枸杞总黄酮类化合物抗脂质过氧化研究

利用Ｆｅ２＋－Ｃｙｓ－Ｈｉｓ体系诱发鼠肝线粒体和红细胞产生脂质过氧化的方法,研究了枸杞总黄酮类化合物（ＴＦＬ）的抗脂质过氧化作用。结果表明,ＴＦＬ可阻断该体系诱发的鼠肝线粒体脂质过氧化,当ＴＦＬ终浓度在０．０２５～２．０ｍｇ／ｍｌ范围时,对丙二醛（ＭＤＡ）生成阻断率为３８．３８％～９９．９６％,呈剂量－效应关系,同时具有保持线粒体膜流动性的作用。扫描电镜观察到ＴＦＬ对脂质过氧化所致红细胞形态结构的破坏有保护作用。     

酸枣、山楂、葡萄的体外抗氧化作用研究

采用Ｆｅ２＋－半胱氨酸诱发大鼠肝微粒体生成丙二醛（ＭＤＡ）和用过氧化叔丁醇（ｔｅｒｔ－ｂｕｔｙｌｈｙ－ｄｒｏｐｅｒｏｘｉｄｅ）损伤大鼠红细胞生成ＭＤＡ两种损伤体系,分别观察酸枣、山楂、葡萄３种果汁的体外抗脂质过氧化作用。结果表明,在２．５～３．３ｍｇ／ｍｌ浓度下,葡萄、山楂和酸枣３种果汁对Ｆｅ２＋－半胱氨酸诱发大鼠肝微粒体ＭＤＡ生成的抑制率分别达到４６．２％、９８．３％和９９．１％,这３种果汁对过氧化叔丁醇所致大鼠红细胞生成ＭＤＡ的抑制率分别为葡萄汁（５５．６ｍｇ／ｍｌ）５８．５％、山楂汁（１３．９ｍｇ／ｍｌ）３８．７％和酸枣汁（８．３ｍｇ／ｍｌ）３８．７％。采用ＥＳＲ测定３种果汁对Ｏ－２和ＯＨ自由基的清除作用。结果表明高浓度时,葡萄汁（１３４ｍｇ／ｍｌ）、山楂汁（５０ｍｇ／ｍｌ）和酸枣汁（５０ｍｇ／ｍｌ）对Ｏ－２的清除率分别为７４．７％、８５．８％和８４．０％,对ＯＨ自由基的清除率分别为８６．３％、９７．８％和９６．７％。上述结果表明,这３种果汁具有较强的抗氧化作用。     

大豆纤维对实验性高脂大鼠动脉粥样硬化的预防作用和抗氧化效果

研究大豆纤维（ＳＦ）对实验性高脂大鼠的血液和肝组织脂质过氧化物（ＬＰＯ）水平、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性和血脂指标的影响。结果表明，大豆纤维膳能明显降低血清总胆固醇（ＴＣ）、低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）和致动脉粥样硬化指数（ＡＩ）（Ｐ＜０．０５）。血清和肝组织ＬＰＯ水平明显下降，ＧＳＨ－Ｐｘ活力显著提高（Ｐ＜０．０５）．ＳＦ对血脂降低和对氧化低密度脂蛋白（Ｏｘ－ＬＤＬ）的阻断作用可能对防止动脉粥样硬化（ＡＳ）的形成起主要作用。     

绿茶及绿茶多酚抗羟自由基诱导的大鼠肝脂质过氧化作用

本研究采用Ｆｅ２＋，Ｈ２Ｏ２反应生成ＯＨ·诱导大鼠离体肝脏脂质过氧化反应体系，用ＧＴ和ＧＴＰ作为抗氧化剂观察对肝脂质过氧化的阻抑作用。随ＧＴ和ＧＴＰ浓度的升高对ＭＤＡ的抑制率分别为０．７７４～０．８９２，０．８１４～０．９７６，浓度与ＭＤＡ之间存在剂量效应关系。     

两种调合油对人群血脂及丙二醛的影响

将茶油、菜油、玉米油、棕榈油及麻油等食油按一定比较配成１、２号调合油。Ⅱ型高脂血症人群食用１号调合油１个月后，血清Ｔｃ、ＬＤＬ－Ｃ及ＴＧ分别下降１１．０％、１３．５及１７．９％（Ｐ〈０．０１），血清丙二醛（ＭＤＡ）下降１９．１％（Ｐ〈０．０１），而ＨＤＬ－Ｃ／Ｔｃ升高１９．９％（Ｐ〈０．０１）。表明１号调油具有降血脂及抗脂质过氧化的作用，可作为高脂血症患者的辅助治疗食油。血脂正常人群食用２号调合油     

三氧化二锑中毒性肝损害的实验研究

每天给小鼠腹腔注射４０ｍｇ／ｋｇ体重三氧化二锑后可引起明显的肝损害。进入体内的锑主要蓄积于肝脏；染毒２８天时，染毒组肝匀浆及肝线粒体中丙二醛（ＭＤＡ）分别为３０．２７±１．８９μｍｏｌ／Ｌ和４７．２７±１．２１μｍｏｌ／Ｌ，显著高于对照组（Ｐ＜０．０１）；肝线粒体Ｎａ＋Ｋ＋－ＡＴＰ酶及Ｃａ２＋－ＡＴＰ酶活性下降至４．８３５６±０．２６５和２．８０７２±０．１４９活力单位，明显低于对照组（Ｐ＜０．０１）。结果提示：肝脏是锑的主要蓄积器官之一，锑中毒性肝损害发病机理可能与肝脏脂质过氧化及肝线粒体ＡＴＰ酶活性受到抑制有关。     

紫苏油和松籽油对大鼠机体脂类和脂质过氧化的影响

在高脂饲料中分别加入６％的紫苏油和松籽油，在实验动物总能量与主要营养素摄入基本相同、脂肪占总能量３２．６％的条件下饲喂Ｗｉｓｔａｒ雄性成年大鼠３周。结果表明，紫苏油和松籽油对高脂血症大鼠均有一定的调整血脂作用。紫苏油和松籽油组大鼠血清甘油三酯（ＴＧ）、总胆固醇（ＴＣ）、低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）、ＬＤＬ－Ｃ与高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）的比值（ＬＤＬ－Ｃ／ＨＤ－Ｌ－Ｃ）、致动脉粥样硬化指数（ＡＩ）的增加值和ＨＤＬ－Ｃ／ＴＣ、卵磷脂胆固醇酰基转移酶（ＬＣＡＴ）活性的下降均不同程度地低于单纯食猪油的高脂对照组。紫苏油尚可提高高脂血症大鼠血清ＨＤＬ－Ｃ、高密度脂蛋白亚组分Ⅱ胆固醇（ＨＤＬ２Ｃ）水平及ＨＤＬ２－Ｃ与高密度脂蛋白亚组分Ⅲ胆固醇（ＨＤＬ３－Ｃ）比值（ＨＤＬ２－Ｃ／ＨＤＬ３－Ｃ）；松籽油未见显著升高ＨＤＬ－Ｃ作用。各组动物血清ＨＤＬ３－Ｃ水平无显著差异。紫苏油和松籽油组大鼠肝体比值低于高脂对照组。紫苏油组大鼠肝脏过氧化脂质（ＬＰＯ）含量高于松籽油和高脂对照组。但与正常组比较，紫苏油、松籽油和高脂对照组大鼠肝体比值、肝脂质含量、肝组织病理学检查显示的肝脂变程度和肝脏ＬＰＯ含量均增高，而肝组织中谷胱?     

绿茶及混合茶抑制二乙基亚硝胺诱发大鼠肝癌前期病变的抗氧化机理研究

用二乙基亚硝胺（ＤＥＮ）诱发Ｗｉｓｔａｒ大鼠肝癌前期病变（Ｓｏｌｔ－Ｆａｒｂｅｒ模型）。实验前６周给大鼠饮用２％绿茶水及０．５％混合茶水，于实验第８周末宰杀动物。结果发现，绿茶组及混合茶组肝ｒ－ＧＴ异常病灶数均明显低于阳性对照组（Ｐ＜０．０１）。经ＨＰＬＣ法分离肝微粒体脂质过氧化产物丙二醛（ＭＤＡ）、乙醛（ＡＣＴ）、戊醛（ＰＰ）、丙酮（ＡＣＯＮ），与阳性对照组相比，绿茶组和混合茶组的各种脂质过氧化产物均有不同程度的降低。此外，对多种抗氧化酶和Ⅱ相代谢酶活性进行检测，其中绿茶组ＳＯＤ、ＧＳＴ、ＱＲ活性明显高于阳性对照组；混合茶组ＣＡＴ、ＳＯＤ、ＧＳＴ、ＱＲ活性明显高于阳性对照组。结果表明，绿茶和混合茶对ＤＥＮ诱发大鼠肝癌的发生均有显著的预防作用。其作用机理可能和诱导抗氧化酶及某些Ⅱ相代谢酶活性，以及抑制脂质过氧化作用有关。     

食用油对血脂、脂质过氧化、膜磷脂脂肪酸及血小板功能的影响

大鼠分别喂饲猪油、花生油、茶油、豆油、麻油及牛油高胆固醇饲料１～３个月，发现：１．麻油及牛油组血清总胆固醇（ＴＣ）及低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）水平远低于诸油及花生油组（Ｐ＜０．０５），且高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）水平最高（Ｐ＜０．０５）。茶油及豆油组ＴＣ与ＬＤＬ－Ｃ居中。甘油三酯以豆油组最高，茶油组最低（Ｐ＜０，０５）。２．各组红细胞膜、心肌线粒体及肝微粒体磷脂脂肪酸与饲料脂肪酸水平呈正相关。ＲＢＣ膜及心肌线粒体磷脂中，猪油及牛油组饱和脂肪酸含量较高，茶油组的单不饱和脂肪酸含量较高，麻油及花生油组的多不饱和脂肪酸（ＰＵＦＡ）含量较高。３．茶油组血清、肝及脑丙二醛（ＭＤＡ）水平最低，其余各组均较高。豆油组的肝ＭＤＡ最高。４．血清、肝超氧化物歧化酶（ＳＯＤ）水平以花生油及豆油组较低。５．血小板聚集率及血栓素Ｂ２（ＴＸＢ２）／６－酮－前列腺索Ｆ＿（１ａ）（６－Ｋ－ＰＧＦ＿（１ａ））比值以麻油组最低、豆油组较高。６．茶油组的生物膜流动性较大，而猪油及牛油组较小。     

橄榄油和鱼油对大鼠血脂和脂质过氧化的影响

研究富含单不饱和脂肪酸的橄榄油和富含多不饱和脂肪酸的鱼油对高血脂大鼠血脂水平及脂质过氧化的影响。方法：选用健康雄性Ｗｉｓｔａｒ大鼠共４０只,实验开始前按血清胆固醇和体重分为四组,正常对照组喂饲常备饲料,高脂对照组喂高脂饲料,橄榄油组和鱼油组除喂高脂饲料外,每日按每１００ｇ体重灌胃０．４ｍｌ相应的油脂,实验期为６周。高脂饲料含有５％猪油,１％胆固醇和０．２％的牛胆盐。每周称体重和记录进食量。实验末测定血清胆固醇（ＴＣ）、甘油三酯（ＴＧ）、高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）、血清丙二醛（ＭＤＡ）、红细胞超氧化物歧化酶（ＳＯＤ）活性。结果：１．橄榄油组和鱼油组大鼠的体重增长和进食量与高脂对照组相比无差异,但体重增长明显高于正常对照组。２．橄榄油组和鱼油组肝／体比值与高脂对照组比明显降低,而肾脏周围和睾丸周围的脂肪与体重的比值只有鱼油组与高脂对照组相比有明显的降低。３．橄榄油组与鱼油组ＴＣ和ＴＧ明显低于高脂对照组（Ｐ＜０．０５）,并且鱼油较橄榄油效果好。（ＴＣ分别为９６３．０、６３１．９、１５３３．５ｍｇ／Ｌ;ＴＧ分别为８１７．６、６９８．３、１５８４．５ｍｇ／Ｌ）鱼油能显著提高ＨＤＬ－Ｃ的水平（Ｐ＜０．０５）,橄榄?     

莲房原花青素对氧自由基和脂质过氧化的作用

目的 :　观察莲房原花青素 ( LSPC)对活性氧自由基 O·-2 、· OH和肝脂质过氧化损伤的作用。方法 :　 ( 1 )应用化学发光法检测 LSPC对 O·-2 和· OH的清除作用 ;( 2 )体外大鼠红细胞、肝线粒体温育引起肝脂质过氧化物 ( LPO)含量变化 ;( 3)体外大鼠肝匀浆温育 ,Fe2 +、H2 O2 诱导引起 LPO含量变化 ;( 4 )小鼠连续口服不同剂量 LSPC 7d后 ,一次性灌胃 5 % CCl4油溶液 1 0 ml/kg bw,2 4 h后检测肝和血浆中超氧化物歧化酶 ( SOD)活性、谷胱甘肽 S-转移酶 ( GST)活性以及脂质过氧化物 ( LPO)含量。结果 :　 LSPC能有效地清除活性氧自由基 O·-2 和· OH,其 IC50 值分别为 1 69.0 mg/L和 1 0 5 .3mg/L;不同剂量 LSPC能明显抑制体外大鼠红细胞、肝线粒体、肝组织LPO产生 ;口服中、低剂量 LSPC能显著降低 CCl4中毒小鼠体内 LPO含量 ,提高 SOD、GST活性。结论 :　适量 LSPC具有抗活性氧自由基和脂质过氧化的作用 ,可能具有护肝功能。     

Lipid peroxidation of liposome induced by glucosone.

Lipid peroxidation of liposome made of egg lecithin was induced by glucosone (D-arabino-hexos-2-ulose), a secondary product of Maillard reaction or glycation of protein. Lipid peroxidation was assessed with measurement of TBARS (thiobarbituric acid reacting substances), POV (peroxide value), and HPLC measurement of MDA (malondialdehyde). EDTA and DTPA (diethylenetriamine-pentaacetic acid) inhibited the lipid peroxidation assessed by each method described above, indicating involvement of metal ions. The observed reduction of Fe3+ to Fe2+ by glucosone might be a critical step of the lipid peroxidation. Our findings suggest a possible role of lipid peroxidation of low-density lipoproteins (LDL) induced by glucosone in atherosis caused by diabetes mellitus.     

Copper deficiency anemia: altered red blood cell lipids and viscosity in rats

To investigate membrane lipid abnormalities and their possible role in copper deficiency anemia, we studied lipids, osmotic fragility, and viscosity of red blood cells (RBCs) of rats fed diets containing 1.1 mg Cu/kg (deficient, Cu-) and 6.0 mg Cu/kg (supplemented, Cu+) at age 3 wk for 9 wk. Data show an increase in cholesterol of 43% and in phospholipids of 38% per cell in Cu- compared with Cu+ rats. Thin-layer chromatography of RBC lipids showed an increased amount of phospholipid-malonyldialdehyde adduct in Cu- (0.70 +/- 0.35% [means +/- SD] of total phospholipids) compared with Cu+ (0.29 +/- 0.19%) rats, suggesting increased membrane lipid peroxidation in Cu- RBC. Osmotic fragility of RBCs from Cu- rats was lower. RBC viscosity was significantly higher in Cu- than in Cu+ rats at shear rates of 23, 11.5, and 5.75 shear/s and was similar at shear rates 115 and 46 shear/s. Increased cell viscosity caused by lipid loading and crosslinking of membrane components caused by lipid peroxidation may have a role in the reduced RBC survival and anemia in Cu deficiency.     

葡萄籽提取物的体外抗脂质过氧化作用

以大鼠肝、脑组织匀浆为材料研究葡萄籽提取物 (GSE)的抗氧化作用。组织匀浆与GSE共浴后 ,比色法测定丙二醛 (MDA)生成量。组织匀浆与GSE共浴后 ,分别以自由基诱导剂CCl4、H2 O2 和铁离子 -抗坏血酸 (Fe2 + VC)激发脂质过氧化作用 ,以MDA产生和还原型谷胱甘肽 (GSH)耗竭作为脂质过氧化作用程度指标。结果表明 ,GSE可明显降低大鼠肝、脑组织自发性MDA的生成 ,减轻CCl4、H2 O2 、Fe2 + VC所致的肝脏脂质过氧化反应 ,减轻肝组织GSH耗竭。提示GSE具有良好的抗脂质过氧化作用。     

莲房原花青素对大鼠红细胞膜维生素E及膜脂流动性的影响

目的:探讨莲房原花青素(LSPC)对大鼠红细胞膜维生素E(VE)及对膜脂流动性的影响。方法:采用Fenton反应体系产生·OH,诱导大鼠红细胞膜过氧化,通过测定膜中丙二醛(MDA)和VE含量变化,来研究过氧化过程中LSPC对红细胞膜中VE的作用;还采用荧光偏振度法观察LSPC对膜脂流动性的影响。结果:在诱导前后使用两种不同浓度的LSPC(3μg/ml、5μg/ml),均能使膜中MDA含量降低,减少膜中VE的消耗,使膜脂的流动性显著增加(P<0.05和P<0.01)。结论:LSPC能显著抑制膜脂质过氧化,并与膜中天然VE有协同作用且能使其再生;使膜脂的流动性下降程度减轻,甚至基本恢复。     

核黄素缺乏大鼠红细胞膜流动性与脂质过氧化关系的研究

对两组大鼠分别喂饲核黄素缺乏(RD)膳和核黄素添加(RS,22mg/kg饲料)膳。7周后,测定了大鼠红细胞(RBC)膜荧光偏振度(P)和平均微粘度(?),RBC膜丙二醛(MDA)及RBC超氧化物歧化酶(SOD)。结果表明:RD组大鼠RBC膜P值和(?)值(分别为0.2976±0.0198和3.9483±0.3680)均高于RS组(0.2760±0.0207和2.8753±0.4634),差别分别呈显著和极显著统计学意义(P<0.05,P<0.01)。而RD组的RBC膜MDA(0.6868±0.1732nmol/mg蛋白质)和RBC SOD(7.7452±0.0610nU/mg蛋白质)则分别高于和低于RS组(0.5548±0.0980nmol/mg蛋白质和8.2685±0.3010nU/mg蛋白质),差别均有显著统计学意义(P<0.05)。研究表明:核黄素缺乏可引起大鼠RBC膜流动性下降,并与RBC膜脂质过氧化加重、清除自由基能力下降有关。     

吸烟烟气致大鼠肺匀浆和线粒体脂质过氧化及茶多酚的拮抗作用

采用体外实验向大鼠肺匀浆或线粒体通入吸烟烟气的方法，研究了吸烟烟气致大鼠肺匀浆和线粒体脂质过氧化及茶多酚的拮抗作用。结果表明向肺匀浆或线粒体通入烟气后，随着通烟气时间的延长，肺匀浆或线粒体脂质过氧化物（ＬＰＯ）含量显著增加；通入烟气１．０ｍｉｎ后，随着温育时间的延长，肺匀浆ＬＰＯ含量也显著增加。说明吸烟烟气能够导致大鼠肺匀浆和线粒体脂质过氧化。预先向肺匀浆或线粒体中加入茶多酚（０．１ｍｇ／ｍｌ），结果显示茶多酚对吸烟烟气致大鼠肺匀浆或线粒体脂质过氧化具有显著的拮抗作用     

Oxidative Stress Induced by Iron inHydrilla verticillata(l.f.) Royle: Response of Antioxidants

The effect of iron (FeCl₃) on chlorophyll content, lipid peroxidation product, potassium ion leakage (a measure of damage to the permeability barrier), and antioxidants was studied inHydrilla verticillata.The effect of iron-induced damage to the plant was compared with those ofN-ethyl maleimide (NEM), a sulfhydryl reagent, and cumene hydroperoxide (CHP), an organic peroxide known to induce lipid peroxidation by free radical formation. The level of lipid peroxidation product was increased in the plants treated with Fe, CHP, and CHP+NEM but not with NEM alone. A significant increase in potassium ion leakage to the external solution was observed by the addition of Fe, CHP, and CHP+NEM, while this did not increase significantly in NEM-treated plants. When NEM and CHP were added simultaneously, the results were the same as those obtained with high iron concentrations, suggesting a combined effect of thiol depletion and lipid peroxidation by Fe ions. In addition, the results indicated loss of glutathione (GSH) and increased oxidized glutathione (GSSG) under Fe stress, indicative of oxidative stress. The oxidative stress may increase the production of free radicals and subsequently resulted in peroxidation of lipids. Further, addition of iron increased the activity of superoxide dismutase (SOD) which may be due to enhanced production of oxygen free radical and related tissue damage. The results suggest that iron-induced damage in plants can be ascribed to a direct metal action on thiols and by toxic oxygen species. An increase in lipid peroxidation product and K⁺leakage are the primary responses of iron toxicity on membrane damage. However, the decrease in chlorophyll content is part of the overall expression of iron toxicity.     

Xanthurenic acid inhibits metal ion-induced lipid peroxidation and protects NADP-isocitrate dehydrogenase from oxidative inactivation.

Vitamin B6 deficiency increases the lipid peroxidation and the synthesis of xanthurenic acid from tryptophan. Antioxidant properties of xanthurenic acid were examined in relation to the coordination of transition metals. Xanthurenic acid inhibited the formation of thiobarbituric acid-reactive substances as a marker of iron-mediated lipid peroxidation and copper-dependent oxidation of low density lipoprotein. NADP-isocitrate dehydrogenase (EC 1.1.1.42), a principal NADPH-generating enzyme for the antioxidant defense system, was inactivated by reduced iron and copper, and xanthurenic acid protected the enzyme from the Fe2+-mediated inactivation. Xanthurenic acid may participate in the enhanced regeneration of reduced glutathione by stimulating the NADPH supply. Xanthurenic acid further enhanced the autooxidation of Fe2+ ion. Other tryptophan metabolites such as kynurenic acid and various quinoline compounds did not inhibit the lipid peroxidation and the inactivation of NADP-isocitrate dehydrogenase, and they showed little or no effect on the Fe2+ autooxidation. The antioxidant properties of xanthurenic acid are related to the metal-chelating activity and probably to the enhanced oxidation of reduced transition metals as a prooxidant, and this action may be due to the electron deficient nature of this compound.