帕金森病患者血液抗氧化功能的变化及多巴制剂与VitE对 …

目的 探讨帕金森病（ＰＤ）的抗氧化酶（ＳＯＤ）活性和过氧化脂质（ＬＰＯ）代谢水平的变化和多巴药物及ＶｉＴ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ＶｔＥ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－ＬＰＯ、Ｅ－ＬＰＯ）及丙二醛（ＭＤＡ）的变化，并与２０例正常３人对照。     

氧化、脂质过氧化与脑梗死关系的探讨

目的:探讨一氧化氮、氧化、脂质过氧化与脑梗死的关系。方法:检测了１４６例急性脑梗死患者(ＣＩ)和１００例健康志愿者(ＨＶ)血浆中的一氧化氮(Ｐ－ＮＯ)、维生素Ｃ(Ｐ－ＶＣ)、维生素Ｅ(Ｐ－ＶＥ)、β－胡萝卜素(Ｐ－β－ＣＡＲ)和过氧化脂质(Ｐ－ＬＰＯ)含量及红细胞中的超氧化物歧化酶(Ｅ－ＳＯＤ)、过氧化氢酶(Ｅ－ＣＡＴ)、谷胱甘肽过氧化物酶(Ｅ－ＧＳＨ－Ｐｘ)活性和过氧化脂质(Ｅ－ＬＰＯ)含量并作分析比较;同时,检测了其中４４例患者治疗前后的上述生化指标,并作分析比较。结果:与ＨＶ组比较,ＣＩ组的Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ平均值均显著升高(Ｐ＜０．００１),Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ平均值均显著降低(Ｐ＜０．００１);与治疗前比较,治疗后的Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ平均值均显著降低(Ｐ＜０．００１),Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ平均值均显著升高(Ｐ＜０．００１)。结论:脑梗死患者体内ＮＯ代谢异常,一系列自由基连锁反应病理性加剧,氧化抗氧化平衡严重失调,ＮＯ、氧化和脂质过氧化损伤加剧。     

帕金森病血抗氧化酶活性的研究

本文报道６７例帕金森病（ＰＤ）患者血超氧化物歧化酶（ＳＯＤ）．谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ），过氧化氢酶（ＣＡＴ）活性及脂质过氧化物（ＬＰＯ）量的测定结果。ＰＤ病人ＳＯＤ和ＧＳＨ－Ｐｘ活性高于正常对照组，但ＳＯＤ，ＧＳＨ－Ｐｘ和ＣＡＴ的活性及ＬＰＯ量与病程长短无明显关系，也与是否服用美多巴无关。研究结果提示，抗氧化酶活性的改变可能与ＰＤ病因有关。     

血管性痴呆和脑梗塞患者载脂蛋白E基因多态性的分析比较

目的探讨ＡＰＯＥ多态性与血管性痴呆（ＶＤ）和脑梗塞（ＣＩ）的关系。方法应用ＰＣＲ－ＲＦＬＰ技术分析２０例ＶＤ、２４例ＣＩ及２４例健康老年人的ＡＰＯＥ基因型。结果ＶＤ和ＣＩ患者ε３频率均降低（Ｐ＜０．０５），ε４频率均升高（Ｐ＜０．０５），而两组患者间各等位基因频率差异均无统计学意义（Ｐ＞０．０５）；且ε４与血清ＡＰＯＥ、ＡＰＯＢ、ＴＣ、ＬＤＬ－Ｃ正相关，与ＡＰＯＡ、ＨＤＬ－Ｃ负相关。结论ＡＰＯＥ多态性与ＶＤ和ＣＩ的发病机制有关，其在这两种疾病中的作用可能相似。     

实验性迟发性脑血管痉挛时痉挛动脉的自由基代谢

为探讨蛛网膜下腔出血（ＳＡＨ）后迟发性脑血管痉挛（ＤＣＶＳ）时痉挛动脉的自由基代谢变化。通过了对ＤＣＶＳ时痉挛动脉的自由基含量、自由基清除酶超氧化物岐化酶（Ｃｕ－ＺｎＳＯＤ）与过氧化氢酶（Ｃａｔ）活性以及自由基代谢产物脂质过氧化物（ＬＰＯ）含量的测定。结果显示：（１）痉挛动脉的自由基含量比对照组明显升高（Ｐ＜０．０１）；（２）Ｃｕ－ＺｎＳＯＤ活性明显降低（Ｐ＜０．０５），Ｃａｔ活性明显升高（Ｐ＜０．０１）；（３）ＬＰＯ含量明显升高（Ｐ＜０．０１）。本实验结果证实ＳＡＨ后ＤＣＶＳ时痉挛动脉存在自由基的代谢紊乱，自由基介导的病理作用可能在ＤＣＶＳ发病机理中起重要作用。     

脑血管病患者SOD、MDA检测意义及其相关性研究

检测８７例脑血管病（ＣＶＤ）患者血清超氧化物歧化酶（ＳＯＤ）同工酶活性、丙二醛（ＭＤＡ）含量，并对其中３４例患者红细胞内ＳＯＤ（ＲＢＣ－ＳＯＤ）活性进行检测，对其相互间的关系进行了探讨。结果表明，血清总ＳＯＤ（Ｔ－ＳＯＤ）、Ｍｎ－ＳＯＤ活性和ＭＤＡ含量明显高于正常对照组，ＣｕＺｎ－ＳＯＤ活性无变化或显著降低及ＲＢＣ－ＳＯＤ活性均明显低于对照组。其相关性表现为Ｔ－ＳＯＤ及Ｍｎ－ＳＯＤ与ＭＤＡ的改变呈显著正相关（ｒ＝０．９３２３，Ｐ＜０．００１；ｒ＝０．９２１５，Ｐ＜０．００１），ＣｕＺｎ－ＳＯＤ与ＭＤＡ的改变呈显著负相关（ｒ＝－０．８８６１，Ｐ＜０．００１）。提示这些变化可作为判断脑血管病变发展和严重程度的重要参数。     

老年急性脑血管病并多器官功能衰竭患者SIL—2R和T细胞亚…

采用ＥＬＩＳＡ和ＡＰＡＡＰ法对３２例老年急性脑血管病（ＡＣＶＤ）并多器官功能衰竭（ＭＯＦ）患者及４０例老年和３５例非老年ＡＣＶＤ患者血清可溶性白细胞介素２受体（ＳＩＬ－２Ｒ）及Ｔ细胞亚群水平进行了测定。并与３０例对照组比较。结果显示，疾病各组队ＣＤ３外ＳＩＬ－２Ｒ和ＣＤ８均较对照组明显升高ＣＤ４／ＣＤ８比值则明显下降，其中以老年ＡＣＶＤ并ＭＯＦ组变化最为显著，与老年和非老年ＡＣＶＤ组比较，亦有显著     

缺血性脑血管病伴OSAS患者的血压和血管舒缩功能观察

目的 观察缺血性脑血管病（ＩＣＶＤ）伴阻塞型睡眠呼吸暂停综合征（ＯＳＡＳ）患者平均动脉压（ＭＡＢＰ）、血浆降钙素基因相关肽（ＣＧＲＰ）和内皮素（ＥＴ）的变化及相互关系。方法 应用放免方法测量３１例患者血浆ＣＧＲＰ和ＥＴ含量,静息状态下测量血压;多元相关分析。结果 ＩＣＶＤ伴ＯＳＡＳ患者组ＭＡＢＰ、ＥＴ均炕于正常对照组（均Ｐ〈０．００１）,ＣＧＲＰ明显低于对照组（Ｐ〈０．００１）;ＣＧＲＰ与ＭＡＢＰ     

多发梗塞性痴呆患者血浆和脑脊液中若干神经肽含量的变化

用放射免疫法测定了３０例多发梗塞性痴呆（ＭＩＤ）、３５例无痴呆多发脑梗塞患者（ＭＣＩ）及３０名健康人的血浆生长抑素（ＳＳ）、精氨酸加压素（ＡＶＰ）及β－内啡肽（β－ＥＰ）含量，同时测定了部分ＭＩＤ和ＭＣＩ患者脑脊液（ＣＳＦ）中ＳＳ、ＡＶＰ、β－ＥＰ含量。发现ＭＩＤ患者血浆ＳＳ、ＡＶＰ含量比ＭＣＩ组和健康对照组均降低（Ｐ＜０．０５），且随痴呆程度的加重，其含量有递减趋势。而血浆中β－ＥＰ在这三组间差异无显著性意义（Ｐ＞０．０５）。ＭＩＤ组ＣＳＦ中ＳＳ、β－ＥＰ含量低于ＭＣＩ组（Ｐ＜０．０５），而ＣＳＦ中ＡＶＰ含量在两组间无差异（Ｐ＞０．０５），ＣＳＦ中ＡＶＰ含量与痴呆的关系有待进一步研究。     

动脉粥样硬化性血栓性脑梗塞患者血浆氧化修饰低密度脂蛋白含量的研究

目的探讨氧化修饰低密度脂蛋白（ＯＸ－ＬＤＬ）与动脉粥样硬化性血栓性脑梗塞（ＡＴＣＩ）发生、发展的关系。方法应用酶联免疫吸附试验（ＥＬＩＳＡ）双抗夹心法检测了８３例ＡＴＣＩ患者血浆ＯＸ－ＬＤＬ含量变化。结果（１）ＡＴＣＩ组血浆ＯＸ－ＬＤＬ水平显著高于正常对照组（Ｐ＜０．０１）;血浆ＯＸ－ＬＤＬ水平变化与病程有关,但与梗塞部位无关。（２）ＡＴＣＩ患者血浆ＯＸ－ＬＤＬ水平与血糖、血胆固醇呈正相关。结论ＯＸ－ＬＤＬ可能参与了ＡＴＣＩ的发生和发展过程。     

维生素E、C在CVD与PD患者中抗氧化作用的临床研究

目的 探讨维生素E（Vit E)与维生素C（Vit C)在脑血管病（CVD）与帕金森病（PD）中的抗氧化作用。方法 检测CVD162例和PD77例共239例患者服用VitE和VitC前后血浆Vit E、Vit C、过氧化脂质（LPO）水平和红细胞超氧化物歧化酶（SOD）活性,并与对照组进行了比较。结果 服药前两组患者血浆Vit E、Vit C水平和红细胞SOD活性明显低于正常对照组;服药后两组患者的Vit E、Vit C水平和SOD活性无明显变化,而CVD组的LPO值升高。结论 CVD和PD患者可能有Vit E、Vit C水平和SOD活性降低,服用Vit E、Vit C后仅见CVD患者的LPO值升高,但匀不能象健康对照组那样提高Vit E、Vit C水平和SOD活性。     

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。     

Plasma lipid peroxidation in sporadic Parkinson's disease. Role of the L-dopa

Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson's disease (PD). There are several methods to measure oxidative stress, being lipid peroxidation (LPO) one of the most frequently used. Endogenous plasma LPO was determined by a spectrofluorimetric method in fifty two patients with sporadic PD and in forty controls. To know the maximum capacity of lipids to peroxidate, LPO was also measured after co-incubation with Fe2+/H2O2 (exogenous LPO). All PD patients were taken L-dopa and the effect of this treatment on LPO levels was additionally studied. Urine catecholamines and their main metabolites were also analyzed, and their possible correlation to LPO statistically studied. Endogenous plasma LPO levels were 33% higher in PD group than in control group (P<0.001). Exogenous plasma or oxidizability was also higher in PD patients compared to controls (20%, P<0.05). The intake of L-dopa was negatively dose-related to endogenous and exogenous plasma LPO. In conclusion, plasma of PD patients has elevated levels of LPO and also is more prone to peroxidation than that in the control group. The results also suggest an antioxidant effect of L-dopa.     

Antioxidant intervention attenuates oxidative stress in children and teenagers with Down syndrome

We previously demonstrated that systemic oxidative stress is present in Down syndrome (DS) patients. In the present study we investigated the antioxidant status in the peripheral blood of DS children and teenagers comparing such status before and after an antioxidant supplementation. Oxidative stress biomarkers were evaluated in the blood of DS patients (n = 21) before and after a daily antioxidant intervention (vitamin E 400 mg, C 500 mg) during 6 months. Healthy children (n = 18) without DS were recruited as control group. The activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), gamma-glutamyltransferase (GGT), glucose-6-phosphate dehydrogenase (G6PD) and myeloperoxidase (MPO), as well as the contents of reduced glutathione (GSH), uric acid, vitamin E, thiobarbituric acid reactive substances (TBARS), and protein carbonyls (PC) were measured. Before the antioxidant therapy, DS patients presented decreased GST activity and GSH depletion; elevated SOD, CAT, GR, GGT and MPO activities; increased uric acid levels; while GPx and G6PD activities as well as vitamin E and TBARS levels were unaltered. After the antioxidant supplementation, SOD, CAT, GPx, GR, GGT and MPO activities were downregulated, while TBARS contents were strongly decreased in DS. Also, the antioxidant therapy did not change G6PD and GST activities as well as uric acid and PC levels, while it significantly increased GSH and vitamin E levels in DS patients. Our results clearly demonstrate that the antioxidant intervention with vitamins E and C attenuated the systemic oxidative damage present in DS patients.     

Free radical toxicity and antioxidants in Parkinson's disease

Erythrocyte lipid peroxidation, oxidative hemolysis, erythrocyte antioxidant enzymes, viz. superoxide dismutase, glutathione reductase, glutathione peroxidase, catalase and plasma antioxidants, viz. vitamin A, vitamin E, vitamin C and ceruloplasmin have been determined by spectrophotometric methods in 15 patients with Parkinson's disease (PD) and in 50 controls. Lipid peroxidation, oxidative hemolysis and plasma ceruloplasmin were significantly higher in PD patients as compared to normals. Erythrocyte antioxidants in PD patients were not significantly different from the controls. However, plasma vitamin C in PD patients was significantly lower than the controls. It is concluded that these patients are under oxidative stress which points to a possible involvement of free radicals in PD.     

石杉碱甲治疗阿尔茨海默病SOD、LPO浓度变化

目的：用石杉碱甲胶丸治疗阿尔茨海默病（ＡＤ）,观察其红细胞和血浆内超氧化物歧化酶（ＳＯＤ）、过氧化脂质（ＬＰＯ）浓度变化与药物疗效之关系。方法：门诊患者３０例,每日服石杉碱甲胶丸共２月,于疗前、疗后１月、２月分别测定认知功能水平及红细胞和血浆内ＳＯＤ、ＬＰＯ浓度。结果：该药有效率达６３．３３％,能一定程序的改善记忆障碍和痴呆症状,治疗１、２个月后,红细胞和血浆内ＳＯＤ、ＬＰＯ浓度都较疗前有明显改善     

Plasma antioxidant status and motor features in de novo Chinese Parkinson's disease patients

Purpose: This study aimed to explore plasma antioxidant status in de novo Chinese Parkinson's disease (PD) patients and investigate its relationship with specific motor features of PD. Patients and methods: Sixty-four de novo Chinese PD patients and 40 age- and sex-matched healthy controls were recruited. Each motor feature of PD patients was assessed by unified Parkinson's disease rating scale. Plasma antioxidant status, including plasma level of glutathione (GSH) and plasma activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), was detected using enzyme-linked immunosorbent assay. The relationship between the plasma antioxidant status and motor features of PD was evaluated by Spearman's coefficient. Results: Plasma GSH level and plasma activities of GSH-Px, CAT and SOD of PD patients were lower than those of healthy controls. Moreover, the declining activity of plasma CAT was related with the increasing mean postural instability and gait disorder (PIGD) score and growing age. In contrast, the severity of tremor was positively correlated with plasma SOD activity. Conclusion: Our study demonstrates that the plasma antioxidant status is impaired in de novo Chinese PD patients. The complex relationship between the plasma antioxidant status and different motor features indicates that the antioxidant mechanisms underlying tremor and PIGD of PD may be different.     

不同药物对帕金森病患者血浆同型半胱氨酸的影响

目的探讨不同药物治疗方法对帕金森病患者血浆同型半胱氨酸(Hcy)、叶酸、维生素B12的影响,以及PD患者病情程度与血浆Hcy的关系。方法 79例PD患者按服药不同分为4组,比较各组血浆Hcy水平;观察Hoehn-Yahr(H-Y)分期与血浆Hcy水平的关系;观察血浆Hcy水平与病程的关系;观察不同治疗组患者叶酸、维生素B_(12)含量。结果服多巴胺制剂组血浆Hcy水平明显高于未服药组(P0.05);Hcy水平较高者H-Y分期较高(P0.05);病程较长的患者血浆Hcy水平升高(P0.05);服多巴胺制剂组患者叶酸、维生素B12水平均较未服药组明显降低(P0.05)。结论多巴胺制剂可引起血浆Hcy水平升高,使叶酸、维生素B12水平降低,有可能促进PD进展;血浆Hcy水平高者运动障碍分期较高,病程较长,即病情相对较重。     

Mitochondrially targeted vitamin E and vitamin E mitigate ethanol-mediated effects on cerebellar granule cell antioxidant defense systems

Ethanol (EtOH) disrupts the structure and function of the developing nervous system, sometimes leading to birth defects associated with fetal alcohol syndrome (FAS). Animal FAS models indicate that cellular membrane peroxidation, intracellular oxidant accumulation, and suppression of endogenous antioxidant enzymes contribute to the toxic effects of EtOH. Mitochondrially targeted vitamin E (MitoVit E), a chemically engineered form of vitamin E (VE) designed to accumulate in the mitochondria, has been shown to inhibit intracellular oxidant accumulation and cell death more effectively than VE. In previous investigations, we have shown that, in vivo, VE reduces neuronal death in the developing cerebellum of EtOH-exposed animals, and, in vitro, VE prevents apoptotic and necrotic death of EtOH-exposed cerebellar granule cells (CGCs). The present investigation shows that, in a FAS CGC model, 1 nM MitoVit E renders significant neuroprotection against EtOH concentrations as high as 1600 mg/dL. The present study also demonstrates that, in this same model, MitoVit E mitigates EtOH-induced accumulation of intracellular oxidants and counteracts suppression of glutathione peroxidase/glutathione reductase (GSH-Px/GSSG-R) functions, protein expression of gamma-glutamylcysteine synthetase (gamma-GCS), and total cellular glutathione (GSH) levels. In the presence and absence of EtOH, VE amplifies the protein expression levels of gamma-GCS, an enzyme that performs the rate-limiting step for GSH synthesis, and total GSH levels. These results suggest that MitoVit E and VE ameliorate EtOH toxicity through non-oxidant mechanisms-modulations of endogenous cellular proteins-and antioxidant means.