核黄素对大鼠脂质过氧化影响的研究

为探讨核黄素对大鼠脂质过氧化的影响,采用随机区组设计,研究了不同核黄素水平对大鼠核黄素营养状况及脂质过氧化的影响。饲养６周后发现,核黄素缺乏引起大鼠全血谷胱甘肽还原酶活性系数升高及全血还原型谷胱甘肽含量降低,全血丙二醛浓度升高及红细胞超氧化物歧化酶活性降低。结论认为核黄素缺乏会引起大鼠脂质过氧化程度升高     

核黄素和β—胡萝卜素联用对二甲基亚硝胺致大鼠脂质过氧化的影响

为进一步探讨亚硝胺通过过氧化物而致癌的可能途径，以及VB2和β-C联用可能通过抑制脂质过氧化反应而影响亚硝胺致癌的机制，给予二甲基亚硝在（NDMN），同时补充核黄素和β-胡萝卜素，观察大鼠体内抗氧化酶活性和脂质过氧化物含量的变化．结果显示：NDMN可使大鼠血红细胞、肝肾匀浆SOD活性和全血GSH-Px活性下降，血清、肝肾匀浆MDA和血清ROOH产生增多．同时添加核黄素和β-胡萝卜素后，红细胞和肝匀装SOD活性、全血GSH-Px活性显著高于NDMN组．血清、肝匀浆MDA含量和血清ROOH含量显著低于NDMN组．表明该黄素和β-胡萝卜素联用可对抗由NDMN引发的脂质过氧化，提示核黄素和β-胡萝卜素联用有预防NDMN致癌的作用．     

核黄素对脂质代谢影响研究进展

核黄素又称维生素B2,是人体必需的水溶性维生素之一,广泛存在于肉蛋奶及多种蔬菜水果之中,以辅酶形式参与体内各种氧化还原反应,与能量代谢密切相关,核黄素缺乏易导致眼、口角、皮肤炎症,临床主要用于防治口角炎、舌炎、阴囊炎、结膜炎、脂溢性皮炎等核黄素缺乏症。文章综述了核黄素对脂质代谢的调节作用,具体表现为抑制胆固醇生物合成,维持肝脏对脂质的正常转运,降低甘油三酯、游离脂肪酸、低密度脂蛋白与极低密度脂蛋白水平,防止脂质过氧化和脂质蓄积,以期为核黄素作为主要药物或辅助药物在心血管疾病等脂质代谢相关疾病的治疗中发挥作用。     

毒害物质与人体脂质过氧化的关系(综述)

脂质过氧化是近年来发展起来的重要中毒机理学说，它可引起各种生物膜的损伤。谷胱甘肽-S-转移酶(GST)是二相反应的重要酶系，催化具有亲合位点的谷胱甘肽(GSH)，与多种亲电子物质、致癌物、亲脂性化学物质结合，参与细胞代谢解毒，清除自由基。随着自由基学说的发展对脂质过氧化作用的研究不断深入，现就人体受几种毒害物质作用引起脂质过氧化变化加以概述。     

体内脂质过氧化水平的影响因素

脂质过氧化是一种常见的氧化损伤类型,参与多种疾病的病理进程,许多因素均可影响体内脂质过氧化的水平。此文汇总了近年来国内外人群流行病学资料,分别从个体因素(年龄、性别、体重指数)、生活方式(吸烟、饮酒、体育锻炼等)、环境因素方面综述其对脂质过氧化标志物的影响。研究内容显示,不同个体因素对体内脂质过氧化物的影响尚存在争议;吸烟、饮酒等生活方式和来自室内外的空气污染均是升高脂质过氧化水平的危险因素,而规律性体育锻炼则是降低脂质过氧化的保护因素。更多的流行病学证据和深入的机制研究亟待开展以更好认识脂质过氧化的影响因素及其在疾病发生发展中的作用,从而实现慢性病的早期预防。     

甲基汞对大鼠肝细胞脂质过氧化作用的影响

为探讨脂质过氧化作用与甲基汞中毒的机理，采用在体灌注实验和离体模型实验方法，研究了甲基汞在离体大鼠肝细胞脂质过氧化模型中的反应及汞对大体大地细胞脂质过氧化作用，结果表明，甲基汞引起的大鼠游离细胞脂质过氧化作用和细胞失活均匀与汞的浓度和作用时间呈正相关关系。     

免疫毒性的脂质过氧化机制研究进展

免疫系统是机体重要的防御系统，具有免疫防御、免疫监视和免疫稳定的功能。它由免疫器官、免疫细胞和免疫分子组成。脂质过氧化（lipkd peroxidation，LPO）是脂质中不饱和脂肪酸（LH）氧化降解的链反应过程，由启动、延伸、终止三个阶段组成。脂质过氧化过程的延伸阶段产生多种自由基如脂过氧自由基（LOO^-）、脂氧自由基（LO^-）和脂自由基（L^-），终止阶段产生多种小分子产物如丙二醛（MDA）。     

免疫毒性的脂质过氧化损伤机制研究

免疫系统是机体重要的防御系统，具有免疫防御、免疫监视和免疫稳定的功能。它由免疫器官、免疫细胞和免疫分子组成。脂质过氧化（Lipid Peroxidation，LPO）是脂质中不饱和脂肪酸（LH）氧化降解的链反应过程，由启动、延伸、终止3个阶段组成。脂质过氧化过程的延伸阶段产生多种自由基如脂过氧自由基（LOO^-）、脂氧自由基（LO^-）和脂自由基（L^-），终止阶段产生多种小分子产物如丙二醛（MDA）。这些产物可以引起多种细胞功能的损伤，并且和多种疾病的发生、发展关系密切。而脂质过氧化损伤和免疫细胞功能损害之间关系的阐明，则有助于全面理解衰老、癌变等病理过程。     

临床营养学研究中脂质过氧化的评价方法

危害人类健康的许多疾病的发病机制都与营养因素有关，尤其是与自由基引发的氧化作用有直接联系。目前脂质过氧化测定已成为临床诊断氧化损伤相关疾病的重要依据。本文从底物测定和产物测定两方面综述脂质过氧化检测方法，介绍自由基、过氧化物及低密度脂蛋白等多种检测方法，并阐明了各种方法的优缺点及应用领域，以便根据不同的目的和条件进行选择，获得准确可靠的结果，使其成为临床诊断及营养学研究的有效辅助手段。     

炎热干旱环境健康成人血清过氧化脂质,巯基和粘蛋白含量探讨

炎热干旱环境健康成人血清过氧化脂质、巯基和粘蛋白含量探讨刘开泰目前研究已经证实，各种有害物质均可引起过氧化脂质（Ｌｐｏ）、巯基（－ＳＨ）和粘蛋白的异常改变，从而导致机体多种病理性的损害。不同地区因地理环境、气候条件、生活习惯及营养状况等诸因素的不同，...     

RIBOFLAVIN STATUS AND RESISTANCE TO PLASMODIUM

Riboflavin deficiency in host cells enhances resistance to malarial parasites. The mechanism appears to be unrelated to changes in the erythrocyte's defenses against oxidative injury but may be related to metabolism of the parasite.     

煤矽肺患者血中微量元素和脂质过氧化的改变

目的 了解煤矽肺患质过氧化水平。方法 检测煤矽肺患血清中微量元素Cu、Zn含量及MDA、SOD和GSH的水平。结果 煤矽肺患血清中Cu、Zn、MDA、SOD明显高于对照组,GSH明显低于对照组。煤矽肺患工龄、期别不同,其脂质过氧化水平也不同。吸烟可促进脂质过氧化发生改变。结论 煤尘可引起接触人群脂质过氧化紊乱。脂质过氧化可能是影响煤矽肺发生、发展的主要因素之一。     

PULMONARY ARTERIAL LIPID DEPOSITS AFTER INTRAVENOUS LIPID INFUSIONS IN NEONATES

Three neonates who received lipid infusions were found at autopsy to have distinctive lipid lesions in small pulmonary arteries. All had histological evidence of pulmonary hypertension which may have provoked vascular damage.     

半胱氨酸对TNT染毒大鼠毒性保护作用的初探

本文初步探讨了半胱氨酸对TNT急性染毒大鼠肝组织申GSH、GSSG、脂质过氧化产物和血清铜蓝蛋白含量以及GSH-Px、磷酸化酶a活性的影响。结果表明,TNT中毒可使脂质过氧化产物含量升高,加速血清铜蓝蛋白的耗竭。半胱氨酸对治疗和预防TNT中毒有一定的作用。为TNT中毒的硝基还原活化机理提供了参考资料。亦为中毒防治开辟了新途径。     

镍染毒对小鼠脾脏的脂质过氧化损伤

目的从氧化应激角度探讨硫酸镍致小鼠脾脏脂质过氧化水平和抗氧化能力的变化。方法硫酸镍0．8，2．0，5．0mg／kg小鼠每日愎腔注射染毒，连续30d。制备脾脏组织匀浆，采用分光光度法测定脾脏总抗氧化能力(T—AOC)和谷胱甘肽(GSH)含量；黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活力；用TBA法测定丙二醛(MDA)含量。结果镍可抑制小鼠脾脏SOD活力，使T—AOC和GSH含量降低，MDA含量增加，并随染毒剂量增加，其效应逐渐增加。结论硫酸镍可致小鼠脾脏抗氧化能力下降，引起脂质过氧化损伤。     

Ethanol Extract of Liriope platyphylla Root Attenuates Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice via Regulation of Lipogenesis and Lipid Uptake

Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder that causes excess lipid accumulation in the liver and is the leading cause of end-stage liver disease. Liriope platyphylla is a medicinal herb that has long been used to treat cough, obesity, and diabetes. However, the effect of Liriope platyphylla on NAFLD has not been studied. The aim of this study was to investigate the effect of Liriope platyphylla root ethanolic extract (LPE) on hepatic lipid accumulation in high-fat diet (HFD)-induced obese mice. Six-week-old C57BL/6 male mice were fed a HFD for 8 weeks and then treated with LPE (100 or 250 mg/kg/day) by oral gavage for another 8 weeks. Body weight gain and liver weight were significantly lower in the 250 mg/kg LPE-treated HFD group than in the vehicle-treated HFD group. Histological analysis of liver sections demonstrated that LPE treatment reduced lipid accumulation compared to the vehicle treatment. The serum total cholesterol, AST, and ALT levels significantly decreased in the LPE-treated HFD group compared to those in the vehicle-treated HFD group. The LPE significantly decreases the protein expression levels of SREBP1, ACC, p-ACC, FAS, and SCD1, which are involved in lipogenesis, and PPARγ, CD36/FAT, and FATP5, which are involved in fatty acid uptake, both in vivo and in vitro. Thus, LPE may attenuate HFD-induced NAFLD by decreasing lipid accumulation by inhibiting lipogenesis and fatty acid uptake.     

煤矿粉尘接触和人群脂质过氧化水平的观察

目的 为了解煤矿粉尘接触和人群脂质过氧化水平。方法 检测煤矿粉尘接触量和人群脂质过氧化水平。结果 矿井巷道和采煤面粉尘浓度低于国家标准装渣,放炮作业和各工种一次最高浓度均超国标。除矿井出风口外,地面各监测点可吸入粉尘均在容许范围,粉尘接触人群ＳＯＤ活性降低,井下工人ＭＤＡ增加,吸烟者更显著,煤工尘肺患者两项指标同时提高,结论 提示煤尘接触引起人群脂质过氧化代谢紊乱,紊乱程度和粉尘接触量有关,吸烟是     

Polyunsaturated eicosapentaenoic acid changes lipid composition in lipid rafts

Summary Background Polyunsaturated fatty acids (PUFAs) modulate immune responses particularly by affecting T cell function and are applied clinically as adjuvant immunosuppressants in the treatment of various inflammatory diseases. However, the molecular mechanisms of PUFA–induced immunosuppressive effects are not yet elucidated. Membrane lipid rafts are functional plasma membrane microdomains characterized by a unique lipid environment. Since lipid interactions are crucial for the formation of lipid rafts, the immunomodulatory effects of PUFAs may be due to changes of fatty acid composition in lipid rafts. Aim of the study We investigated the effects of eicosapentaenoic acid (EPA, 20:5 n – 3) supplementation on modulating lipid composition and fatty acyl substitution in their cytoplasmic and exoplasmic lipid leaflet in lipid rafts. Methods The human Jurkat E6–1 T cells were cultured in EPA–supplemented medium and the cells treated with stearic acid served as a control. Lipid rafts were isolated by discontinuous sucrose density gradient ultracentrifugation. The lipids in raft and soluble fractions from EPA–treated and control T cells were extracted and separated by gas chromatography. Raft phospholipids were analyzed by mass spectrometry. Results Our results showed that EPA treatment could alter lipid composition resulting in a considerable increase of unsaturated fatty acyl chains in lipid rafts from EPA–treated T cells compared with control cells. Effective incorporation of EPA to rafts was not only in the exoplasmic but also in the cytoplasmic membrane lipid leaflet. EPA treatment altered the lipid environment in lipid rafts. EPA presented an inhibiting effect on Jurkat T cells proliferation and inhibited IL–2Rα expression on the surface of T cells. Conclusions Our data provided evidence for an important modification in lipid composition of membrane lipid rafts and T cell function by EPA supplementation.     

不同食用油对大鼠机体脂类与过氧化脂类含量的影响

本文报告了茶油、菜油、色拉油、豆油和猪油对大鼠机体脂类水平和脂类过氧化作用的影响及两者的相关关系。结果表明:茶油和豆油有良好的阻止血脂升高的作用。血浆卵磷脂胆固醇酰基转移酶的活性在4种植物油组相近(80.26～94.03nmol/ml.h),猪油组最低(57.07nmol/ml.h)。饲猪油者肝及主动脉中脂类含量偏高。血清及心、肝、肾组织中过氧化脂类(LPO)含量以猪油组最高,茶油组较低。此外,豆油有升高组织中LPO含量的作用,而菜油和色拉油相反。实验后,饲以富含单不饱和脂肪酸油脂者,其红细胞超氧化物歧化酶活力升高,饲豆油和猪油者降低。实验末大鼠血清及肝组织中LPO与脂类(TC、TG)含量呈显著正相关(P<0.01),心,脑中此关系不明显。     

Population Semiphysiologic Kinetic Modeling and Simulation of Plasma Triglyceride Levels After Soybean Oil–Based Intravenous Lipid Emulsion Administration in Rats

Background: Soybean oil–based intravenous lipid emulsion (SO‐ILE) has clinical utility as an energy source and in lipid rescue therapy. However, an excessive infusion rate of SO‐ILE in routine use and in lipid rescue therapy may cause serious side effects. There is little information about plasma triglyceride (TG) kinetics following SO‐ILE administration. The present study aimed to develop a population semiphysiologic kinetic model of TG and to predict the TG kinetics even at extremely high concentrations in rats. Materials and Methods: TG concentration profiles after intravenous bolus (0.1, 0.25, 0.5, 1.0, 1.5, and 2.0 g/kg) or infusion (3.0 g/kg/h for 1 hour) of SO‐ILE to rats were analyzed by a kinetic model constructed with 4 pathways: apolipoprotein acquisitions, zero‐order catabolism, first‐order uptake to storage sites, and zero‐order secretion from storage sites. The developed model was subjected to internal and external validation. Results: Plasma TG concentrations appeared to decline in a biphasic manner with nonlinear TG kinetics. The developed kinetic model was well validated and found to accurately predict the external validation data. Conclusions: The proposed kinetic model accurately described TG concentrations after SO‐ILE administration at various infusion rates, including a lipid rescue regimen. The maximum acceptable infusion rate of SO‐ILE in routine use should correspond to the maximum velocity of the apolipoprotein acquisition: 0.619 g/kg/h in rats. The prediction of TG kinetics at extremely high concentrations will provide useful information for lipid rescue therapy.