml/(kg.d),L-Se、M-Se、H-Se组分别予大豆硒蛋白2,4,8g/(kg.d)灌胃。第12w末处死大鼠,检测血糖、血清及心肌组织中SOD、GSH-Px、NOS活性和MDA、NO含量以及心肌组织中Na+-K+-ATPase、Ca2+-ATPase活性。结果与模型组比较,补充外源性大豆硒蛋白后,M-Se、H-Se组可明显降低糖尿病大鼠血糖及MDA含量(均P<0.001),显著增加血清GSH-Px、NOS活性(P<0.001),同时使心肌线粒GSH-Px活性、NO含量明显增加(均P<0.001),并且使心肌组织Na+-K+-ATPase、Ca2+-ATPase活性显著增加(P<0.01,P<0.001)。结论大豆硒蛋白对糖尿病大鼠心肌损伤具有保护作用。     

Effect of nutritional status and ozone exposure on some biomarkers of oxidative stress in rat brain regions

The aim of this study was to analyze the effect of nutritional condition and simulated exposure to ozone on Glutathione (GSH), the activity of Na+/K+ ATPase and lipid peroxidation in rat brain. Male Wistar rats were fed with 7% and 23% protein diets. Two groups were formed for each nutritional condition: one group was exposed for 15 successive days to 0.75 ppm of ozone and the other to air. Subsequently, the brain was dissected in cortex, hemispheres, cerebellum, and brainstem to measure the activity of thiobarbituric acid reactive substances (TBARS), ATPase, and levels of GSH. The activity of Na+/K+ ATPase increased in cerebellum of well-nourished rats exposed to ozone, while total ATPase and TBARS decreased in all studied areas in the malnourished groups. The levels of GSH decreased significantly (P < 0.05) in the brain of rats fed with 7% of protein diet and exposed to ozone but increased in rats fed with normal diet and exposed to ozone. These results suggest that malnutrition causes alterations in the values of Na+/K+ ATPase, total ATPase, GSH, and lipid peroxidation, while ozone contributes to these modifications. As a consequence, both variables are involved in oxidative stress in the rat brain.     

茶多酚对甲基汞致大鼠神经毒性影响

目的研究甲基汞致大鼠神经毒性的作用机制,探讨茶多酚对甲基汞致神经毒性作用的影响。方法36只Wistar大鼠随机分成3组,对照组,染汞组(12μmol/kg),茶多酚干预组(1 mmol/kg),连续干预染毒4周,最后1次染毒后24 h,将大鼠麻醉后处死,断头取脑,冰浴下分离大脑皮质,测定Na+-K+-ATP酶、Ca2+-ATP酶活力及细胞内Ca2+、活性氧簇(ROS)含量及细胞凋亡情况。结果与对照组比较,单纯染汞组Na+-K+-ATP酶[(2.72±0.46)μmol/(h.mg)]、Ca2+-ATP酶活力[(1.52±0.26)μmol/(h.mg)]明显降低(P<0.01),细胞内Ca2+含量(239.52±44.84)nmol/L、ROS含量(313.86±35.11)及细胞凋亡率[(40.84±6.26)%]明显升高(P<0.01);与染汞组比较,茶多酚干预组Na+-K+-ATP酶活力[(3.58±0.71)μmol/(h.mg)]、Ca2+-ATP酶活力[(1.98±0.29)μmol/(h.mg)]明显升高(P<0.05或P<0.01),细胞内Ca2+含量(188.39±7.43)nmol/L、ROS含量(238.03±22.99)及细胞凋亡率[(28.31±4.34)%]明显降低(P<0.05或P<0.01)。结论茶多酚对甲基汞致大鼠神经毒性有一定拮抗作用。     

Effect of norepinephrine on inhibition of mouse brain (Na+ + K+)-stimulated, (Mg++)-dependent, and (Ca++)-dependent ATPase activities by ethanol

Norepinephrine (0.1 mM) has been reported to "sensitize" (Na+ + K+)-ATPase activity of rat brain homogenates to inhibition by ethanol. The present study extends these investigations to the mouse and includes other ATPase activities. We measured the effects of norepinephrine on the sensitivity of ethanol-induced inhibition of (Na+ + K+)-stimulated (E.C. 3.6.1.3), (Mg++)-dependent (E.C. 3.6.1.4) and (Ca++)-dependent ATPase activities. Whole forebrains from C57BL/6J mice were homogenized and assayed in vitro for ATPase activity using standard conditions. Ethanol (0.125-2.0 M) caused a dose-dependent inhibition of all three ATPases. Norepinephrine (0.1 mM) had no appreciable effect on ethanol's inhibition of (Na+ + K+)-stimulated or (Ca++)-dependent ATPase activities, but slightly antagonized ethanol's effect on (Mg++)-ATPase. These results suggest that norepinephrine has little effect on the sensitivities of specific ATPases to ethanol inhibition in mouse brain.     

Erythrocyte lipid peroxidation and (Na+ + K+)-ATPase activity in cholesterol fed rabbits

Cholesterol, phospholipid and lipid peroxide levels in plasma and erythrocytes as well as membrane-bound (Na+ + K+)-ATPase activity were determined in rabbits fed a high-cholesterol diet for 3 months. While cholesterol feeding caused an increase in lipid peroxide levels, (Na+ + K+)-ATPase activity was found to be reduced. According to this, we can assume that, in high-cholesterol fed rabbits, elevated lipid peroxides may be one of the responsible factors for the decreased erythrocyte (Na+ + K+)-ATPase activity.