重组人促红素对老年慢性肾衰病人氧自由基及抗氧化酶活性的 …

目的 探讨重组人促红素（ｒＨ－ＥＰＯ）对慢性肾衰患者体内氧自由基及抗氧化酶活性的影响。方法 测定１９例老年慢性肾衰尿毒症期患者ｒＨ－ＥＰＯ治疗前后血浆ＭＤＡ、ＳＯＤ及红细胞ＧＳＨ－Ｐｘ含量。结果 ｒＨ－ＥＰＯ治疗后慢性肾衰病人ＭＤＡ含量降低，ＳＯＤ、ＧＳＨ－Ｐｘ活性升高。结论 ｒＨ－ＥＰＯ纠正肾性贫血同时，可清除体内氧自由基，提高抗氧化酶活性。     

硒和维生素E对大鼠心肌腺苷酸及氧化损伤的影响

目的：研究低硒（Ｓｅ）低维生素Ｅ（ＶＥ）饮食大鼠心肌腺苷酸含量和氧化损伤的关系。方法：使用高效液相测定心肌腺苷酸含量和使用生化方法测定心肌ＭＤＡ含量和ＳＯＤ、ＧＳＨ－Ｐｘ活性。结果：与补充Ｓｅ和／或ＶＥ饮食大鼠相比，低Ｓｅ低ＶＥ饮食大鼠心肌ＡＭＰ，ＡＤＰ含量无明显差异，而ＡＴＰ含量明显降低，ＭＤＡ含量增加，ＳＯＤ，ＧＳＨ－Ｐｘ活性降低，表明Ｓｅ和ＶＥ影响ＡＴＰ含量与其抗氧化作用有关，而其中以联合补充Ｓｅ和ＶＥ效果最佳     

Ⅱ型糖尿病合并高血压患者氧化损伤及抗氧化酶活性的研究

目的：评价氧化损伤及抗氧化酶活性对型糖尿病（ Ｎ Ｉ Ｄ Ｄ Ｍ）及其伴发高血压（ Ｈ Ｔ）的影响。　方法与结果：采用鲁米诺依赖的中性粒细胞化学发光法,对１３６ 例 Ｎ Ｉ Ｄ Ｄ Ｍ 患者（其中 ７０ 例不伴有 Ｈ Ｔ,６６ 例伴有 Ｈ Ｔ）及３０ 例年龄匹配的健康对照者, 检测其外周血中性粒细胞产生氧自由基（ Ｏ Ｆ Ｒ）的水平。采用化学定量法,测定其血浆脂质过氧化终末产物－ 丙二醛（ Ｍ Ｄ Ａ）的浓度及抗氧化酶－ 超氧化物歧化酶（ Ｓ Ｏ Ｄ）、谷胱甘肽过氧化物酶（ Ｇ Ｓ Ｈ Ｐｘ）的活性。 Ｎ Ｉ Ｄ Ｄ Ｍ 伴发 Ｈ Ｔ组,其 Ｐ Ｍ Ｎ┐ Ｃ Ｌ 峰值、积分和吞噬指数均明显高于 Ｎ Ｉ Ｄ Ｄ Ｍ 不伴 Ｈ Ｔ组及健康对照组;血浆 Ｍ Ｄ Ａ浓度较后两组也明显升高（ Ｐ均＜ ０．０１）; Ｎ Ｉ Ｄ Ｄ Ｍ 组及 Ｎ Ｉ Ｄ Ｄ Ｍ 伴发 Ｈ Ｔ组的血浆 Ｓ Ｏ Ｄ和 Ｇ Ｓ Ｈ Ｐｘ 活性较正常对照组均明显降低（ Ｐ均＜ ０．０１）;但与 Ｎ Ｉ Ｄ Ｄ Ｍ 组相比, Ｎ Ｉ Ｄ Ｄ Ｍ 伴发 Ｈ Ｔ组的血浆 Ｓ Ｏ Ｄ 和 Ｇ Ｓ Ｈ Ｐｘ 活性其差异无显著性（ Ｐ均＞ ０．０５）; Ｐ Ｍ Ｎ┐ Ｃ Ｌ峰值与 Ｍ Ｄ Ａ呈明显正相关（ｒ＝ ０．７４８６, Ｙ＝ １５９．８ Ｘ＋ １３２．２, Ｐ＜ ０．０１,     

老年冠心病患者红细胞磷脂与过氧化反应关系的研究

实验观察老年冠心病人红细胞磷脂和血中ＬＰＯ、ＳＯＤ及ＧＳＨ－Ｐｘ含量的变化，并对其相互关系进行了分析。结果表明，各组老年冠心病患者红细胞磷脂中ＬＰＣ、ＳＭ、ＰＳ、ＰＥ和ＳＭ／ＰＣ、ＰＳ／ＰＣ均明显升高，而ＰＣ则显著下降，心肌梗塞组更为明显，标志老年冠心病人细胞老化指数升高，红细胞粘滞性增高，心肌梗塞组ＬＰＯ显著升高，ＳＯＤ、ＧＳＨ－Ｐｘ和ＳＯＤ／ＬＰＯ，ＧＳＨ－Ｐｘ／ＬＰＯ明显降低，说明老年冠心病患者体内氧化与抗氧化平衡失调。逐步回归分析表明，红细胞磷脂各成分与ＬＰＯ和ＳＯＤ有密切关系。     

宫颈癌与妇科良性疾病患者血中抗氧化指标的检测及其临床意义

检测了２７例宫颈癌、３０例宫颈炎和３０例子宫肌瘤患者的血清ＳＯＤ及其同功酶、全血ＧＳＨ－Ｐｘ、ＣＡＴ等的活性水平以及血清ＬＰＯ含量。结果表明，与健康对照组相比，宫颈癌患者血清Ｃｕ，Ｚｎ－ＳＯＤ、总－ＳＯＤ（Ｔ－ＳＯＤ）活性明显降低（Ｐ＜０．０１），ＬＰＯ含量明显增高（Ｐ＜０．０５）；宫颈炎患者血清Ｍｎ－ＳＯＤ、Ｔ－ＳＯＤ活性明显降低（Ｐ＜０．０１），全血ＧＳＨ－Ｐｘ活性与血清ＬＰＯ含量明显增高（Ｐ＜０．０１）；子宫肌瘤患者血清Ｍｎ－ＳＯＤ、Ｃｕ、Ｚｎ－ＳＯＤ、Ｔ－ＳＯＤ与全血ＧＳＨ－Ｐｘ活性均明显降低（Ｐ＜０．０１），血清ＬＰＯ含量明显增高（Ｐ＜０．０１）。可见，血清Ｔ－ＳＯＤ活性降低和ＬＰＯ含量升高是宫颈癌、宫颈炎与子宫肌瘤患者自由基代谢紊乱的共同特点，提示体内病理性氧自由基反应和脂质过氧化反应明显增强是上述患者共同的病理基础。     

紫外线照射自血回输对肺心病患者血液抗氧化能力的影响

为进一步探讨紫外线照射自血回输（ＡＵＶＩＢ）对肺心病急性加重期患者辅助治疗的机理，对４８例肺心病患者ＡＵＶＩＢ治疗前后血液中超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）、过氧化氢酶（ＣＡＴ）活性进行了检测，并以正常人作对照。结果发现：肺心病患者ＳＯＤ水平虽高于正常对照组，但无显著差异（Ｐ＞００５），ＭＤＡ含量显著高于正常对照组（Ｐ＜００１），而ＧＳＨ－Ｐｘ与ＣＡＴ活性明显低于正常对照组（Ｐ＜００５）。经ＡＵＶＩＢ辅助治疗后，ＧＳＨ－Ｐｘ与ＣＡＴ活性显著升高（Ｐ＜００５），ＭＤＡ水平显著降低（Ｐ＜００５）。说明ＡＵＶＩＢ能提高肺心病患者血液抗氧化能力     

一氧化氮等自由基与脑出血关系的研究

目的探讨一氧化氮等自由基与脑出血的关系。方法检测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）、β－胡萝卜素（Ｐ－β－ＣＡＲ）和过氧化脂质（Ｐ－ＬＰＯ）含量及红细胞超氧化物歧化酶（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。结果与对照组比较,患者组Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ均值显著升高（Ｐ＜０．００１）,Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ均值显著降低（Ｐ＜０．００１）;逐步回归发现,患者病情（ＮＤＳ）与Ｐ－ＮＯ、Ｐ－ＶＣ、Ｅ－ＬＰＯ值相关最为密切,颅内血肿量与Ｐ－ＮＯ、Ｐ－ＶＥ、Ｅ－ＬＰＯ值相关最为密切。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     

地方性砷中毒患者生物膜损伤机制的探讨

对病区地砷病患者，病区非地砷病患得及对照组居民体的脂质过氧化及唾液酸水平进行了检测。结果表明，病区非病人组全血ＧＳＨ－Ｐｘ活力明显低于对照组，血清ＳＡ及尿ＭＤＡ含量明显高于对照组，病区病人组全血ＧＳＨ－ＰｘＳＯＤ活力明显低于对照组，血中ＧＳＨ，ＳＡ，ＭＤＡ含量及尿中ＭＤＡ水平均明显高于对照组，相关分析发现，病区病人尿砷含量与尿中ＭＤＡ水平呈呈相关（ｒ＝０．４６，Ｐ〈０．０５），提示：砷可导致生物膜     

IGF-I对ISP损伤大鼠心肌MDA、GSH-Px变化影响的实验研究

目的 研究胰岛素样生长因子－Ｉ（ＩＧＦ－Ｉ）对异丙肾上腺素（ＩＳＰ）致大鼠心肌损伤丙二醛（ＭＤＡ）,谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的变化影响。方法 采用大鼠ＩＳＰ心肌损伤动物模型,以ＩＧＦ－Ｉ作保护因素,分别检测ＭＤＡ的含量及全血ＧＳＨ－Ｐｘ的活力。结果 ＩＳＰ组大鼠全血ＧＳＨ－Ｐｘ活力明显低于ＩＧＦ－Ｉ＋ＩＳＰ组。结论 ＩＧＦ－Ｉ能减少ＩＳＰ所致心肌损伤时氧自由基的产生,减轻氧自由基对细胞膜     

NO和脂质过氧化与老年矽肺关系的研究

目的　探讨ＮＯ和脂质过氧化与老年矽肺的关系。方法　检测８５ 例老年矽肺患者和８０ 例健康老年人的血浆ＮＯ（Ｐ－ＮＯ）、过氧化脂质（Ｐ－ＬＰＯ）及红细胞超氧化物歧化酶（Ｅ－ＳＯＤ）、过氧化氢酶（Ｅ－ＣＡＴ）、谷胱甘肽过氧化物酶（Ｅ－ＧＳＨ－Ｐｘ）、过氧化脂质（Ｅ－ＬＰＯ）值。结果　与对照组比较,患者组Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ 均值显著降低,Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ 均值显著升高（Ｐ＜ ０．００１）;直线回归和相关分析表明上述各检测值与患者病程均有相关;逐步回归表明患者病情、肺功能状态与Ｐ－ＮＯ、Ｅ－ＳＯＤ、Ｅ－ＬＰＯ 值相关最密切。结论　矽肺患者体内ＮＯ 代谢异常,氧化抗氧化平衡严重失调,氧化和脂质过氧化反应病理性加剧。     

氟对大鼠脂质过氧化和抗氧化能力的影响

目的 探讨氟对大鼠血和各组织丙二醛（MDA）水平、超氧化物歧化物（SOD）活力及全血谷胱苷肽过氧化物酶（GSH-Px）活力的影响。方法 运用动物实验,采用饮水加氟的方法。结果 染氟可使大鼠血清、肝脏、肾脏、脑中MDA含量显著增加;全血和肝脏、肾、心脏、睾丸的SOD活性显著降低;全血GSH-Px活性降低。结果 氟可促进机体脂质过氧化,抑制抗氧化酶（SOD,GSH-Px）的活力。     

外源性一氧化氮对旋毛虫感染小鼠抗氧化能力的影响

目的探讨外源性NO供体亚硝基铁氰化钠(SNP)对旋毛虫病小鼠肝脏、外周血中抗氧化酶活性及脂质氧化的影响。方法采用消化法分离旋毛虫肌幼虫,感染BALB/c小鼠,400条/只。42 d后,收集感染鼠及正常小鼠外周血、肝脏。设A组(感染鼠肝脏匀浆物+SNP)、B组(正常鼠肝脏匀浆物+SNP)、C组(感染鼠外周血+SNP)、D组(正常鼠外周血+SNP)。每组内设5个SNP反应终浓度,分别为0(空白对照)、2、5、10、30μmol/L,37℃反应30 min,测定各组超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)及脂质氧化(MDA)含量。结果与正常鼠相比,旋毛虫感染鼠肝脏、外周血中SOD、CAT、GSH-Px活性上升,MDA含量增加,差异均有统计学意义(P均0.05);在A、B组中,10、30μmol/L SNP作用下SOD、CAT、GSH-Px活性较空白对照降低(P均0.05);与2~30μmol/L SNP反应后,MDA含量较空白对照明显升高(P均0.05)。在C、D组中,30μmol/LSNP作用下SOD、CAT、GSH-Px活性显著下降,MDA浓度升高,与空白对照比较差异均有统计学意义(P均0.01)。在2~30μmol/L浓度区间,SNP浓度与旋毛虫感染鼠肝脏、外周血中SOD、CAT、GSH-Px活性呈负相关(r肝SOD=-0.901,r肝CAT=-0.802,r肝GSH-Px=-0.847,r血SOD=-0.899,r血CAT=-0.685,r血GSH-Px=-0.635,P均0.05),与MDA含量呈正相关(r肝MDA=0.697,r血MDA=0.764,P均0.05)。结论旋毛虫感染可致小鼠肝脏、外周血中活性氧自由基产生增加,SOD、CAT、GSH-Px活性升高;外源性NO可降低旋毛虫感染小鼠SOD、CAT、GSH-Px活性,抑制小鼠的抗氧化能力。     

Oxidative stress and antioxidant parameters in a Turkish group of patients with active and inactive systemic lupus erythematosus

Aim: Although the pathogenesis of systemic lupus erythematosus (SLE) is likely to be multifactorial, the inflammatory nature of SLE implies that a state of oxidative stress may exist in this disease, which may contribute to immune cell dysfunction, auto‐antigen production and auto‐antibody reactivity. This study was conducted to investigate the oxidant/antioxidant status of patients with SLE and to correlate this with disease activity. Methods: Sixteen clinically active, 12 clinically inactive SLE patients and 11 healthy controls were included into the study and antioxidant potential (AOP), catalase (CAT), glutathione peroxidase (GSH‐Px), superoxide dismutase (SOD), adenosine deaminase (ADA), malondialdehyde (MDA), and xanthine oxidase (XO) activity levels in erythrocytes and AOP, GSH‐Px, MDA, and XO activity levels in plasma were measured. Results: In erythrocytes; AOP was higher in SLE patients (both active and inactive), CAT activity was higher in inactive SLE patients, GSH‐Px, SOD and XO activity were lower in SLE patients (active and inactive) than the control group. In plasma; SLE patients (active and inactive) had higher AOP levels, activity of GSH‐Px was lower in SLE groups (active and inactive), activity of MDA was lower in active SLE patients, and activity of XO was higher in the active SLE patients than the control group. Conclusion: Antioxidant status was impaired in SLE patients but there was no significant difference between the active and inactive SLE groups, so oxidative stress may play a role in the pathogenesis of SLE but probably is not correlated with disease activity.     

Melatonin ameliorates chronic renal failure-induced oxidative organ damage in rats

Chronic renal failure (CRF) is associated with oxidative stress that promotes production of reactive oxygen species (ROS). Melatonin, the chief secretory product of the pineal gland, was recently found to be a potent free radical scavenger and antioxidant. The aim of this study was to examine the role of melatonin in protecting the aorta, heart, corpus cavernosum, lung, diaphragm, and kidney tissues against oxidative damage in a rat model of CRF, which was induced by five of six nephrectomy. Male Wistar albino rats were randomly assigned to either the CRF group or the sham-operated control group, which had received saline or melatonin (10 mg/kg, i.p.) for 4 wk. CRF was evaluated by serum blood urea nitrogen (BUN) level and creatinine measurements. Aorta and corporeal tissues were used for contractility studies, or stored along with heart, lung, diaphragm, and kidney tissues for the measurement of malondialdehyde (MDA, an index of lipid peroxidation), protein carbonylation (PC, an index for protein oxidation), and glutathione (GSH) levels (a key antioxidant). Plasma MDA, PC, and GSH levels and erythrocytic superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in CRF. In the CRF group, the contraction and the relaxation of aorta and corpus cavernosum samples decreased significantly compared with controls (P < 0.05-0.001). Melatonin treatment of the CRF group restored these responses. In the CRF group, there were significant increases in tissue MDA and PC levels in all tissues with marked reductions in GSH levels compared with controls (P < 0.05-0.001). In the plasma, while MDA and PC levels increased, GSH, SOD, CAT, and GSH-Px activities were reduced. Melatonin treatment reversed these effects as well. In this study, the increase in MDA and PC levels and the concomitant decrease in GSH levels of tissues and plasma and also SOD, CAT, GSH-Px activities of plasma demonstrate the role of oxidative mechanisms in CRF-induced tissue damage, and melatonin, via its free radical scavenging and antioxidant properties, ameliorates oxidative organ injury. CRF-induced dysfunction of the aorta and corpus cavernosum of rats was reversed by melatonin treatment. Thus, supplementing CRF patients with adjuvant therapy of melatonin may have some benefit.     

Protective effect of melatonin on random pattern skin flap necrosis in pinealectomized rat

Random pattern skin flaps are still widely used in plastic surgery. However, necrosis in the distal portion resulting from ischemia is a serious problem, increasing the cost of treatment and hospitalization. Free oxygen radicals and increased neutrophil accumulation play an important role in tissue injury and may lead to partial or complete flap necrosis. To enhance skin flap viability, a variety of pharmacological agents have been intensively investigated. The aim of this study is to test the effects of melatonin, the chief secretory product of the pineal gland and a highly effective antioxidant, on random pattern skin flap survival in rats. Herein, to investigate the physiological and pharmacological role of melatonin on dorsal skin flap survival. Pharmacological (0.4, 4 and 40 mg/kg) levels of melatonin were given intraperitoneally (i.p.). For this, pinealectomized (Px) and sham operated (non-Px) rats were used. The effects of melatonin on levels of malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH) and the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were measured in the skin flap. The ratio of skin flap necrosis was compared among the experimental groups by using planimetry. MDA and NO levels were found to be higher in Px than non-Px rats; while GSH levels and GSH-Px, and SOD activities were reduced. Melatonin administration to Px rats reduced MDA and NO levels and increased GSH, GSH-Px, SOD levels. Melatonin also reduced the ratio of flap necrosis determined by using planimetry and supported through the photography. In conclusion, these results show that both physiological and pharmacological concentrations of melatonin improve skin flap viability.     

硒与GSH联合对氟致大鼠脂质过氧化作用的影响

目的　研究抗氧化剂硒及与不同剂量 GSH联合对氟所致脂质过氧化作用的影响。方法　采用动物实验。结果　饮含氟化钠 (15 0 mg/ L)水可使大鼠肝、肾及血清中 L PO含量显著增加 ;SOD活性、GSH- Px活性、GSH含量均显著下降 ;饮含氟水同时给亚硒酸钠 ,可使血清中 L PO含量显著下降 ;SOD活性、GSH- Px活性、GSH含量显著升高。说明硒对氟引起的脂质过氧化有拮抗作用。饮含氟水同时给 Se与不同剂量 GSH后 ,结果显示 :Se与低、中、高 3个剂量 GSH均可使血清中 L PO含量显著下降 ,全血中 SOD活性显著增强 ,呈剂量—效应关系 ,使肝、肾及全血中 GSH- Px活性不同程度增强 ,表明 Se与 GSH联合可有效拮抗氟所致的脂质过氧化作用 ,恢复机体抗氧化能力。结论　 1氟可引起大鼠肝、肾及全血中脂质过氧化物含量升高 ,抗氧化能力下降 ;2硒及与不同剂量 GSH联合具有不同程度拮抗氟诱导的脂质过氧化作用 ,恢复机体的抗氧化能力     

D-半乳糖催老大鼠氧化水平和抗氧化能力的变化

目的　研究人工催老大鼠氧化水平和抗氧化能力的改变。方法　采用D 半乳糖 6 0mg/kg皮下注射 4 2d ,复制人工催老大鼠模型 ,以观察催老大鼠血中丙二醛 (MDA)、一氧化氮 (NO)的含量、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)、一氧化氮合酶 (NOS)和脑单胺氧化酶 (MAO)等活性的变化。结果　催老大鼠与正常大鼠相比 ,血清中MDA含量增高 ,SOD和GSH Px活性降低 ,脑MAO活性增高 ,NO含量和NOS活性无明显改变。结论　D 半乳糖可以使催老大鼠氧化水平增加 ,抗氧化能力下降 ;且两者变化无性别差异。     

染料木黄酮对ICR小鼠抗氧化能力及AGE水平的影响

目的　了解染料木黄酮 (Genistein)对 ICR小鼠组织抗氧化能力及高级糖基化终末产物 (AGE)水平的影响。方法　分别用不同剂量的染料木黄酮灌胃 1 6月龄的 ICR小鼠 30 d,然后分别对小鼠脑、肝等组织 AGEs、总活性氧 (ROS)、丙二醛 (MDA)水平以及谷胱甘肽过氧化物酶(GSH- Px)活性进行测定。结果　染料木黄酮灌胃小鼠肝组织 AGEs、ROS及 MDA水平均显著下降 (P<0 .0 5) ,GSH- Px活性升高 (P<0 .0 5) ;灌胃组小鼠脑组织 AGEs水平及 GSH- Px活性均与对照组小鼠无显著差异 ,而 ROS和 MDA水平不同程度下降 (P<0 .0 5)。结论　染料木黄酮可提高小鼠的抗氧化能力及肝组织细胞中 GSH- Px活性 ,从而有效降低肝组织中的氧化应激水平 ,抑制肝组织中 AGEs的形成 ;而其对脑组织 AGEs水平及GSH- Px活性均未产生明显影响。     

砷对大鼠肝脏抗氧化作用影响的动态观察

为探讨砷对大鼠肝脏脂质过氧化和抗氧化能力的影响,采用亚慢性动物试验的方法对染砷不同时间大鼠肝脏脂质过氧化和抗氧化水平进行了动态观察。结果表明,在染砷第３０ｄ、第９０ｄ和第１８０ｄ大鼠肝脏丙二醛（ＭＤＡ）含量与对照组无明显差异（Ｐ〉０．０５）。提示砷对肝脏脂质过氧化反应的增强无明显作用;在染砷第３０ｄ、第９０ｄ和第１８０ｄ大鼠肝脏谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性均明显低于对照组（Ｐ〈０．０５,