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。     

高血压患者血中SODLPO与维生素E的关系初探

探讨高血压患者血中SOD、LPO及维生素E之间的相互关系。检测46例高血压及50例正常对照组血中SOD、LPO及维生素E含量并做相关分析。结果显示观察组中SOD均值较对照组明显降低（P＜0．01），LPO均值较对照组显著升高（P＜0．05）二者呈负相关系。观察组中取维生素E者血中维生素E水平可以提高（P＜0．05）。提示SOD、LPO及维生素E在高血压的发展中有一定的协同作用，氧自由基（OFR）能促进动脉粥样硬化的发展，维生素E具有抗氧化作用。     

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     

不同病期脑梗死患者血浆脂酰氢过氧化物和维生素E水平的变化

目的　探讨血浆脂质过氧化物与抗氧化物在缺血性脑梗死不同病期的变化及其意义。方法　采用紫外及可见分光光度法测定 4 8例脑梗死不同病期患者血浆脂酰氢过氧化物 (AHP)和维生素E的含量并与正常人比较。结果　脑梗死急性期组患者 (19例 )血浆AHP水平显著升高 ,血浆维生素E水平显著降低 ,与正常对照组比较差异均有显著性 (P <0 0 1,P <0 0 5 ) ;恢复期组患者 (17例 )血浆AHP水平明显下降 ,与急性期组比较差异有显著性 (P <0 0 1) ,而血浆维生素E水平未见明显回升 ;后遗症期组 (12例 )患者血浆AHP水平与恢复期组比较差异无显著性 (P >0 0 5 ) ,血浆维生素E水平与急性期组比较无显著提高 (P >0 0 5 )。结论　对缺血性脑梗死患者应常规监测血中过氧化脂质及抗氧化物含量 ,抗氧化治疗可能有利于脑梗死患者的康复和预防脑卒中的复发。     

一氧化氮与脑出血关系的研究

目的：探讨一氧化氮与脑出血的关系。方法：检测了133例脑出血患者和100例健康对照者血浆一氧化氮（P－NO）、维生素C（P－VC）、维生素E（P－VE）含量。结果：与对照组比较，患者组P-NO平均值显著升高，P－VC、P－VE平均值均显著降低；患者临床病情（NDS）和颅内血肿量均与P－NO呈正相关，而与P－VC、P－VE呈负相关。结论：脑出血患者体内自由基反应病理性加剧，氧化抗氧化平衡严重失调，宜及早抗氧化治疗。     

帕金森病患者血浆β—内啡肽含量的变化及其临床意义

目的：探讨帕金森病（Parkinson disease,PD)患者血浆β－内啡肽（β-endorphin,β－EP）含量的变化及其临床意义。方法：采用放射免疫分析法测定35例PD患者血浆β－EP含量，并与30例正常者对照。结果：PD患者血浆β－EP含量校正常对照组明显降低（P＜0．05）；高岭、病情重及伴痴呆和抑郁的抑郁的患者血浆β－EP含量降低更显著（P＜0．05）。结论PD患者血浆β－EP含量显著降低，与PD发病密切相关，高龄、病情重及伴痴呆和抑郁的患者血浆β－EP含量低更明显，有助于对病情进展及预后进行评估。     

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。     

维生素E辅助治疗癫痫患者的临床疗效及作用机制探讨

目的：探讨维生素E辅助治疗癫痫的临床疗效，并分析其作用机制。方法选择我院神经内科收治的140例癫痫患者作为研究对象，其中观察组70例采用常规癫痫药物联合维生素E治疗，对照组70例采用常规癫痫药物治疗，比较2组临床疗效，并分析其作用机制。结果观察组总有效率82.86％，明显高于对照组，差异有统计学意义（ P＜0.05）；观察组血浆T-Aoc水平较对照组明显增加，而MDA水平较对照组明显降低，差异均有统计学意义（P＜0.05）。结论维生素E辅助治疗癫痫患者具有显著疗效，改善体内自由基水平，保护脑组织，阻止神经元放电，值得临床推广和应用。     

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。     

Vitamin D and Parkinson's disease--a hypothesis.

Parkinson's disease (PD), a common disease of the elderly, is a movement disorder characterized by tremor, akinesia, and loss of postural reflexes, leading to immobility and frequent falls. It results from selective loss (death) of dopaminergic neurons in the substantia nigra region of the brain, largely developed prior to clinical diagnosis, and continuous after diagnosis, despite use of current therapeutic modalities. In PD in the United States the cause and mechanism of continued neuron cell death in the substantia nigra is currently unknown. We hypothesize, based upon several lines of evidence, that documented chronically inadequate vitamin D intake in the United States, particularly in the northern states and particularly in the elderly, is a significant factor in the pathogenesis of PD. This hypothesis implies that dietary aid for prevention and therapy for PD is possible.     

Vitamin D from different sources is inversely associated with Parkinson disease

An inverse association between Parkinson disease (PD) and total vitamin D levels has been reported, but whether vitamin D from different sources, that is, 25(OH)D2 (from diet and supplements) and 25(OH)D3 (mainly from sunlight exposure), all contribute to the association is unknown. Plasma total 25(OH)D, 25(OH)D2, and 25(OH)D3 levels were measured by liquid chromatography–tandem mass spectrometry in PD patients (n = 478) and controls (n = 431). Total 25(OH)D was categorized by clinical insufficiency or deficiency; 25(OH)D2 and 25(OH)D3 were analyzed in quartiles. Vitamin D deficiency (total 25[OH]D < 20 ng/mL) and vitamin D insufficiency (total 25[OH]D < 30 ng/mL) are associated with PD risk (odds ratio [OR] = 2.6 [deficiency] and 2.1 [insufficiency]; P < 0.0001), adjusting for age, sex, and sampling season. Both 25(OH)D2 and 25(OH)D3 levels are inversely associated with PD (P_trend < 0.0001). The association between 25(OH)D2 and PD risk is largely confined to individuals with low 25(OH)D3 levels (P_trend = 0.0008 and 0.12 in individuals with 25[OH]D3 < 20 ng/mL and 25[OH]D3 ≥ 20 ng/mL, respectively). Our data confirm the association between vitamin D deficiency and PD, and for the first time demonstrate an inverse association of 25(OH)D2 with PD. Given that 25(OH)D2 concentration is independent of sunlight exposure, this new finding suggests that the inverse association between vitamin D levels and PD is not simply attributable to lack of sunlight exposure in PD patients with impaired mobility. The current study, however, cannot exclude the possibility that gastrointestinal dysfunction, a non‐motor PD symptom, contributes to the lower vitamin D2 levels in PD patients. © 2014 International Parkinson and Movement Disorder Society     

Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease

The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [?30%], PSP [?21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [?20%]). GSH levels were normal in all examined normal and degenerating extra‐nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (?19 to ?30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD. © 2003 Movement Disorder Society     

Serum glutathione peroxidase,xanthine oxidase,and superoxide dismutase activities and malondialdehyde levels in patients with Parkinson’s disease

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Oxidative stress has been hypothesized to play a major role in the development of PD in various studies. This study assessed to investigate oxidative and anti-oxidative status in PD patients. We evaluated oxidant/antioxidant status by measuring serum malondialdehyde (MDA) levels, xanthine oxidase (XO) activities, and activities of antioxidant enzymes, namely, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). The study included 29 patients with PD and 32 healthy subjects as controls. Comparison of oxidative parameters in the patient and control groups revealed significantly higher GSH-Px and XO activities in the patient group. Serum MDA and SOD activities in PD patients were not significantly different from the controls. MDA was negatively correlated with duration of the PD and positively with age of onset. There was a negative correlation between SOD and Hoehn and Yahr (H&Y) stage. According to these results, we suggest that oxidative stress may contribute to the development of PD.     

Dietary intake of antioxidant vitamins and risk of Parkinson’s disease: a case–control study in Japan

Background: Antioxidant vitamins are expected to protect cells from oxidative damage by neutralizing the effects of reactive oxygen species. However, epidemiological evidence regarding the associations between antioxidant vitamin intake and Parkinson’s disease (PD) is limited and inconsistent. We investigated the relationship between dietary intake of selected antioxidant vitamins, vegetables and fruit and the risk of PD in Japan using data from a multicenter hospital‐based case–control study. Methods: Included were 249 patients within 6 years of onset of PD. Controls were 368 inpatients and outpatients without a neurodegenerative disease. Information on dietary factors was collected using a validated self‐administered diet history questionnaire. Adjustment was made for sex, age, region of residence, pack‐years of smoking, years of education, body mass index, dietary intake of cholesterol, alcohol, total dairy products, and coffee and the dietary glycemic index. Results: Higher consumption of vitamin E and β‐carotene was significantly associated with a reduced risk of PD after adjustment for confounders under study: the adjusted odds ratio in the highest quartile was 0.45 (95% confidence interval [CI]: 0.25–0.79, P for trend = 0.009) for vitamin E and 0.56 (95% CI: 0.33–0.97, P for trend = 0.03) for β‐carotene. Stratified by sex, such inverse associations were significant only in women. No material relationships were shown between intake of vitamin C, α‐carotene, cryptoxanthin, green and yellow vegetables, other vegetables, or fruit and the risk of PD. Conclusions: Higher intake of vitamin E and β‐carotene may be associated with a decreased risk of PD.     

Serum heme oxygenase‐1 levels are increased in Parkinson’s disease but not in Alzheimer’s disease

Mateo I, Infante J, Sánchez‐Juan P, García‐Gorostiaga I, Rodríguez‐Rodríguez E, Vázquez‐Higuera JL, Berciano J, Combarros O. Serum heme oxygenase‐1 levels are increased in Parkinson’s disease but not in Alzheimer’s disease.
Acta Neurol Scand: 2010: 121: 136–138.
© 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objective – Oxidative stress is implicated in Parkinson’s disease (PD) and Alzheimer’s disease (AD), and heme oxygenase‐1 (HO‐1) is a potent antioxidant overexpressed in PD substantia nigra and AD cerebral cortex and hippocampus, indicating a possible up‐regulation of antioxidant defenses in both neurodegenerative diseases. The role of HO‐1 in peripheral blood of PD and AD patients remains unresolved. Methods – We measured serum HO‐1 levels in 107 patients with PD, 105 patients with AD, 104 controls for PD and 120 controls for AD. Results – The median serum concentration of HO‐1 was significantly higher in PD patients (2.04 ng/ml) compared with that of PD controls (1.69 ng/ml, P = 0.016), with PD patients predominating over controls in the upper tertile of serum HO‐1 levels, whereas there was more PD controls than PD patients in the lower tertile (P = 0.006). Median serum levels of HO‐1 did not differ significantly between AD patients and AD controls. Conclusion – The increase of serum HO‐1 levels in PD patients could indicate a systemic antioxidant reaction related to a chronic oxidative stress state in PD brain.     

Desferrioxamine and vitamin E protect against iron and MPTP-induced neurodegeneration in mice

Summary To elucidate the neuroprotective effects of the iron chelator desferrioxamine (DFO) and the antioxidant vitamin E on excessive iron-induced free radical damage, a chronic iron-loaded mice model was established. The relationship between striatal iron content, oxidized to reduced glutathione ratio, hydroxyl radical (.OH) levels and dopamine concentrations were observed in DFO or vitamin E pretreated iron-loaded/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated C57BL/6 mice. The results demonstrated that both DFO and vitamin E inhibit the iron accumulation and thus reverses the increase in oxidized glutathione (GSSG), oxidized to reduced glutathione ratios, .OH and lipid peroxidation levels. The striatal dopamine concentration was elevated to normal value. Our data suggested that: (1) iron may induce neuronal damage and thus excessive iron in the brain may contribute to the neuronal loss in PD; (2) iron chelators and antioxidants may serve as potential therapeutic agents in retarding the progression of neurodegeneration.     

Decreased serum selenium concentrations in patients with Parkinson's disease

Selenium is an essential component of the antioxidant enzyme glutathione peroxidase. The activity of this enzyme is reduced in the substantia nigra of patients with Parkinson's disease (PD), but the results of studies on erythrocytes are controversial. We compared the serum levels of selenium and the 24 h urinary selenium excretion (measured by hydride generation atomic absorption spectrophotometry) in 29 PD patients and 30 matched controls. Serum selenium levels were significantly lower in PD patients than in controls (34.6 ± 2.35 and 45.2 ± 3.83 μg/l, p < 0.05) while urinary excretion was similar for both groups (47.1 ± 6.25 and 45.5 ± 5.38 μg/24 h). These values were not influenced by antiparkinsonian drugs, and they did not correlate with age, age at onset and duration of the PD, scores of the Unified PD Rating Scale or the Hoehn and Yahr staging in the PD group. These results might suggest a possible role of low serum selenium levels in the risk for, or a consequence of the oxidative stress in PD.