ADVANTX LCV＋血管造影机微动开关等器件替换2例

１床旁控制面板（ＴＡＢＬＥＳＩＤＥＰＡＮＥＬ）上微动开关及旋钮的替换。ＧＥ公司生产的ＡＤＶＡＮＴＸＬＣＶ +血管造影机（ＤＳＡ）使用了人机一体的设计理念 ,术者可以通过设在床边的床旁控制器（ＴＡＢＬＥＳＩＤＥＰＡＮＥＬ）、智能手柄（ＳＭＡＲＴＨＡＮＤＬＥ）和遥控器（ＲＥＭＯＴＥＣＯＮＴＲＯＬＤＥＶＩＣＥ） ,在床旁完成对设备的全部操作。使用非常方便。但是 ,设在床旁控制器上的光栅控制钮（ＩＲＩＳＣＯＮＴＲＯＬＫＮＯＢ）和轮廓滤波控制钮（ＣＯＮＴＯＵＲＦＩＬＴＥＲＣＯＮＴＲＯＬＫＮＯＢ）设计得非常单薄 ,极…     

矽肺与抗氧化剂、抗氧化酶关系的探讨

目的：探讨矽肺与抗氧化剂、抗氧化酶的关系。方法：检测了７３例矽肺患者和６０例健康对照者的血浆维生素Ｃ（Ｐ－ＶＣ）、维生素Ｅ（Ｐ－ＶＥ）、β－胡萝卜素（Ｐ－β－ＣＡＲ）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。结果：与对照组比较,患者组的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）;各检测值与患者病程、病情、肺功能状态均有相关;逐步回归表明患者病程、病情、肺功能状态与Ｐ－ＶＥ、Ｅ－ＳＯＤ值相关最为密切。结论：矽肺患者体内氧化抗氧化平衡严重失调,氧自由基反应病理性加剧。     

一氧化氮等自由基对吸烟者损害效应的研究

检测１２５５例康康吸烟者和５２４例健康非吸烟者血浆一氧化氮（Ｐ－ＮＯ）、维生素Ｃ（Ｐ－ＶＣ）、维生素Ｅ（Ｐ－ＶＥ）、β－胡萝卜素（Ｐ－β－ＣＡＲ）含量和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，并做６５对配比实验，结果表明，与非吸烟组比较，吸烟组的Ｐ－ＮＯ平均含量显著升高（Ｐ＜０．００１），Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ平均含量和Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－ＰＸ平均活性皆显著降低（Ｐ＜０．００１）。随吸烟时间和吸烟量的增加，其Ｐ－ＮＯ含量也增高，Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ含量和Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－ＰＸ活性降低，并均呈一定程度的的直线相关（Ｐ＜０．００１）。提示吸烟者体内的氧化和抗氧化平衡严重失调，氧自由基反应明显加剧。     

IQ CT阴极输出模块故障维修实例

故障现象机架工作正常,控制台高压ＲＥＡＤＹ灯不能点亮,即高压不能上电。打开机架,在高压控制及输出部分分别发现模拟控制板（ＡＮＡＬＯＧＹＣＯＮＴＲＯＬＬＢＯＡＲＤ）的ＤＳ７灯点亮,提示板上 １５Ｖ控制电源（ １５ＶＳＷＩＴＣＨ）故障;在阴极输出模块（ＣＡＴＨＯＤＯＵＴＰＵＴＭＯＤＵＬＥ）上ＤＳ９灯亮,提示模块 １５Ｖ控制电源（ １５ＶＳＷＩＴＣＨ）故障;在逆变诊断控制板（ＩＮＶＥＲＴＥＲＤＩＡＧＮＯＳＴＩＣＢＯＡＲＤ）上的ＤＳ１５灯点亮,提示板上 １５Ｖ控制电源（ １５ＶＳＷＩＴＣＨ）故障;在系统控制板（ＳＹＳ…     

一氧化氮等自由基对矽肺患者损伤效应的研究

检测７３例矽肺患者和６０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）、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）和过氧化脂质（Ｅ－ＬＰＯ）值的结果表明,与对照组比较,患者组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）,Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ平均值均显著升高（Ｐ＜０．００１）;上述检测值与患者病程、病情、肺功能状态均有相关;逐步回归表明,患者病程与Ｐ－ＮＯ、Ｐ－ＶＥ、Ｅ－ＳＯＤ、Ｅ－ＬＰＯ值相关最为密切;提示矽肺患者体内一氧化氮和氧自由基反应病理性加剧,氧化抗氧化平衡严重失调     

美国INVIVO公司TVS型监护仪维修2例

美国ＴＶＳ型多功能监护仪是美国ＩＮＶＩＶＯＲＥＳＥＡＲＣＨＩＮＣ公司产品 ,可监测心电、无创血压、血氧饱和度、脉搏、呼吸、体温、有创血压等参数 ,其硬件电路包括有电源部分（ＡＢ０６Ｌ、ＡＢ０６Ｗ）、主处理板部分（ＡＢ３０）、矢量逻辑板（ＡＢ０６Ｃ）、矢量模拟板（ＡＢ０６Ｃ）、信号处理板（ＡＢ０６Ｆ１）、血压测试板（ＡＢ０６ＤＪ）、有创血压板（ＡＢ０６Ｓ）、血氧饱和度测试板（ＡＢ３６）、心电测试部分（ＡＢ０６Ｅ、ＡＢ０６Ｋ）、体温和呼吸测试板（ＡＢ０６Ｔ）、偏转放大器（ＡＢ０６Ｈ）、显示器ＣＲＴ、ＣＲ…     

库尔特MD10血球计数仪改MD18的方法

１软件库尔特ＭＤ１０（Ｅ版本）在一张高密小盘上载有：（１）ＤＯＳ５．０系统文件５个：ＩＯ．ＳＹＳ、ＭＳ－ＤＯＳ．ＳＹＳ、ＣＯＭＭＡＮＤ．ＣＯＭ、ＨＩＭＥＭ．ＳＹＳ、ＲＡＭ－ＤＲＩＶＥＲ·ＳＹＳ。其中前三个文件是ＤＯＳ的核心，完成操作系统的基本功能；ＨＩＭＥＭ．ＳＹＳ可以提供上位内存，ＲＡＭＤＲＩＶＥＲ．ＳＹＳ可用建立一个虚拟盘。（２）系统配置、自动批处理文件各１个：ＣＯＮ－ＦＩＧ．ＳＹＳ、ＡＵＴＯＥＸＥＣ．ＢＡＴ。前者为程序的运行提供运行环境，包括用ＨＩＭＥＭ．ＳＹＳ开辟上位内存和用ＲＡＭＤＲＩ…     

产ESBL肺炎克雷伯菌医院感染分子流行病学研究

目的 明确产ＥＳＢＬ肺炎克雷伯菌医院感染发生率及其流行病学特征。方法 收集,分离菌株,进行药敏实验和ＥＳＢＬ检测;ＰＣＲ扩增ｂｌａＴＥＭ和ｂｌａＳＨＶ基因,等电聚焦测定β－内酰胺酶的等电点,染色体ＤＮＡ的ＰＦＧＥ分型以及进行病例资料分析。结果 共分离到１０４株非重复肺为克雷伯菌,产ＥＳＢＬ株占１３．５％。感染株ＥＳＢＬ阳性率明显高于院外感染株．;ＥＳＢＬ阳性菌对ＣＰＤ,ＣＴＸ,ＣＡＺ,ＣＴＲ,ＡＴ     

吸烟对抗氧化类维生素和抗氧化酶活性的影响

为探讨吸烟与抗氧化类维生素及氧自由基的关系，我们检测了８７１例健康吸烟者和３４８例健康非吸烟者血浆维生素Ｃ（Ｐ－ＶＣ）、维生素Ｅ（Ｐ－ＶＥ）、β－胡萝卜素（Ｐ－β－ＣＡＲ）、过氧化脂质（Ｐ－ＬＰＯ）含量及红细胞超氧化物歧化酶（Ｅ－ＳＯＤ）活性。结果表明，与非吸烟组比较，吸烟组的Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ显著降低，Ｐ－ＬＰＯ显著升高；６５例相同年龄男性吸烟者的Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ和Ｅ－ＳＯＤ均随吸烟史及吸烟量的增加而降低，Ｐ－ＬＰＯ随吸烟史及吸烟量的增加而升高，并均呈一定程度的直线相关；提示吸烟者体内的氧化和抗氧化平衡严重失调，氧自由基反应和脂质过氧化反应明显加剧。     

抗氧化营养素对主动脉内皮细胞脂质过氧化损伤的影响

探讨抗氧化营养素硒（Ｓｅ）、维生素Ｅ（ＶＥ）、维生素Ｃ（ＶＣ）及β－胡萝卜素（ＢＣ）防治动脉粥样硬化形成的可能作用及机制。方法：以原代培养的小牛主动脉内皮细胞（ＢＡＥＣ）为模型、以ｏｘＬＤＬ为损伤因素,利用硫代巴比妥酸荧光比色法（ＴＢＡ）和单核细胞（ＨＬ－６０）粘附计数法观察抗氧化营养素对ＢＡＥＣ脂质过氧化及单核细胞粘附性的影响。在体外培养的ＢＡＥＣ中加入不同剂量的抗氧化营养素：Ｓｅ的终浓度（μｍｏｌ）分别为１．０、５．０、１０．０;ＶＥ的终浓度（μｍｏｌ）分别为１２．５、２５．０、５０．０;ＶＣ的终浓度（μｍｏｌ）分别为２０．０、５０．０、１００．０;ＢＣ的终浓度（μｍｏｌ）分别为１．０、５．０、１０．０;共同培养１２ｈ后,再与终浓度为０．１ｍｇＰｒ／ｍｌ的ｏｘＬＤＬ继续培养２４ｈ,取贴壁细胞及培养液进行检测。结果：（１）抗氧化营养素组细胞培养上清液中脂质过氧化物（ＭＤＡ）的含量明显地低于ｏｘＬＤＬ组。其中Ｓｅ的三个剂量组培养上清液中ＭＤＡ分别降低了５．１１％、１５．２２％和１９．３６％;ＶＥ的三个剂量组降低１０．８９％、１８．０２％和２９．０９％;ＶＣ的三个剂量组降低了７．４２％、１７．２４％和２１．１?     

Antioxidant supplementation effects on low-density lipoprotein oxidation for individuals with type 2 diabetes mellitus.

OBJECTIVE: This study compared susceptibility to oxidation of low-density lipoproteins (LDL) of non-diabetic and diabetic (Type 2) men and examined the response of diabetic men to antioxidant supplementation (alpha-tocopherol, beta-carotene and ascorbate). RESEARCH DESIGN AND METHODS: Twenty adult non-diabetic and 20 diabetic men were recruited. Oxidation of LDL was assessed by four different assay systems, and the extent of oxidation was assessed by four different measurements. Diabetic men received eight weeks of placebo ("baseline"), twelve weeks of antioxidant supplements ("treated") and eight weeks of placebo ("post-treatment"). Supplements provided 24 mg of beta-carotene, 1000 mg of ascorbate and 800 IU of alpha-tocopherol daily. RESULTS: With Cu oxidation at 37 degrees C, thiobarbituric reactive substances (TBARS) formation was significantly higher (p=0.032) and loss of free amine groups was significantly greater (p=0.013) in the LDL from diabetic subjects than controls. Antioxidant supplementation of diabetic subjects significantly decreased all parameters of LDL oxidation with Cu at 30 degrees C and 37 degrees C. At 30 degrees C the lag phase increased from 55 to 129 minutes (p<0.0001); conjugated diene formation decreased from 1.23 to 0.62 OD units (p<0.0001); TBARS formation decreased from 78 to 33 nmoles MDA/mg LDL protein (p<0.0001); and free amine loss decreased from 41 to 12% (p<0.0001). With Cu oxidation at 37 degrees C, similar changes occurred. CONCLUSIONS: These studies indicate that the LDL from diabetic subjects are more susceptible to oxidation than LDL from non-diabetic subjects. Supplementation of diabetic subjects with antioxidant vitamins significantly decreases susceptibility of LDL to oxidation by Cu. These studies are consistent with epidemiological and intervention studies suggesting that antioxidant vitamin use significantly decreases risk for coronary heart disease.     

大豆异黄酮对低密度脂蛋白氧化修饰的抑制作用

为探讨大豆异黄酮 (SI)在体外及体内对低密度脂蛋白 (LDL)氧化修饰的作用特点及其与α 生育酚的异同 ,采用密度梯度超速离心法分离制备血清LDL后 ,建立了Cu2 + 诱导LDL氧化修饰反应模型 ,体外向模型中直接加入SI和α 生育酚后 ,通过监测反应体系中硫代巴比妥酸反应物质 (TBARS)和共轭双烯生成量的变化观察它们的作用。体内实验通过先补加SI于高脂饲料喂饲大鼠 ,再测定血中LDL对Cu2 + 诱导氧化的敏感性以反映SI的效果。结果表明 ,体外无论在启动LDL氧化反应前还是反应后加入SI,均显著降低体系中TBARS和共轭双烯的生成 ,并呈现剂量相关关系 ;仅在启动LDL氧化反应前加入α 生育酚显示良好的抑制效果 ,当启动LDL氧化反应后加入α 生育酚则未表现任何防护作用。在大鼠喂饲实验中 ,高脂饲料导致动物LDL对氧化修饰的敏感性增加 ,补加SI对此有明显的拮抗作用。可见 ,在体外SI是与α 生育酚作用有所区别的一类天然抗氧化剂 ,它在体外和体内均能显著抑制LDL的氧化修饰     

维生素C在低密度脂蛋白氧化修饰中作用的体外实验

目的：研究维生素C（VC）在预防低密度脂蛋白（LDL）氧化修饰中的作用。方法：在Cu^2 介导的无细胞体系中分别加入VC10,50,100,200μmol/L,巨噬细胞体中分别加入VC50,100,200μmol/L,以维生素（200μmol/L）为阳性对照,不添加维生素C组（VC0）为阴性对照,测定荧光物质（lipofusin),硫代巴比妥酸反应物质（TBARS）,LDL电泳迁移率（Rf),氧化型低密度脂蛋白（Ox-LDL),LDL氧化过程中的停滞时间等LDL的氧化修饰情况。结果：Cu^2 介导的无细胞体系中,高剂量VC（100,200μmol/L）在3,6,9h均能发挥其抗氧化作用,抑制TBARS,Ox-LDL生成,而VC低剂量（10,50μmol/L）则无此作用,相反在3h表现出促Ox-LDL生成作用,在巨噬细胞体系中,高剂量组（100,200μmol/L)能显著降低荧光物质,TBARS和LDL电泳迁移率（Rf),延长LDL氧化过程中的停滞时间,并存在剂量反应关系。结论：VC在LDL氧化修饰中具有双重作用,低剂量时能促进LDL氧化,高剂量时表现出抗氧化作用。     

镁对人体低密度脂蛋白氧化修饰的影响

目的 :　观察镁对人体低密度脂蛋白 (LDL)氧化修饰的影响。方法 :　一次性密度梯度超速离心法制备人天然 LDL,共轭二烯法检测 Mg2 +对 Cu2 +介导的 LDL氧化反应敏感性的影响 ,硫代巴比妥酸反应物 (TBARS)法检测 Mg2 +对 Cu2 +和内皮细胞介导的 LDL氧化修饰程度的影响。结果 :　 1 .LDL+Cu2 + +Mg2 +各剂量组 LDL氧化反应潜伏期较 LDL+Cu2 +组明显延长 ;2 .LDL+Cu2 + +0 .3mmol/L Mg2 +组和 LDL+Cu2 + +0 .6mmol/L Mg2 +组 TBARS低于 LDL+Cu2 + 组 ,P<0 .0 1 ;3.在内皮细胞介导的 LDL氧化体系中 ,补 Mg2 + 各剂量组 TBARS低于空白对照组 ,LDL+Mg2 +各剂量组 TBARS低于 LDL组 ,差异均具有显著性 (P<0 .0 5)。结论 :　在一定实验条件下 Mg2 +可阻断 LDL的氧化反应     

镁对氧化低密度脂蛋白致内皮细胞损伤的保护作用

为探讨镁对内皮细胞的保护作用 ,用一次性密度梯度超速离心法制备人低密度脂蛋白 (LDL) ,以共轭二烯法和改良八木法检测Mg2 +(0 3、0 6、1 2和 2 4mmol L)对Cu2 +介导LDL氧化反应潜伏期和氧化修饰程度的影响。另将传至 2～ 3代的人脐静脉内皮细胞分为正常对照组、ox LDL对照组、补镁组和ox LDL +Mg2 +组 ,改良八木法测定细胞脂质过氧化物水平 ,黄嘌呤氧化法测定细胞外SOD活性 ,DTNB法测定含硒和不含硒GSH Px活性。结果显示 ,(1)Mg2 +各剂量组明显延长Cu2 +介导LDL氧化反应潜伏期 ,0 3和 0 6mmol LMg2 +显著降低TBARS的生成 ;(2 )与ox LDL组相比 ,ox LDL +Mg2 +各剂量组TBARS生成量显著下降 ,SOD活性显著升高 ,含硒GSH Px酶活力显著升高 ,不含硒GSH Px活力显著升高。提示镁抑制LDL的氧化修饰 ,补镁能降低细胞脂质过氧化物水平 ,增强抗氧化酶的的活性     

HDL oxidability and its protective effect against LDL oxidation in Type 2 diabetic patients

Low density lipoprotein (LDL) oxidation is a crucial step in the atherosclerotic process. High density lipoprotein (HDL)-associated enzymes such as paraoxonase could exert a protective effect on LDL oxidation in the arterial wall, an effect which could be impaired in Type 2 diabetes mellitus (T2DM). We studied copper-induced oxidation in LDL and HDL isolated from 17 T2DM patients with fair glycaemic control and HDL-cholesterol within normal range and 17 healthy normolipidaemic control subjects. To evaluate the effect of HDL on LDL oxidation in diabetic and control subjects, we assessed copper-induced oxidation in HDL/LDL mixtures, with each lipoprotein isolated from the same subject. Relationships with HDL chemical composition, alpha-tocopherol content and serum paraoxonase activity were investigated. Oxidation was promoted by lipoprotein incubation with copper and then thiobarbituric acid reactive substances (TBARS), conjugated diene production and electrophoretic mobility in agarose gel were measured. In T2DM subjects HDL oxidation was higher than in controls. However, HDL from diabetics was as effective as control HDL to inhibit LDL oxidation. Neither HDL chemical composition nor serum paraoxonase activity showed any difference as compared to control subjects. In contrast, HDL from T2DM subjects showed a higher alpha-tocopherol content which positively correlated with HDL oxidability. Paraoxonase activity positively and strongly correlated with HDL inhibitory effect on LDL oxidation in patients and controls belonging to the heterozygous activity phenotype. Besides, LDL oxidability showed no differences between patients and controls. These results suggest that fairly-controlled T2DM patients with HDL-cholesterol levels within normal range show: 1) normal HDL ability to inhibit LDL oxidation related to normal paraoxonase activity; 2) higher HDL oxidability in spite of its high alpha-tocopherol content, which could favour tocopherol-mediated peroxidation and 3) normal LDL oxidability possibly due to the lack of significant lipoprotein structural alterations.     

维生素E和β胡萝卜素对巨噬细胞氧化修饰低密度脂蛋白的影响

目的 :　研究维生素 E(VE)、β胡萝卜素 (βC)对巨噬细胞 (MΦ )介导的低密度脂蛋白 (LDL)氧化修饰能力的影响。方法 :　于培养成熟的 MΦ中分别加入不同剂量的 VE(40、1 0 0、2 0 0 μmol/L)和 βC(0 .5、1 .0、2 .0 μmol/L) 37℃孵育 2 4 h,通过测定培养物上清液中硫代巴比妥酸反应物 (TBARS)、荧光物质 (Lipofusin)、LDL电泳迁移率 (Rf)及共轭二烯 (Dienes)的形成 ,反映LDL的氧化修饰程度。结果 :　体外补充 VE可以显著降低培养物上清液中 TBARS、荧光物质以及共轭二烯的形成 ,明显抑制 LDL的电泳迁移率 ,随剂量增大作用加强 ;βC低剂量组 (0 .5μmol/L)可显著降低培养物上清液中 TBARS、荧光物质以及共轭二烯的形成 ,明显抑制 LDL的电泳迁移率 ,其余各组无明显影响。结论 :　 VE、βC均可抑制 MΦ介导 LDL氧化修饰的能力 ,并具一定的量效关系 ,提示在 MΦ氧化修饰 LDL的可调节因子中 ,抗氧化营养素是一种有效措施     

beta-Carotene and alpha-tocopherol concentration and antioxidant status in buccal mucosal cells and plasma after oral supplementation

The uptake of alpha-tocopherol and beta-carotene and their antioxidative effect in plasma and buccal mucosal cells after oral application in twelve subjects is demonstrated in our study. The effect on the antioxidative status was evaluated using a modified thiobarbituric acid-reactive substance (TBARS) method. As expected, the supplement of 134.2 mg alpha-tocopherol/d and 25 mg beta-carotene/d for 7 d resulted in a significant increase of alpha-tocopherol and beta-carotene concentration in plasma (P<0.05). In buccal mucosal cells, the concentration of beta-carotene increased after supplementation (P<0.05), whereas the concentration of alpha-tocopherol remained constant. A decrease in TBARS (P<0.05) was found in buccal mucosal cells but not in plasma. In conclusion, an uptake of the supplemented antioxidants was detected in plasma and in buccal mucosal cells. There was significant change in beta-carotene concentration and oxidative stress as measured using a modified TBARS test in buccal mucosal cells, but not in the plasma.     

Effects of tomato juice consumption on plasma and lipoprotein carotenoid concentrations and the susceptibility of low density lipoprotein to oxidative modification

Effects of tomato juice supplementation on the carotenoid concentration in lipoprotein fractions and the oxidative susceptibility of LDL were investigated in 31 healthy Japanese female students. These subjects were randomized to one of three treatment groups; Control, Low and High. The Control, Low and High groups consumed 480 g of a control drink, 160 g of tomato juice plus 320 g of the control drink, and 480 g of tomato juice, providing 0, 15 and 45 mg of lycopene, respectively, for one menstrual cycle. The ingestion of tomato juice, rich in lycopene but having little beta-carotene, increased both lycopene and beta-carotene. Sixty-nine percent of lycopene in plasma was distributed in the LDL fraction and 24% in the HDL fraction. In the Low group, the lycopene concentration increased 160% each in the VLDL+IDL, LDL and HDL fractions (p<0.01). In the High group, the lycopene concentration increased 270% each in the VLDL+IDL and LDL fractions, and 330% in the HDL fraction (p<0.01). Beta-carotene also increased 120% and 180% in LDL fractions of the Low and the High groups, respectively. Despite these carotenoid increases in LDL, the lag time before oxidation was not prolonged as compared with that of the Control group. The propagation rate decreased significantly after consumption in the High group. Multiple regression analysis showed a positive correlation between lag time changes and changes in the alpha-tocopherol concentration per triglyceride in LDL, and a negative correlation between propagation rate changes and changes in the lycopene concentration per phospholipid in LDL. These data suggest that alpha-tocopherol is a major determinant in protecting LDL from oxidation, while lycopene from tomato juice supplementaion may contribute to protect phospholipid in LDI, from oxidation. Thus, oral intake of lycopene might be beneficial for ameliorating atherosclerosis.     

Long-chain n-3 polyunsaturated fatty acid from fish oil modulates aortic nitric oxide and tocopherol status in the rat

In spite of their high oxidisability, long-chain n-3 PUFA protect against CVD. Dietary fatty acids modulate the fatty acid composition of lipoproteins involved in atherosclerosis. We thought that if long-chain n-3 PUFA were able to increase NO production by the aorta, then by its antioxidant activity the NO will prevent lipid peroxidation. However, the beneficial effect of NO in vivo on VLDL + LDL oxidation would only be possible if NO could diffuse to their lipidic core. Rats were fed maize oil- or fish oil as menhaden oil- (MO) rich diets for 8 weeks, to study the effects of MOon aortic NO production, NO diffusion into VLDL + LDL, the extent of oxidation in native VLDL + LDL and their oxidisability ex vivo. Aortic NO production and its alpha-tocopherol content were increased and n-3 PUFA were incorporated into the VLDL + LDL. In spite of the higher peroxidisability and the low alpha-tocopherol in native VLDL + LDL from rats fed MO, native VLDL + LDL from the two groups shared similar electrophoretic patterns, conjugated dienes, thiobarbituric acid-reactive substances, total antioxidant capacity, and NO diffusibility on VLDL + LDL, indicative of an in vivo protection against oxidation. However, these results do not correlate with the ex vivo oxidisability of VLDL+ LDL, as NO is lacking. Thus, the in vivo beneficial effects can be explained by increased a-tocopherol in aorta and by a compensatory effect of NO onVLDL + LDL against the low alpha-tocopherol levels, which may contribute to the anti-atherogenic properties of fish oil.