帕金森病血抗氧化系统变化及L-多巴的影响

目的　观察帕金森病 (PD)血抗氧化系统变化及 L-多巴的影响。方法　对 3 0例病程 1～ 5年的轻、中度PD采用化学比色法分别测定 L-多巴治疗前后外周静脉血一氧化氮 (NO)、一氧化氮合成酶 (NOS)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH-Px)和脂质过氧化物 (LPO)血浆活性 ,并与同时期 2 0例健康人对照。结果　与对照组比较 ,PD患者 NOS、SOD、GSH-Px降低 ,LPO增高 (P <0 .0 1 ) ;L-多巴治疗后 ,NO、NOS、SOD、GSH-Px进一步降低 ,LPO进一步增高 (P <0 .0 5 )。 结论　PD存在抗氧化酶活性降低 ,过氧化脂质代谢增强现象 ;L-多巴可加强这一异常变化。     

帕金森病血抗氧化系统的变化及临床意义

探讨帕金森病（ＰＤ）患者体内抗氧化系统水平及其在ＰＤ发病中的可能作用。方法观测了７０例ＰＤ患者和７０例正常人的血浆维生素Ｃ、Ｅ浓度（Ｐ－ＶＣ，Ｐ－ＶＥ），血浆及红细胞膜超氧化物歧化酶（Ｐ－ＳＯＤ，Ｅ－ＳＯＤ）活性，血浆及红细胞过氧化脂质（Ｐ－ＬＰＯ，Ｅ－ＬＰＯ）水平的变化。结果与正常对照组相比，ＰＤ患者的Ｐ－ＶＣ、Ｐ－ＶＥ浓度及Ｐ－ＳＯＤ、Ｅ－ＳＯＤ活性均明显降低，而Ｐ－ＬＰＯ、Ｅ－ＬＰＯ水平则显著增高。并且Ｐ－ＶＣ、Ｐ－ＶＥ、Ｅ－ＳＯＤ水平与ＰＤ患者的病情和病程呈负相关。结论提示ＰＤ患者可能存在血抗氧化系统缺陷而使内源性氧自由基堆积，导致黑质神经元退变     

帕金森病血抗氧化系统变化及其临床意义

为探讨帕金森病（PD）患者体内抗氧化系统水平及其在PD发病中的作用，对70例PD患者血浆维生素C（P－VC）、维生素E（P－VE）、血浆及红细胞超氧化物歧化酶（P－SOD，E－SOD）、血浆与红细胞过氧化脂质（P－LPO，E－LPO）的水平进行了检测并与正常对照组比较。结果表明：PD组P-VC、P-VE水平及P-SOD、E-SOD活性均比正常对照组显著降低，而P-LPO、E-LPO则显著增高，并且P-VC、P-VE、E-SOD与病情和病程呈负相关，提示抗氧化系统缺陷及内源性氧自由基堆积与PD发病有密切关系。     

帕金森病患者血液抗氧化功能的变化及多巴制剂与Vit E对其影响的研究

目的　探讨帕金森病 (PD)的抗氧化酶 (SOD)活性和过氧化脂质 (L PO)代谢水平的变化和多巴药物及 Vit E对其的影响 ,找出反映氧化异常的客观生化指标。方法　对 96例 PD患者动态检测了服用 L-多巴和 Vit E前后的血浆及红细胞膜超氧化物岐化酶 (P- SOD、E- SOD)和谷胱甘肽过氧化物酶 (GSH- Px)活性 ,血浆及红细胞过氧化脂质 (P- L PO、E- L PO)及丙二醛 (MDA)的变化 ,并与 2 0例正常人对照。结果　未服用药物患者的血抗氧化酶活性基本正常 ,加服 L-多巴后 P- SOD、GSH- Px降低 ,L PO和 MDA水平明显升高。已服用多巴药物的患者血 SOD活性降低 ,L PO水平显著升高 ,增加服用 Vit E后 L PO和 MDA水平均无改变。结论　提示 PD患者伴有抗氧化酶活性降低 ,过氧化脂质代谢增强 ,但病程早期并不显著 ,而多巴制剂、特别是 L-多巴可加速这一变化过程 ,Vit E对其无影响     

还原型谷胱甘肽治疗帕金森病的临床研究

目的探讨还原型谷胱甘肽(GSH)治疗帕金森病(PD)患者的临床疗效。方法 63例帕金森病患者随机分为2组,治疗组32例,对照组31例,均予抗PD药物治疗,其中治疗组加用0.9%氯化钠注射液100 mL+还原型谷胱甘肽1.2～2.4 g静滴,1次/d,共21 d。治疗前后分别采用PD统一评分量表(UPDRS)、Hoehn-Yahr分级量表进行临床评价,行血清谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)测定。结果与对照组比较,GSH组UPDRS评分、Hoehn-Yahr分级有显著改善(P0.05或0.01),GSH-Px、SOD值较治疗前明显升高(P0.01),而对照组改变不明显。结论 GSH治疗帕金森病疗效显著。     

诱导脑缺血耐受影响脑组织抗氧化活力

目的建立诱导脑缺血耐受的缺血预处理模型并研究其对脑组织超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-PX)活性的影响.方法动物分别给予假预处理(SHAM)、一侧颈内动脉注射生理盐水(SI)、双侧颈总动脉夹闭(BCAO)和双侧颈总动脉夹闭同时一侧颈内动脉注射生理盐水(BS),24h后腔内线栓法制作大脑中动脉阻断(MCAO)模型.观察MCAO后72h4组脑梗死体积,观察各组预处理24h和MCAO 24h、48h缺血侧脑组织SOD和GSH-PX活力.结果BS 组脑梗死体积明显低于其它3组(P<0.05),预处理后24h BS组缺血侧脑组织SOD和GSH-PX活力明显高于其它组(P<0.01);MCAO24h、48h 4组缺血侧脑组织SOD和GSH-PX活力均明显降低,BS组SOD和GSH-PX活力明显高于其它3组(P<0.01).结论双侧颈总动脉夹闭同时一侧颈内动脉注射生理盐水能诱导缺血耐受,该缺血预处理增高脑组织抗氧化活力,可能是缺血耐受产生的机制之一.     

PEP-1介导铜锌超氧化物歧化酶对帕金森病小鼠氧化应激损伤的保护作用

目的 观察PEP-1-铜、锌超氧化物歧化酶(PEP-1-SOD1)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)所致帕金森病小鼠行为学和氧化应激损伤的影响,探讨其可能的神经保护机制.方法 36只C57/BL小鼠随机分为正常组、模型组和PEP-1-SOD1组.模型组给MPTP腹腔注射,连续5 d;PEP-1-SOD1组连续腹腔注射MPTP 5 d前给予PEP-1-SOD1腹腔注射3 d.通过爬杆实验观察小鼠行为学变化.取小鼠纹状体通过黄嘌呤氧化酶法检测铜/锌超氧化物歧化酶(SOD1)和谷胱甘肽过氧化物酶(GSH-Px)活性,通过TBA法检测MDA含量.结果 模型组小鼠爬杆能力明显下降,PEP-1-SOD1组处理的小鼠行为学异常明显改善(P＜0.01).模型组小鼠纹状体SOD1和GSH-Px活性明显降低,MDA含量显著升高(P＜0.01).同模型组比较,PEP-1-SOD1组小鼠纹状体SOD1和GSH-Px活性显著增高,MDA含量明显减少(P＜0.01).结论 PEP-1-SOD1具有神经保护作用,其机制可能与减轻氧化应激损伤、增强抗自由基损伤能力有关.     

帕金森病患者氧化应激与运动功能的相关性研究

目的探讨帕金森病(PD)患者氧化应激与运动功能的相关性。方法对PD患者运用HoehnYahr(H-Y)分级和帕金森病联合评分标准(UPDRS)-Ⅲ的运动功能评分量表进行运动功能评分,同时检测患者血浆中超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、丙二醛(MDA)的水平,并与健康对照组比较。结果与对照组相比,PD组患者SOD、GSH水平明显降低,MDA水平升高,差异均有统计学意义(P<0.01、0.05)。PD患者SOD及GSH的水平随着H-Y分级的增高而下降,与UPDRS-Ⅲ运动评分负相关;MDA水平随着H-Y分级的升高而升高,与UPDRS-Ⅲ运动评分正相关。结论 PD患者氧化代谢产物的增加与运动功能障碍呈正相关。     

急性脑梗死患者血液微量元素和抗氧化酶变化的研究

目的　了解急性脑梗死（ Ａ Ｃ Ｉ） 患者血浆和红细胞中微量元素以及抗氧化酶 Ｓ Ｏ Ｄ,谷胱苷肽过氧化物酶（ Ｇ Ｓ Ｈ Ｐ Ｘ） 变化的临床意义。方法　对４５ 例急性脑梗死患者进行配对研究。结果　 Ａ Ｃ Ｉ 组血浆锌、硒及红细胞硒明显减低;而血浆及红细胞铜、锰含量明显增高（ Ｐ＜ ００１） ;血液的 Ｓ Ｏ Ｄ, Ｇ Ｓ Ｈ Ｐ Ｘ 活性也明显低于对照组;红细胞及血浆铜、锰;红细胞硒与 Ｇ Ｓ Ｈ Ｐ Ｘ 均呈明显正相关; Ｂａｙｅｓ 逐步回归判别表明血液 Ｇ Ｓ Ｈ Ｐ Ｘ, Ｓ Ｏ Ｄ,红细胞硒与 Ａ Ｃ Ｉ 病情变化关系最密切。结论　本研究结果提示血液中锌的降低和铜含量的增高可能与应激反应有关;硒的改变与动脉粥样硬化及 Ａ Ｃ Ｉ 的发生、发展密切相关。     

原花青素在D-半乳糖致衰老大鼠大脑、心脏组织中的抗氧化作用

目的 探讨原花青素(PC)在D-半乳糖致衰老大鼠大脑、心脏组织中的抗氧化作用.方法 取健康6月龄Wistar大鼠50只,雌雄各半,分性别随机均分为正常对照组、衰老模型组、维生素E(VE)组、PC 120 mg/kg和60 mg/kg 2个剂量组等5组(各10只),分别给予相应的处理.测定各组大鼠大脑、心脏组织中的超氧化...     

Polymorphonuclear leukocyte nitrite content and antioxidant enzymes in Parkinson's disease patients

OBJECTIVE: The present study was undertaken to evaluate the alteration in the peripheral neuronal nitric oxide synthase (NOS) activity in Parkinson's disease patients. Therefore, basal nitrite content in PMNs, platelets and in the plasma of PD and control Indian population were evaluated. MATERIALS AND METHODS: We estimated nitrite, the nitric oxide (NO) metabolite, in neutrophils (PMNs), platelets and in plasma of control and in L-dopa treated Parkinson's disease (PD) patients. We also measured the activity of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the PMNs. RESULTS: We observed a significant increase in the basal nitrite content in PMNs of PD patients without any alteration in the plasma and platelets. Thus, the change was specific to PMNs. Catalase activity was significantly less in the PMNs of PD patients, but SOD and GPx remained unaltered. CONCLUSION: Results obtained in the PD patients exhibit an increase in the NOS activity in PMNs. Thus, involvement of NO is suggested in PD.     

抗氧化酶类对大鼠感染性脑损伤的内源性防护作用

目的 通过测定脑组织丙二醛（ＭＤＡ）、超氧化物歧化酶（ＣｕＺｎ－ＳＯＤ和Ｍｎ－ＳＯＤ）、过氧化氢酶（ＣＡＴ）及谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）活性的变化,探讨抗氧化酶类在大鼠感染性脑损伤内生防护机制听作用。方法 向大鼠左颈内动脉注射百日咳菌悬浮液,诱发感染性脑损伤模型。４０只大鼠随机分为生理盐水对照组（ＮＳ）和右日咳杆菌悬浮液组（ＢＰＳ）,观察时间为４ｈ和２４ｈ。用可见光和紫外分光光度法分别测定     

Serum S100B and antioxidant enzymes in bipolar patients

Bipolar disorder (BD) is a chronic, severe, and highly disabling psychiatric disorder; peripheral markers have been used to assess biochemical alterations associated with BD and/or possibly involved in its pathophysiology. Beyond neuronal commitment, many groups have proposed the involvement of glial activity in psychiatric disorders. Other biochemical markers, particularly associated with oxidative stress, have been studied in BD. In the present study, we evaluated glial involvement and oxidative stress in patients with BD. Glial activity was assessed by measuring serum S100B content; oxidative stress was assessed using serum thiobarbituric acid reactive substances (TBARS) and activities of antioxidant enzymes in BD patients during different episodes of disease. We found a significant increment of serum S100B during episodes of mania and depression, but not in euthymic patients. Superoxide dismutase (SOD) activity, as well the SOD/glutathione peroxidase plus catalase ratio, was also increased in manic and depressed patients. On the other hand, TBARS levels were increased in BD patients regardless of the phase of the disorder. These findings suggest a potential oxidative damage in BD patients. This peripheral oxidative imbalance indicates that systemic changes are taking place during the active phases of the illness. Such changes appear to relate to astrocyte function, as indicated by serum S100B elevation.     

神经症患者超氧化物歧化酶、谷胱甘肽超氧化物酶及脂质超氧化物含量的变化

为研究氧自由基与神经症之间的关系，分别采用邻苯三酚自氧化法、二硫对硝基苯甲酸直接法、硫代巴比妥酸比色法，测定了８７例神经症和５５名健康人超氧化物歧化酶（ＳＯＤ）、谷胱甘肽超氧化物酶（ＧＳＨ－Ｐｘ）和脂质超氧化物（ＬＰＯ）含量。结果显示，神经症组ＳＯＤ与ＧＳＨ－Ｐｘ两种酶含量均低于对照组，神经症组治疗前低于治疗后；ＬＰＯ为治疗前高于治疗后，差异均有显著性。从单胺类的代谢与生成氧自由基的生化联系以及机体内ＳＯＤ、ＧＳＨ－Ｐｘ、ＬＰＯ之间的相互关系上对结果进行了分析，提示体内单胺类物质代谢过程中产生的氧自由基在神经症的病理过程中可能发挥一定的作用。     

Peripheral blood cell activities of monoamine oxidase B and superoxide dismutase in Parkinson's disease

Summary Monoamine oxidase type B (MAO-B) and superoxide dismutase (SOD) are two enzyme stystems that are potentially relevant to an oxidative stress model of Parkinson's disease (PD) causation. Activities of MAO-B in platelets (nmol/10⁸ cells/hr) and total SOD in lymphocytes (U/mg protein) were assayed among 28 cases of idiopathic PD and 22 controls. As anticipated, MAO-B was lowest in PD cases on selegiline (L-deprenyl) therapy (mean 1.10). There was a slight deficit of MAO-B among male cases not taking selegiline compared to controls (3.78 vs. 4.15), but the opposite trend was observed for females (6.18 vs. 4.16). SOD was slightly higher in cases (7.40), than controls (6.81). Excess SOD among PD cases was seen irrespective of gender, age, or selegiline treatment, although none of the differences was statistically significant Future research on SOD should take advantage of the availability of assays specific for the cytosolic and mitochondrial forms of the enzyme.     

自由基代谢与精神分裂症临床症状和药物治疗的关系

目的：探讨自由基代谢与精神分裂症临床症状和药物治疗的关系。方法：是否治疗的慢性精神分裂症患者各４０例分别评定定阳性和阴性症状量表（ＰＡＮＳＳ）,并测定膜脂质过氧化物丙二醛（ＭＤＡ）含量、铜／锌超氧化物歧化酶（Ｇｕ－ＺｎＳＯＤ）和谷胱苷肽过氧化物酶（ＧＳＨ－Ｐｘ）活性。结果：与健康对照组相比,未治疗组患者ＭＤＡ含量和ＧＳＨ－Ｐｘ活性显著增加,治疗组患者无显著改变;而两组患者ＳＯＤ活性显著降低;未治疗     

Parkinson's disease is associated with oxidative stress: comparison of peripheral antioxidant profiles in living Parkinson's, Alzheimer's and vascular dementia patients

Summary. Antioxidant profiles in Parkinson's disease (PD; n = 15), dementias of Alzheimer's type (DAT; 18) and Vascular (VD; 15), and control subjects (C; 14) were studied. Cu-Zn superoxide dismutase (SOD), catalase (CAT), glutathione system (GLU) and thiobarbituric acid reactive substances (TBARS) were measured in erythrocytes; antioxidant capacity (TRAP) in plasma. Biochemical variables were analyzed simultaneously using multivariate and non-parametric methods. Clinical diagnostic resulted associated with the main source of variability in antioxidant variables (Kruskal-Wallis: H = 32.58, p = 0.000001). Comparison of PD and C resulted highly significant (z = 4.47, p = 0.000047), demonstrating an association between oxidative stress and PD. SOD and TBARS were significantly higher in pathological groups against C (p = 0.0000001, p = 0.051); TRAP resulted lower (p = 0.00015). Discriminant functions constructed using biochemical variables separated pathological groups (93% success) from C, and DAT (88.9%) from VD (73.3%); but not PD from DAT or VD. Antioxidant profiles of PD patients showed characteristics overlapping with DAT (60%) and with VD (40%), suggesting biochemical similarities between them. Received October 5, 2000; accepted June 1, 2001     

Platelet monoamine oxidase-B activity in Parkinson's disease

Summary Platelet MAO-B levels have been investigated in seventeen consecutively diagnosed and previously untreated patients with idiopathic Parkinson's disease using the non-hydroxylated catecholamine, -phenylethylamine, as substrate. Patients with Parkinson's disease had MAO-B activity levels that were considerably higher than sex and age matched normal controls or patients with Motor neurone disease or Myasthenia gravis.