冠心病患者血清过氧化脂质的变化及其与动脉硬化关系的研究

对３０例不稳定型心绞痛（ＵＡ）、１９例急性心肌梗塞（ＡＭＩ）患者血清过氧化脂质（ＬＰＯ）、血清总胆固醇（ＴＣ）、甘油三酯（ＴＧ）、高密度脂蛋白胆固醇（ＨＤＬ－ｃ）进行了测定，并计算动脉硬化指数（ＡＩ）。发现ＵＡ及ＡＭＩ患者ＬＰＯ、ＴＣ、ＴＧ、ＡＩ值均显著高于正常人，ＨＤＬ－ｃ均低于正常人。ＵＡ与ＡＭＩ患者血清ＬＰＯ及血脂诸值比较差异均无显著性。ＵＡ与ＡＭＩ两组患者的ＬＰＯ水平均与ＡＩ呈显著正相关。     

内皮细胞脂质过氧化损伤对单核细胞粘附的影响

以巯基氧化剂联胺作用于培养人血管内皮细胞，引发细胞过氧化脂质蓄积与质过氧化损伤，研究内皮细胞脂质过氧化损伤对人血单核细胞粘附的影响，结果发现，内皮细胞脂质过氧化损伤使单核细胞对内皮细胞的粘附增加，单核细胞主要粘附于受损伤的内皮细胞表面和间隙，提示单核细胞对内皮细胞粘附增加，是内皮细胞脂质过氧化损伤促进和加重动脉粥样硬化病变形成的一个重要机制。     

动脉粥样硬化与血浆抗氧化活性

目的:探讨高胆固醇血症所致动脉粥样硬化(AS)发病过程中脂质过氧化激活机制。方法:选择健康雄性家兔，每天定量加胆固醇饲料(0.25 g/kg)饲养。时间 12周，每隔2周从兔耳取静脉血，测量血清铜蓝蛋白-转铁蛋白系统的抗氧化活性及血清胆固醇(Ch)和雨二醛(MDA)含量。结果:饲养12周后，部分兔血清钢蓝蛋白-转铁蛋白系统抗氧化活性明显增强，Ch含量增加 3倍，MDA含量明显下降。其余兔血清铜蓝蛋白-转铁蛋白系统抗氧化活性无明显变化，Ch含量增加 10倍，MDA含量显着提高。结论:高胆固醇血症所致AS的发生过程可能是多种脂质过氧化激活机制综合作用的结果，增强血浆抗氧化活性可在一定程度上抑制Ch和脂质过氧化物(LPO)积累，延缓AS的发生。     

脂质过氧化对血管内皮细胞源性生长因子分泌的影响

脂质过氧化对血管内皮细胞源性生长因子分泌的影响杨向红陈铁镇一、材料和方法（１）牛主动脉内皮细胞的培养：于无菌条件下取牛主动脉，以消化法进行内皮细胞的原代培养。培养液为含１０％小牛血清的ＤＭＥＭ培养液。第２～５代继代细胞用于实验。（２）脂质过氧化实验：...     

垂体腺苷酸环化酶激活肽对动脉粥样硬化形成过程中脂质过氧化的影响

目的　探讨垂体腺苷酸环化酶激活肽 (PACAP)对家兔实验性动脉粥样硬化 (AS)形成过程中脂质过氧化的影响。方法　 80只雄性新西兰家兔 ,随机分为 3组 :(1)对照组 (C组 ) :喂饲普通颗粒兔饲料 ;(2 )AS模型组 :每只兔每日喂饲含胆固醇 1 5g的颗粒兔饲料 ;(3)PACAP组 (P组 ) :喂饲与AS组同样的饲料 ,另从耳缘静脉注射PACAP。分别于实验的 0、4、8、12周末记录兔体重 ,同时从兔耳中央动脉取空腹血 ,测定丙二醛 (MDA)含量 :并取若干兔的主动脉标本作苏丹Ⅳ染色 ,测量斑块面积。结果　 (1)AS组及P组血清MDA含量均显著高于C组 ;而P组显著低于AS组。 (2 ) 4周末时P组斑块面积显著小于AS组。结论　PACAP具有抗脂质过氧化作用 ,可能与抗AS有关     

脂质过氧化对人内皮细胞的损伤及抗氧化剂的保护作用

以氢过氧化估烯作为培养人内皮细胞脂质过氧化反应的引发剂，以亚硒酸钠、维生素E、超氧化物歧化酶作为抗氧剂，应用光镜、脂质过氧化物测定及放射免疫分析等方法观察了抗氧剂对脂质过氧化损伤的内皮细胞形态结构和功能的保护作用。结果表明：氢过氧化枯烯激发和促进了内皮细胞的脂质过氧化反应；而硒、维生素E、超氧化物歧化酶使细胞脂质过氧化物含量减少，由过氧化作用造成的细胞收缩、生物膜系统的损伤程度减轻，对细胞前列腺素（PGI2）合成的抑制作用减弱。提示：上述抗氧剂可能通过对内皮细胞的保护作用，阻止动脉粥样硬化病变的形成和发展。     

脂质过氧化和氧自由基酶活性变化与强迫症临床症状的关系 …

目的：探讨强迫症患者体内氧化、抗氧化系统的状态及其与临床症状的关系。方法：采用超氧化物歧化酶超微量快速测定法、ＤＴＮＢ直接法、改良红细胞还原型谷胱甘肽二硫双硝基苯甲酸定量测定法和ＴＢＡ法。测３０例强迫症患者,３０例正常对照血中ＳＯＤ、ＧＳＨ－ＰＸ活性,ＧＳＨ含量和血清中ＬＰＯ含量并做ＳＡＳ－ＳＤＳ、Ｙ－ＢＯＣＳ评分。结果：强迫症组ＬＰＯ含量,ＳＯＤ活性明显高于正常组,ＧＳＨ含量则显著降低（Ｐ〈００     

脂蛋白胆固醇、载脂蛋白B与抗氧化酶脂质过氧化物的关系

用胆固醇喂家兔塑造动脉粥样硬化（ＡＳ）模型，观察脂蛋白胆固醇、载脂蛋白Ｂ与抗氧化酶［红细胞超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）］脂质过氧化物的关系。结果表明：高胆固醇血症高载脂蛋白Ｂ血症抑制抗氧化酶活性，促使自由基和脂质过氧化物（ＬＰＯ）堆积，使ＬＤＬ氧化修饰为Ｏ－ＬＤＬ。Ｏ－ＬＤＬ通过清道夫受体摄入，引起细胞内胆固醇堆积，促进Ａ８的形成。     

超氧化物歧化酶、过氧化脂质和谷胱甘肽过氧化物酶变化与急性有机磷农药中毒的关系

本文对３３例急性有机磷农药中毒（ＡＯＩＰ）患者检测了超氧化物歧化酶（ＳＯＤ－１），过氧化脂质（ＬＰＯ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ），ＡＯＩＰ组的ＳＯＤ－１、ＧＳＨ－Ｐｘ较对照组明显降低（Ｐ＜０．０１）。而ＬＰＯ较对照组明显升高（Ｐ＜０．０１）。ＳＯＤ－１含量与胆碱酯酶活性呈正相关（ｒ＝０．６０２，Ｐ＜０．０１）。研究结果说明，氧自由基参于了有机磷农药对机体的损伤过程。     

缺血预处理对肺再灌注损伤脂质过氧化的影响

目的：观察缺血预处理对在体兔肺常温缺血再灌注损伤脂质过氧化的影响。方法：采用阻断左肺门的肺缺血再灌注损伤模型。硫代巴比妥酸法及UFN13直接法测肺组织丙二醛（MDA）、超氧化物歧化酶（SOD）、谷航甘肽过氧化物酶（GSHpx)及肺组织光镜观察。结果：缺血再灌组左肺MDA较假手术组和缺血组为高,而SOD和GSHpx活性较低（P＜0．01）,肺组织损伤较重。与缺血再灌组比较,缺血预处理 缺血再灌组有较低的MDA含量和较高的SOD与GSHpx活性（P＜0．05）,肺损伤亦较轻。结论：缺血预处理可减轻兔肺常温缺血再灌注诱导的脂质过氧化反应。     

Hyperbaric oxygen modulates antioxidant enzyme activity in rat skeletal muscles

In skeletal muscle the activity of the enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) is regulated in response to generation of reactive oxygen species (ROS). Increased activity of these enzymes is observed after repeated bouts of aerobic exercise, a potent stimulus for intracellular ROS production. Hyperbaric oxygen (HBO) inhalation also stimulates intracellular ROS production although the effects of HBO on skeletal muscle SOD, GPx and CAT activity have not been studied. We tested the hypothesis that SOD, GPx and CAT activity is modulated in skeletal muscles in response to acute and repeated HBO administration. In adult male rats acute HBO inhalation (60 min at 3 atmospheres absolute) reduced catalase activity by approximately 51% in slow-twitch soleus muscles. Additionally, repeated HBO inhalation (twice daily for 28 days) increased Mn²⁺-superoxide dismutase activity by approximately 241% in fast-twitch extensor digitorum longus muscles. We conclude that both acute and repeated HBO inhalation can alter enzymatic antioxidant activity in skeletal muscles. Electronic Publication     

内毒素对大鼠脑线粒体的损伤及与氧自由基的关系

本文观察了在较低剂量(2mg/kg)E.Coli内毒素纯制剂腹腔注射后,大鼠脑组织线粒体的过氧化脂质和与氧自由基代谢及线粒体完整性密切相关的酶的活性变化。结果表明,在内毒素注射后14小时鼠脑线粒体LPO较对照组升高21%(P<0.01),SOD、GSH-Px、SDH活性均明显下降,分别较对照组低18%、30%、22.3%(均P<0.01)。24小时开始恢复,即LPO下降,其它酶学指标回升。48小时各项指标均基本回到对照组水平。电镜观察证实内毒素注射后14小时脑组织线粒体肿胀。上述结果提示:这种剂量的内毒素造成了脑组织的可逆性损害。自由基清除能力降低,膜脂质过氧化作用增强是引起大鼠脑线粒体损害的重要原因。     

Effects of sprint exercise on oxidative stress in skeletal muscle and liver

Although numerous studies have tested the effects of continuous exercise regimens on antioxidant defences, information on the effect of sprint exercise on the antioxidant defence system and lipid peroxidation levels of tissues is scant. The present study was designed to determine the effects of sprint exercise on the lipid peroxidation and antioxidant enzyme system in liver and skeletal muscle during the post-exercise recovery period in untrained mice. Mice performed 15 bouts of exercise, each comprising running on a treadmill for 30 s at 35 m·min^–1 and a 5° slope, with a 10-s rest interval between bouts. They were then killed by cervical dislocation either immediately (0 h), 0.5 h, 3 h or 24 h after completion of the exercise. Their gastrocnemius muscle and liver tissues were quickly removed. It was found that blood lactate levels increased immediately after the exercise, but had returned to control levels by 0.5 h post-exercise. This exercise regimen had no effect on the activity of superoxide dismutase and glutathione peroxidase in these tissues. Levels of muscle thiobarbituric acid reactive substances (TBARS) had increased at 0.5 and 3 h post-exercise, and then returned to control levels by 24 h post-exercise. In conclusion, acute sprint exercise in mice resulted in an increase in TBARS levels in skeletal muscle; no change was observed in the liver. Antioxidant enzyme activities remained unaffected by acute sprint exercise in these tissues. Electronic Publication     

过氧化与胎儿窘迫

目的：探讨过氧化与胎儿窘迫的关系。方法 测定63例晚孕妇女静脉血及脐血中超氧化物歧化酶(SoD)及过氮化脂质(LPO)含量，其中40例为正常晚孕妇女(对照组)。23例为胎儿宫内窘迫孕妇(胎窘组)。结果 胎窘组孕妇血及脐血LPO值明显高于对照组，差异有显著性(P＜0．01)，而SOD显著低于对照组(P＜0．01)。LPo含量与脐血pH、PO2显著负相关(P＜0．05)，与POC2显著正相关(P＜0.01)。结论 机体过氮化与胎窘发生有密切的关系。     

Acute effect of ionic high osmolar contrast medium on renal antioxidant enzyme activity in streptozotocin-induced diabetic rats

Abstract Acute contrast medium-induced nephrotoxicity was estimated in 3%–12% of patients receiving cardiac angiography, especially in advanced age, renal insufficiency and diabetic patients. As intrinsic renal antioxidant enzyme activities may play a crucial role in defence against renal oxidant injury, this study was designed to investigate the acute effect of ionic high osmolar diatrizoate meglumine/diatrizoate sodium on renal antioxidant activities in normal or streptozotocin (STZ)-induced diabetic rats at two time points (1 h and 24 h). A total of 40 Wistar rats were separated to normal and STZ-induced diabetic groups. Ten of each group were injected with diatrizoate (10 ml/kg) via tail vein and 10 with 10 ml/kg of 0.9% NaCl as control. This study shows that diabetic rats had higher renal glutathione peroxidase (GPx) activities than those of normal rats. GPx activities decreased significantly after diatrizoate injection at the first hour (717.4±104.0 to 578.6±92.1 mU/mg in the diabetic group, 466.4±30.6 to 371.4±75.5 mU/mg in the normal group, all P=0.032) but the difference faded 24 h later. The increase of superoxide dismutase (SOD) activities was enhanced (673.5±100.2 to 750.4±129.8 U/mg, P=0.04) in the normal group, but not in the diabetic group (624.1±156.6 to 671.1±136.7 U/mg, P=0.15) after diatrizoate injection at the first hour. At 24 h, renal SOD activities were still significantly higher in the diatrizoate injection group. In summary, intrinsic renal antioxidant activities are adapted in STZ-induced diabetes and ionic high osmolar diatrizoate could modify their activities. Furthermore, diabetics have abnormal response of renal antioxidant activities by contrast media and are at risk for contrast-mediated nephrotoxicity.     

Lipoic acid effects on lipid peroxidation level,superoxide dismutase activity and monoamines concentration in rat hippocampus

The purposes of the present work were to verify lipid peroxidation level, superoxide dismutase (SOD) activity and monoamines (dopamine (DA), norepinephrine (NE), serotonin (5-HT)), and their metabolites (3,4-hydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA)) contents in rat hippocampus after lipoic acid (LA) administration. Wistar rats were treated with 0.9% saline (i.p., control group) and LA (10, 20 or 30 mg/kg, i.p., LA10, LA20 and LA30 groups, respectively). After the treatments all groups were observed for 24 h. In LA20 group only there was a significant decrease in lipid peroxidation level. However, no alteration was observed in SOD activity in groups treated with LA. The NE and DA levels were increased only in 20 mg/kg dose of LA in rat hippocampus. Serotonin content and their metabolite 5-HIAA levels was decreased in same dose of LA. On the other hand, DOPAC and HVA levels did not show any significant change. The reduction in lipid peroxidation level and alterations in hippocampal monoamines can be suggested as a possible brain mechanism from this antioxidant. The outcome of the study may have therapeutic implications in the neurodegenerative diseases.     

家兔内毒素性DIC时血清LPO含量、红细胞SOD活力的变化及意义

本实验用内毒素复制家兔DIC模型,以硫代巴比妥酸法测定血清LPO含量,以邻苯三酚法测定红细胞SOD活力,探讨二者变化及自由基反应在内毒素性DIC病理过程中的意义。结果表明:模型组血清LPO含量(9.36±2.65)与对照组(6.62±1.91)比较明显增高(P<0.01),而红细胞SOD活力(1676.41±374.01)与对照组(2225.66±411.85)比较明显降低(P<0.005)。提示自由基可能参与了DIC的病理过程并且是致组织损伤的重要因素之一。本文对该病理过程中自由基增多可能的机制进行了讨论。