慢性肾功能衰竭患者脂质过氧化物,超氧化物歧化酶的变化及其临？…

研究慢性肾功能衰竭患者氧自由基损伤情况,方法测定８０例ＣＲＦ患者和３０例正常人血清ＬＰＯ含量,总ＳＯＤ、ＣｕＺｎ－ＳＯＤ、Ｍｎ－ＳＯＤ活性水平。结果ＣＲＦ患者血清ＬＰＯ含量,总ＳＯＤ、ＣｕＺｎ－ＳＯＤ、Ｍｎ－ＳＯＤ活性均较正常人明显增高,     

慢性肾功能衰竭患者脂质过氧化物、超氧化物歧化酶的变化及其临床意义的探讨

目的研究慢性肾功能衰竭（ＣＲＦ）患者氧自由基损伤情况。方法测定８０例ＣＲＦ患者和３０例正常人血清ＬＰＯ含量、总ＳＯＤ、ＣｕＺｎ—ＳＯＤ、Ｍｎ—ＳＯＤ活性水平。结果ＣＲＦ患者血清ＬＰＯ含量、总ＳＯＤ、ＣｕＺｎ—ＳＯＤ、Ｍｎ—ＳＯＤ活性均较正常人明显增高（Ｐ＜００５～００１）,且总ＳＯＤ、ＣｕＺｎ—ＳＯＤ、Ｍｎ—ＳＯＤ活性与Ｓｃｒ呈显著正相关,与ＧＦＲ呈显著负相关。结论①ＣＲＦ患者存在氧自由基的蓄积,脂质过氧化反应病理亢进和超氧化物歧化酶代偿性增高的病理改变;②血ＳＯＤ活性可作为反映肾功能损害的可靠指标。     

肺表面活性物质功能不良的机制探讨

对蛋白是否抑制肺表面活性物质（ＳＡＭ）活性，进行了大白鼠体内外实验。体外实验，测定了不同浓度的血浆蛋白和ＳＡＭ混和液标本的最小表面张力（ＳＴｍｉｎ）和最大表面张力（ＳＴｍａｘ）；体内实验，将大白鼠随机分为血浆组、生理盐水组和对照组，分别向前两组动物肺内注入血浆或生理盐水。结果发现，体外实验随蛋白浓度的增高，ＳＴｍｉｎ和ＳＴｍａｘ也增高，呈现浓度依赖关系；体内实验血浆组和盐水组大鼠空气机械通气３０分钟后ＰＯ２和顺应性明显低于对照组，继续纯氧通气１０分钟，两组动物ＰＯ２仍明显低于对照组，而血浆组ＰＯ２又明显低于盐水组。作者认为，盐水组ＰＯ２下降主要与生理盐水稀释ＳＡＭ有关，血浆组ＰＯ２下降主要是血浆蛋白抑制了ＳＡＭ活性，使其功能不良     

重型颅脑伤患者红细胞免疫功能与脂质过氧化物,超氧化…

探讨颅脑伤患者红细胞免疫功能改变与超氧化物歧化酶，过氧化脂质的关系。检测３０例重型颅脑伤患者红细胞免疫功能及ＳＯＤ，血清ＬＰＯ变化。结果；红细胞Ｃ３ｂ受体花环率及红细胞免疫粘附促进率均明显降低，红细胞免疫复合物花环率及红细胞免疫抑制率则明显 高；红细胞ＳＯＤ活性明显降低，血清中ＬＰＯ则明显升高。     

80例慢性肾功能衰竭患者脂质过氧化物超氧化物歧化酶的变化

目的：研究肾功能衰竭患者氧自由基对肾的损伤作用。方法：测定８０例ＣＲＦ患者和３０例正常人血清脂质过氧化物含量,超氧化物歧化酶的活性水平。结果;ＣＲＦ患者血清ＬＰＯ含量,总ＳＯＤ,铜锌超氧化歧化酶,锰超氧化歧酶活性均较正常人明显增高,且总ＳＯＤ,ＣｕＺｎ－ＳＯＤ,Ｍｎ－ＳＯＤ活性与血清肌酐呈显著正相关,与肾小球滤过率呈显著负相关。     

旋磁场对脑缺血再灌注损伤大鼠血液流变学的影响

目的对脑缺血再灌注损伤大鼠应用旋磁场后,观察超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）、前列环素（ＰＧＩ２）、血栓素（ＴＸＡ２）及血液流变学指标的变化。方法 实验运行分３组,每组１２只,对照组做假手术,再灌组,旋磁组双侧颈总动脉夹闭３０ｍｉｎ,再灌注３０ｍｉｎ（旋磁组大鼠夹闭颈总动脉后置于旋磁场内,鼠体中心部分距磁极为６ｃｍ,磁感应强度为３０ｍＴ）,腹主动脉取血进行观察。结果 旋磁组ＳＯＤ海拔 力     

抗氧化剂治疗大鼠肾病模型的初步探讨

目的：探讨抗氧化剂对大鼠肾模型治疗作用。方法：给大鼠１次性静脉注射阿霉素（ＡＤＲ）制作肾病模型。选用抗氧化剂维生素Ｅ（ＶＥ）为治疗因素，测定血清中脂质过氧化物（ＬＰＯ），红细胞超氧化物歧化酶（ＳＯＤ）水平及相关血尿生化指标。结果：模型物组动物实验第１４天出现典型肾病综合征表现，血清中ＬＰＯ水平明显升高、红细胞ＳＯＤ活性明显降低。ＶＥ治疗组动尿、血生化指标及病理改变明显改善，且血清ＬＰＯ水平明显降低，红细胞ＳＯＤ活性明显高于ＡＤＲ组动物。结论：氧自由基，脂质过氧化损伤与ＡＤＲ肾病发生密切相关，ＶＥ能通过清除自由基、阻断脂质过氧化物对ＡＤＲ肾病起一定治疗作用     

肺癌病人手术前后血清超氧化物歧化酶的动态研究

本实验用邻苯酚法，对４６例肺癌，２５例良性胸部疾患病人进行手术前后血清ＳＯＤ活性的动态检测，并以１０５例健康人作对照。结果显示，肺癌病人术前ＳＯＤ活性明显低于良性胸部疾患病人和正常人，其降低的程度与肺癌的病期、原发肿瘤大小、淋巴结转移和组织学类型有密切关系。肺癌行根治术后，血清ＳＯＤ活性逐渐升高，术后２周可达正常水平。     

肺癌病人手术前后血清超氧化物歧化酶的动态研究

本实验用邻苯酚法，对４６例肺癌，２５例良性胸部疾患病人进行手术前后血清ＳＯＤ活性的动态检测，并以１０５例健康人作对照。结果显示，肺癌病人术前ＳＯＤ活性明显低于良性陪疾患病人和正常人，其降低的程序与肺癌的病期，原发肿瘤大小，淋巴结转移和组织学类型有。根治术后，血清ＳＯＤ活性逐渐升高，术后２周可达正常水平。     

旋磁场并高压氧对脑卒中患者自由基代谢的影响

旋磁场并高压氧对脑卒中患者自由基代谢影响的研究结果表明，采用０．１ＭＰａ高压氧，每日１次，４０分钟，连续治疗１０次为１疗程，高压氧升高血浆过氧化脂质（ＬＰＯ）含量和抑制红细胞超氧化物歧化酶（ＳＯＤ）活性的作用不明显（Ｐ〉０．０５），但能明显降低红细胞谷胱甘肽（ＧＳＨ）含量和谷胱甘肽过氧化物酶（ＧＳＨｐｘ）的活性（Ｐ〈０．０５）。旋磁场，磁片两块异名极并置，磁感应强度为０．２５Ｔ，旋转（２５００ｒ／     

旋磁场对大鼠实验性缺血心肌保护作用的机制研究

目的　观察旋磁场对垂体后叶素致心肌缺血的保护作用并探讨其机制。方法　大鼠 3 0只 ,采用静脉注射垂体后叶素 (2U/kg体重 )造成急性心肌缺血动物模型 ,经旋磁场作用后 ,观察心电图ST段升高幅度、T波振幅 ;血清一氧化氮 (NO)含量 ;血清和心肌超氧化物歧化酶 (SOD)活力和脂质过氧化物丙二醛(MDA)含量的变化。结果　 40mT旋磁场作用 3 0min ,能减轻垂体后叶素引起的大鼠心肌缺血时血清及心肌SOD的活力降低 (0 .1>P >0 .0 5,P <0 .0 1) ;抑制MDA的生成 (P <0 .0 5) ;增加血清NO含量 ,且在 3 0min时更明显 (P <0 .0 1) ;心电图中ST段升高幅度、T波振幅均较缺血组显著降低 (P <0 .0 5)。结论　在适当场强作用下 ,旋磁场通过增加血清和心肌SOD活力、降低MDA含量 ,增加血清NO含量对大鼠实验性缺血心肌发挥保护作用     

迷迭香酸对系膜增生性肾炎系膜细胞抗氧化应激的影响

目的探讨在系膜增生性肾小球肾炎(M sPGN)中系膜细胞氧化损伤与抗氧化系统的改变及迷迭香酸的干预作用。方法培养大鼠肾小球系膜细胞,以PDGF刺激系膜增生及RAD干预;另外,用兔抗大鼠胸腺细胞免疫血清(ATS),制备大鼠抗THy1.1系膜增生性肾小球肾炎模型,并以迷迭香酸干预。体外及体内实验均设正常对照组、肾炎组、单纯迷迭香酸组和迷迭香酸干预组。利用分光法分别测定培养细胞和肾脏组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性。结果在抗THy1.1肾炎的肾脏组织及PDGF刺激肾小球系膜细胞中MDA含量升高和SOD减少;迷迭香酸的干预后MDA的产生降低,而SOD增加。结论氧自由基及其诱发的脂质过氧化在系膜增生性肾小球肾炎的致病中起重要作用,而迷迭香酸则能抑制肾炎系膜细胞的上述改变,具有抗氧化活性。     

Lecithinization of superoxide dismutase potentiates its protective effect against Forssman antiserum-induced elevation in guinea pig airway resistance.

We synthesized lecithinized superoxide dismutase (PC-SOD), in which a lecithin derivative was covalently bound to recombinant human SOD. We selected PC4-SOD (4 molecules of the lecithin derivative bound to each SOD dimer) and PC10-SOD (10 molecules of the derivative to each SOD dimer) for our study. Both of these PC-SOD retained SOD activity in vitro and showed delayed plasma disappearance in vivo in rats. PC-SOD also had 4 to 20 times higher affinity in vitro for several kinds of cells than that of unmodified SOD. Because Forssman antiserum is known to induce bronchial obstruction in guinea pigs via actions of O2-, we studied the effect of PC-SOD on Forssman antiserum-induced respiratory resistance. Unmodified SOD was ineffective at the doses of 1,000 to 30,000 U/kg, whereas PC-SOD showed a dose-dependent inhibitory effect over the range of 10 to 1,000 U/kg. The ED50 of PC4-SOD and PC10-SOD were 140 and 240 U/kg, respectively, at 30 min after the challenge with Forssman antiserum. These findings suggest that the pharmacological potency of PC-SOD is over 200 times more than that of unmodified SOD, and that PC-SOD may have the potential for various clinical applications.     

啤酒对血清酶活性影响的体内外实验

目的:观察体内外实验中受试者饮用啤酒后各种血清酶活性的变化情况。设计:观察对比实验。单位:泰山医学院基础医学研究所。对象:实验于2005-03/04在泰山医学院基础医学研究所完成。选择泰山医学院学生17名,年龄19～35岁,包括本科生和研究生,实验前均签署同意书。方法:①体内实验:受试者统一正常饮食后3h采静脉血3mL,作为对照。然后立即口服啤酒4mL/kg,分别于15,30,45,60,90,120,180min后各采血3mL,测定血液中丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶、碱性磷酸酶、肌酸激酶、乳酸脱氢酶、淀粉酶、脂肪酶活性的变化。②体外实验:选取17份新鲜受试者血清,分别加入两个试管中,每管0.5mL。对照管加入20μL生理盐水;测定管中加入20μL啤酒溶液,观察啤酒对以上各种酶活性的直接影响。主要观察指标:体内外实验中血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶、碱性磷酸酶、肌酸激酶、乳酸脱氢酶、淀粉酶及脂肪酶的活性。结果:纳入17名学生,全部进入结果分析,无脱落。①体内实验:啤酒可显著降低血清天冬氨酸氨基转移酶活性(418.08±58.68,383.41±63.01)nkat/L,显著升高血清碱性磷酸酶活性(3678.57±436.25,3962.96±400.91)nkat/L(χ2=19.00～20.00,P<0.01),其余酶活性均有不同程度的升高。②体外实验:啤酒在体外对各种酶活性均有一定程度的抑制作用。结论:啤酒在体内外对酶活性均有一定影响,从而影响机体代谢,过量饮用会影响健康。在常规血清酶学检测中,应避免患者饮用啤酒所造成的干扰,以确保实验结果的准确可靠。     

蝙蝠葛酚性碱对家兔心脑缺血-再灌注损伤保护作用的研究

目的　探讨蝙蝠葛酚性碱 (PAMd)抗心、脑同时缺血再灌注损伤的机制。方法　采用结扎家兔左冠状动脉前降支及双侧颈总动脉 30 m in后再灌注造成心、脑缺血再灌注模型 ,观察 PAMd对缺血前后及再灌注后不同时间血清、左心室、海马、皮质及小脑中丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活性的影响。结果　家兔心、脑缺血再灌注 10 min后血清 MDA含量显著升高 ,SOD活性显著降低 (P均 <0 .0 5 )。PAMd3.5 mg/ kg显著降低心、脑缺血再灌注后血清及组织 MDA含量 ,升高 SOD活性 (P均 <0 .0 5 )。结论PAMd通过减轻脂质过氧化所造成的损伤 ,提高 SOD活性 ,对心、脑缺血再灌注损伤具有一定保护作用。     

50 Hz电磁场对小鼠骨髓间充质干细胞增殖的影响

目的　探讨小鼠骨髓间充质干细胞经脉冲电磁场辐射不同时间后其细胞增殖水平的变化。方法　用密度梯度离心法分离小鼠骨髓间充质干细胞 ,再经贴壁筛选法筛选 ,对生长良好的第 3代小鼠骨髓间充质干细胞进行不同时间的脉冲电磁场辐射 (频率 50Hz、正弦波形、不同强度 ) ,用MTT法、流式细胞仪法测定细胞生长增殖水平及细胞周期变化。结果　小鼠骨髓间充质干细胞经脉冲电磁场辐射 3d(每天 2次 ,每次 3 0min)后 ,各实验组细胞增殖水平均有明显提高 ,差异有显著性意义 (P <0 .0 5)。采用流式细胞仪测定细胞周期 ,发现各实验组 (S G2 /M )期细胞数量较对照组均有不同程度的增长 ,差异有显著性意义 (P <0 .0 5)。各组均未发现DNA倍体异常细胞。结论　小鼠骨髓间充质干细胞经频率为 50Hz、正弦波形、强度分别为 4mT ,3mT ,2mT ,1mT的脉冲电磁场辐射 3d(每天 2次 ,每次 3 0min ,间隔 12h)后 ,能明显促进该细胞体外培养的增殖水平     

In vitro and in vivo effects of dapsone on neutrophil and lymphocyte functions in normal individuals and patients with lepromatous leprosy

The effects of dapsone on polymorphonuclear leukocyte functions and lymphocyte mitogen-induced transformation were assessed in vitro and in vivo in normal individuals and in newly diagnosed untreated patients with lepromatous leprosy. The effects of dapsone on the cell-free generation of superoxide by the xanthine: xanthine oxidase system and iodination of bovine serum albumin by horseradish peroxidase were also investigated. In normal individuals dapsone mediated stimulation of polymorphonuclear leukocyte migration in vitro and vivo. Dapsone had no effect on postphagocytic hexose monophosphate shunt activity in vivo. Similar effects were found in patients with lepromatous leprosy. Dapsone also decreased the inhibitory activity of serum from patients with lepromatous leprosy on normal polymorphonuclear leukocyte migration in vitro. Progressive loss of serum-mediated inhibition of migration was observed after ingestion of dapsone by the patients. Further experiments showed that stimulation of polymorphonuclear leukocyte motility was related to inhibition of lymphocyte transformation at high concentrations in vitro, but had slight stimulatory activity on phytohemagglutinin-induced transformation in controls and patients in vivo.     

New quinoline di-Mannich base compounds with greater antimalarial activity than chloroquine, amodiaquine, or pyronaridine.

We have compared the ex vivo antimalarial activity of 12 new quinoline di-Mannich base compounds containing the 7-dichloroquinoline or 7-trifluoromethylquinoline nucleus with amodiaquine, chloroquine, and pyronaridine using the Saimiri-bioassay model. Each compound was administered orally (30 mg/kg of body weight) to three or more noninfected Saimiri sciureus monkeys, and serum samples were collected at various times after drug administration and serially diluted with drug-free (control) serum. In vitro activity against the multidrug-resistant K1 isolate of Plasmodium falciparum was determined in serum samples by measuring the maximum inhibitory dilution at which the treated monkey serum inhibited schizont maturation in vitro. Of the 12 Mannich bases tested, 8 were associated with levels of ex vivo antimalarial activity in serum greater than those of amodiaquine, chloroquine, or pyronaridine 1 to 7 days after drug administration. Further studies were carried out with four of these compounds, and the results showed that the areas under the serum drug concentration-time curves for the four compounds were between 7- and 26-fold greater than that obtained for pyronaridine. Activity against four multidrug-resistant strains of P. falciparum was also much greater in serum samples collected from monkeys after administration of these four compounds than in serum samples collected after administration of pyronaridine or chloroquine. These findings suggest that these four quinoline Mannich base compounds possess a very marked and prolonged antimalarial activity and that further studies should be performed to determine their value as antimalarial drugs.     

Protective Role of Superoxide Dismutase against Diabetogenic Drugs

Copper-zinc superoxide dismutase (SOD) is present in relatively high concentrations in the beta-cells of human islets. The activity of the extracted enzyme is partially inhibited upon incubation with the diabetogenic drugs alloxan, streptozotocin, or Vacor. The role of this enzyme in protecting beta-cells against chemically induced diabetes was further investigated.Incubation of intact canine islets with alloxan (0.2 mg/ml) and 4 mM glucose decreased the insulin secretory response by 87% during subsequent exposure to 28 mM glucose. Concomitantly the SOD-specific activity (units of enzyme activity per milligram immunoreactive SOD) decreased 50% in alloxan-exposed islets. When islets were protected from alloxan toxicity by including 28 mM glucose with alloxan, the insulin secretory response and SOD specific activity remained identical to controls. Thus, SOD specific activity correlates with maintenance of beta-cell function.To test the effectiveness of SOD against streptozotocin in vitro, canine islets were incubated 10 min with or without streptozotocin (0.1 mg/ml) with 4 mM glucose; their functional integrity was tested subsequently as the insulin secretory response to 28 mM glucose. Exposure to streptozotocin alone decreased the response by 70%; inclusion of SOD (1.5 mg/ml) before and during exposure to streptozotocin completely prevented this effect. Cyanide-inactivated SOD was not effective.The potential of SOD to prevent streptozotocin-induced diabetes was tested in rats in vivo. SOD injected 10 s or 50 min before streptozotocin prevented or significantly attenuated diabetes. Injection of SOD and streptozotocin simultaneously was much less effective, and cyanide-inactivated SOD was ineffective. No protection was afforded by injection of SOD 12 or 24 h before streptozotocin.Our results support hypotheses that (a) oxygen radicals mediate the beta-cell toxicity of both alloxan and streptozotocin, and (b) beta-cells may be particularly vulnerable to oxygen radical damage.