Addition of vitamin E to long-chain polyunsaturated fatty acid-enriched diets protects neonatal tissue lipids against peroxidation in rats

Summary Background: Tissue 10:4(n-6) and 22:6(n-3) status have been correlated with neonatal development and growth. Artificial formulas for neonates have been supplemented with long chain polyunsaturated fatty acids (LCP) from animal and marine sources which may enhance sensitivity of cellular membranes to oxidative damage. Diet-derived antioxidants like vitamin E play a key role in the protection of tissue lipids against oxidation. Aim of the study: We seek to determine the influence of dietary vitamin E on tissue sensitivity to oxidative stress in rats fed for 4 weeks on diets enriched in (n-3) and (n-6) long-chain polyunsaturated fatty acids. Methods: Weanling rats received 10% fat diets that provided 18:1(n-9), 18:2(n-6) and 18:3(n-3) in a similar ratio to that of rat milk (group A), supplemented with fish oil (groups B and B+E) and supplemented with (n-6) and (n-3) LCP from an animal phospholipid concentrate (groups C and C+E). Vitamin E (500 mg vitamin E/kg fat) was added to diets B+E and C+E. Tissue fatty acid content and the activities of catalase, superoxide dismutase, glutathione transferase und glutathione peroxidase in liver and brain were measured. Glutathione status, vitamin E and the production of thiobarbituric acid reactive substances (TBARs) after incubation of erythrocyte, liver and brain lipids with inducers of enzymatic or non-enzymatic lipid peroxidation was measured. Results: Group B registered significantly lower total superoxide dismutase acitvity than group B+. Catalase activity was significantly higher in group C than in group C+E. Hepatic total and reduced glutathione levels were decreased in vitamin E supplemented groups compared to unsupplemented ones. TBARs production in erythrocyte lipids was significantly higher in groups B and C compared to vitamin E supplemented groups B+E and C+E. Conclusions: This study shows that the addition of vitamin E protected erythrocyte and liver microsome lipids enriched in (n-3) and (n-6) LCP from lipid peroxidation during the postnatal development of rats. The protection was more effectively in group C+E than in group B+E. Received: 14 January 1999, Accepted: 14 June 1999     

核黄素缺乏大鼠红细胞维生素E水平的变化及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（Ｒ８，２２ｍｇ／ｋｇ饲料）膳８周后，测定了两组大鼠的红细胞维生素Ｅ（ＲＢＬＶｅ）、红细胞超氧化物歧化酶（ＳＯＤ）和红细胞丙二醛（ＭＤＡ）的水平。结果发现：ＲＤ组ＲＢＣＶｅ水平（４．７１７３±０．７７１０ｍｇ／ｇ蛋白质）显著低于ＲＳ组（５。３８６８±１．１５３７ｍｇ／ｇ蛋白质，Ｐ＜０．０５）。而ＲＤ组的ＲＢＣＳＯＤ（７７４５．２±６１０．１ｕ／ｇ蛋白质）和ＭＤＡ（０．６８６８±０．１３７２μｇ／ｇ蛋白质）则分别显著低于和高于ＲＳ组（８２６８．５±３０１．０ｎｕ／ｇ蛋白质，０．５５４８±０．０９８０，Ｐ＜０．０５）。研究提示，核黄素缺乏引起细胞膜脂质过氧化加重可能ＲＢＣＶｅ消耗增加。     

Effect of vitamin E,selenium and age on lipid peroxidation events in rat cerebrum

The effect of 8 and 20 weeks of dietary vitamin E (200 IU/kg diet) and/or selenium (0.2 ppm) supplementation or deficiency on oxidative processes in cerebrum of 1 and 15 month old male F344 rats was examined. After 8 weeks of treatment a 32-fold difference in plasma and a 3-fold difference in cerebrum alpha-tocopherol (a-T) level was found between vitamin E supplemented and deficient young rats. These differences were 1.8- and 1.5-fold, respectively, in old rats and increased to 8- and 2-fold differences, respectively, after an additional 12 weeks of treatment. Selenium deficiency had a significant effect on plasma glutathione peroxidase activity and a slight sparing effect on plasma a-T content. Endogenous lipid peroxides (thiobarbituric acid reactants present without incubation) in cerebrum were not correlated with a-T concentration or age. However, incubation of cerebrum homogenates with or without the addition of 0.1 mM Fe²⁺, 0.25 mM ascorbic acid, or 100 mg % acetaldehyde revealed that dietary vitamin E has a major role and selenium has a minor role in the protection against ex-vivo and possibly in vivo lipid peroxidation in cerebrum.     

2-乙氧基乙醇染毒对大鼠某些脂质过氧化相关指标的影响

目的：观察2－乙氧基乙醇（EE）染毒大鼠与脂质过氧化过程有关的某些生化指标的变化,并探讨EE染毒是否诱发血清脂质过氧化（LPO）升高及其可能机理。方法：选取雄性Wistar大鼠,随机分为4组：对照组、EE分别为200、400、800mg/kg组,每组30只。每天染毒1次,每周6次,持续6周。分别于染毒每周后,将各组动物随机处死5只,对血液及肝脏中的脂质过氧化相关指标进行测定。结果：血清LPO水平显著升高;血清铜蓝蛋白（CP）、血清超氧化物歧化酶（SOD）和肝脏SOD活性显著升高;肝脏过氧化氢酶（CAT）活性显著下降,肝脏GSH－Px活性变化不明显。结论：EE长期染毒可诱发大鼠LPO水平升高,这可能是EE诱发大量活性氧（ROS）产生和影响大鼠抗氧化机制共同作用的结果。     

Paraoxonase 1 Q192R (PON1-192) polymorphism is associated with reduced lipid peroxidation in R-allele-carrier but not in QQ homozygous elderly subjects on a tomato-rich diet

Summary. Background: The oxidative modification of LDL is considered to play a central role in the pathogenesis of atherosclerosis and coronary heart disease (CHD). Paraoxonase (PON1) protects LDL from oxidation and may therefore retard the developement of atherosclerosis. The PON1–192 polymorphism is associated with diminished PON1 concentrations and an increased risk for CHD in RR-allele subjects. Aim of the study: To investigate the effect of tomato juice consumption on PON1 activity and other parameters related to oxidative stress in healthy elderly subjects. Furthermore, the PON1–192 genotype has been determined in the volunteers in order to see whether possible treatment effects are related to the PON1–192 polymorphism. Methods: Fifty elderly subjects were randomly assigned to control (mineral water) or intervention group (tomato juice). Subjects of the tomato juice group consumed daily 330 mL tomato juice for 8 weeks. Antioxidant status was measured as LDL oxidation, plasma malondialdehyde, ferric reducing ability of plasma (FRAP) and PON1 activity. The PON1–192 polymorphism was determined by restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR). Plasma carotenoids were analyzed by HPLC. Results: Tomato juice consumption reduced LDL-oxidation and improved antioxidant status in R-allele carriers, but not in the QQ genotype group. PON1 activity increased irrespective of the genotype in both, control and intervention group. Conclusions: The changes in antioxidant status after tomato juice consumption seem to depend on the PON1–192 genotype. Healthy elderly, carrying the R-allele, could specificly reduce their higher cardiovascular risk by changing dietary habits. Received: 9 October 2002, Accepted: 28 October 2002 Correspondence to: Achim Bub     

实验性高脂血症大鼠的血硒、维生素E、GSH－Px及脂质过氧化物的改变

采用幼年ＳＤ雄性大鼠３０只，随机分成３组，分别饲喂基础饲料，猪油饲料（１０％猪油和１．５％胆固醇）和玉米油饲料（１０％玉米油和１．５％胆固醇）。９周后，玉米油组和猪油组的大鼠形成高脂高胆固醇血症，第１０周处死动物，取血测定全血硒（Ｓｅ），谷胱甘肽过氧化物酶（６ＧＳＨ－Ｐｘ），血清维生素Ｅ（ＶＥ）和脂质过氧化物（ＬＰＯ）含量。结果由猪油和玉米油诱导的高血脂大鼠血Ｓｅ水平低于基础饲料组的大鼠，基础组、猪油组和玉米油组的血Ｓｅ值分别为０．０９６、０．０８１和０．０８０ｍｇ／Ｌ，而且随着饲养时间的延长，血Ｓｅ趋于下降，但各组间的差异无显著性意义。基础组和猪油组大鼠的ＧＳＨ－Ｐｘ活性分别为２０．０４和２１．０１ｍｍｏｌ／（ｍｉｎ．Ｌ），而玉米油组最低，仅为１１．０８ｍｍｏｌ／（ｍｉｎ．Ｌ），玉米油组与基础组和猪油组之间呈极显著差异（Ｐ＜０．０１）。血清ＬＰＯ含量在各组之间未观察到显著性差异（基础组１７．５８，猪油组１７．４４，玉米油组１７．７３μｍｏｌ／Ｌ）。但值得注意的是玉米油组的ＧＳＨ－Ｐｘ／ＬＰＯ比值为０．６３，明显低于基础组（１．１３）和猪油组（１．１９），说明玉米油组大鼠体内抗氧化能力减弱。猪油组血清ＶＥ浓?     

维生素E对二硫化碳致雄性大鼠睾丸组织脂质过氧化的拮抗作用

目的探讨二硫化碳(CS2)对雄性大鼠睾丸组织氧自由基及抗氧化水平的影响,同时观察维生素E(VE)对其的拮抗作用。方法取健康Wistar雄性大鼠36只随机分为6组,以不同浓度CS2(0、50、250、1250mgm3)静式吸入染毒,共10周,另设1250mgm3(CS2)加VE(250mgkg)组和单纯VE(250mgkg)组,VE拌入饲料中,染毒结束后,处死动物取出睾丸制备组织匀浆,分别测定各组SOD、MDA、GST、GSH、GSHpx、NO、总NOS和iNOS水平,同时检测VE对其的拮抗水平。结果睾丸组织中SOD活力下降,MDA含量上升,与对照组比较有显著差异(P<0.05);GSH含量、GST、GSHpx活力总体趋势下降,与对照组比较有显著差异(P<0.05或P<0.01);NO含量及总NOS、iNOS活力均下降,有随染毒浓度增加而降低的趋势,与对照组比较有显著差异(P<0.05或P<0.01)。但用VE干预后,SOD、GST、GSHpx、总NOS、iNOS活力均有不同程度上升,GSH、NO含量亦是如此,而MDA含量则下降。结论VE对CS2致睾丸组织脂质过氧化有拮抗作用。     

Effect of vitamin E and vitamin C on the DNA synthesis of human umbilical arterial endothelial cells

Summary Background Endothelial cell growth and reendothealization after vascular injury protect the vessel wall against endothelial dysfunction which is believed to play a major role in the pathogenesis of atherosclerosis. Aim of the study To investigate a possible protective role of antioxidant vitamins in the present study, the effect of vitamin E (α-tocopherol) alone and in combination with vitamin C on the DNA synthesis of human umbilical arterial endothelial cells (HUAEC) was examined. Furthermore, because oxidized low-density lipoprotein (ox-LDL) is thought to be involved in atherogenesis, the combined effect of vitamin E and vitamin C with ox-LDL and the influence of vitamin-pretreated LDL on HUAEC proliferation were investigated. Methods DNA-synthesis was determined by measurement of [³H]thymidine incorporation into the cell DNA. Results Vitamin E alone and in combination with vitamin C resulted in an increase in [³H]thymidine incorporation into cell DNA, especially in the presence of basic fibroblast growth factor (bFGF). All vitamin-pretreated LDL samples and ox-LDL led to a nearly complete inhibition of endothelial DNA-synthesis. The ox-LDL-induced effect could not be prevented by vitamin E alone nor in combination with vitamin C. Conclusions It seems that once LDL oxidation is in process, vitamin E alone and in combination with vitamin C is ineffective to exert its antioxidative capacity under the conditions used. Thus, vitamin E alone and combined with vitamin C may act as antiatherogens by inducing endothelial cell growth. Received: 3 January 2001, Accepted: 17 July 2001     

富硒蒜对实验性高脂血症大鼠血脂及脂质过氧化作用的影响

为了观察富硒蒜对实验性高脂血症大鼠脂和抗氧化能力的影响，取76只成年Wistar大鼠分为6组，雌雄各半，A组为正常对照组，B组为高脂（HFD）对照组，C组为HFD＋亚硒酸钠组，D组为HFD＋富硒蒜组，E组为HFD＋普通蒜组，F组为HFD＋普通蒜＋亚硒酸钠组，A，B、E组饲料硒水平为0．08mg/kg，其它三组为2．7mg/kg，实验期12周，结束时取血及肝，肾组织进行生化测定和肝病理检查，结果表明，C，D和F组动物血清总胆固醇，甘油三酯和低密度脂蛋白胆固醇含量都显著低于高脂对照组，而高密度脂蛋白胆固醇则高于高脂对照组，雌鼠的血脂对高脂饲料的反应比雄鼠更敏感。C，D，E，F组动物体内过氧化状态升高的程度均显著低于高脂对照组动物，表现为肝组织内脂质过氧化物丙二醛的含量显著降低及肝组织及红细胞内谷胱甘肽过氧化物酶活力和血浆内过氧化物歧化酶活力不同程度地升高，D，F组雄性动物肝，肾中硒含量高于C组，最显著的是在该两组雌雄动物红细胞中大量蓄积硒，病理检查发现，四个实验组动物肝组织含量高于C组，最显著的是在该两组雌雄动物红细胞中大量蓄积硒，病理检查发现，四个实验组动物肝组织脂肪变性的程度显著轻于高脂对照组动物，在D组动物中表现得尤明显结果说明，从预防高血脂和对抗脂质过氧化作用的角度，富硒蒜优于亚硒酸钠或普通蒜，也稍优于合并使用普通蒜和亚硒酸钠。     

阿维菌素与高效氯氰菊酯联合对大鼠脂质过氧化影响

目的 通过动物实验观察阿维菌素与高效氯氰菊酯的联合毒性作用,并从氧化损伤的角度探讨其联合作用的机制。方法 将大鼠随机分为4组,分别为对照组、阿维菌素组、高效氯氰菊酯组以及混合组,灌胃染毒30 d,观察大鼠一般状况及体重变化,计算脏器系数及检测血清中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活力和丙二醛（MDA）含量。结果 混合组大鼠中毒症状较各单剂组加重,持续时间延长;与对照组比较,阿维菌素组、高效氯氰菊酯组及其混合组体重均降低,仅雄性大鼠体重差异有统计学意义（P<0.05）;阿维菌素组、高效氯氰菊酯组及其混合组大鼠血清中MDA含量显著增加,SOD和GSH-Px酶活力显著降低（P<0.05）;析因分析结果显示,阿维菌素和高效氯氰菊酯对大鼠血清中MDA含量（F=0.324,P=0.57）,SOD（F=2.86,P=0.09）和GSH-Px（F=2.29,P=0.14）酶活力没有交互作用,联合作用方式均为相加作用。结论 阿维菌素与高效氯氰菊酯联合作用毒性较各单剂量组增加,氧化损伤可能是其联合毒性作用机制之一。     

孕期铁营养不良对成年大鼠血脂与脂质过氧化影响的实验研究

目的:通过建立大鼠孕期铁营养不良模型探讨孕期低铁干预对成年大鼠脂质过氧化及血脂的影响。方法:将健康Wistar雌性大鼠随机分为二组,实验组(即低铁组)饲喂低铁饲料(含铁7.4 mg/kg);对照组饲喂加铁饲料(含铁274 mg/kg)。与健康成年Wistar雄鼠同笼交配2周(即孕1周)后,开始铁干预至子鼠出生后23周时转至普通颗粒饲料喂养即铁平衡期,持续8个月测定大鼠血浆甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、脂蛋白a[LP(a)]、游离脂肪酸(FFA),血清超氧化物歧化酶(SOD)活力和丙二醛(MDA)。结果:实验组与对照组相比成年期大鼠铁蛋白(SF)、FFA、SOD升高;HDL降低(P<0.05)。结论:孕期铁营养不良可造成成年大鼠对脂代谢的调节能力下降,出现血脂紊乱,促进体内脂质过氧化反应的同时抗氧化酶类SOD活性上升。     

3－硝基丙酸脂质过氧化作用的实验研究

９只雄性大鼠以８０ｍｇ／ｋｇ３－硝基丙酸（３－ＮＰＡ）经口染毒后１５、３０和４５ｍｉｎ时，在肝脏中用电子自旋共振仪可检测到较强的自由基信号。肾上腺素红法测定发现５×１０－３～１０－２ｍｏｌ／Ｌ３－ＮＰＡ可明显促进肝与脑微粒体和线粒体产生自由基。８０ｍｇ／ｋｇ３－ＮＰＡ灌胃染毒大鼠肝和脑中ＳＯＤ和ＧＳＨ－Ｐｘ活性上升，ＭＤＡ含量升高。因此３－ＮＰＡ在体内和体外均有诱发脂质过氧化作用的能力。     

三氯乙烯和四氯乙烯对体外培养皮肤KC细胞氧化损伤及维生素E的保护作用

目的探讨三氯乙烯（TCE）、四氯乙烯（PCE）对体外培养人皮肤角质形成细胞（KC）氧化损伤作用及维生素E的保护作用。方法将来源于3个或3个以上不同健康个体的皮肤KC细胞混合培养于K—SFM培养基中，利用中性红吸附实验确定其半数抑制浓度（IC50），并据此确定TCE、PCE染毒浓度。染毒4h后，测定细胞内丙二醛（MDA）、超氧化物歧化酶（SOD）、活性氧（ROS）水平；维生素E保护组使用不同浓度维生素E预作用2h后，再分别换入0．5mmol／LTCE或0．2mmol／LPCE与不同浓度维生素E混合物作用4h后，测定细胞内MDA、SOD、ROS水平。结果TCE、PCE能引起体外培养人皮肤KC细胞氧化损伤，且具有浓度一反应关系。而维生素E对其具有保护作用，能下调其氧化损伤，且具有浓度一反应关系。结论TCE、PcE能引起体外培养人皮肤KC细胞氧化损伤，而维生素E对其具有保护作用。     

3－硝基丙酸脂质过氧化作用的实验研究

９只雄性大鼠以８０ｍｇ／ｋｇ３－硝基丙酸（３－ＮＰＡ）经口染毒后１５、３０和４５ｍｉｎ时，在肝脏中用电子自旋共振仪可检测到较强的自由基信号。肾上腺素红法测定发现５×１０－３～１０－２ｍｏｌ／Ｌ３－ＮＰＡ可明显促进肝与脑微粒体和线粒体产生自由基。８０ｍｇ／ｋｇ３－ＮＰＡ灌胃染毒大鼠肝和脑中ＳＯＤ和ＧＳＨ－Ｐｘ活性上升，ＭＤＡ含量升高。因此３－ＮＰＡ在体内和体外均有诱发脂质过氧化作用的能力。     

Vitamin C and vitamin E antagonistically modulate human vascular endothelial and smooth muscle cell DNA synthesis and proliferation

Summary Background Vitamin C and E are suggested to play a preventive role in the pathogenesis of atherosclerosis. They reduce oxidation of low density lipoproteins (oxLDL), thereby protecting human vascular arterial endothelial and smooth muscle cells from oxLDL induced damages. Aims of the Study Since vascular arterial endothelial and smooth muscle cells are both involved in atherosclerotic plaque formation, we simultaneously examined the effect of vitamin C, E and oxLDL on their DNA synthesis and proliferation to further elucidate their joint role in this process. Methods Human umbilical arterial endothelial cells (HUAEC) and human arterial smooth muscle cells (HUASMC) were incubated with “preventive concentrations” of vitamin C (60μM) and E (30μM) and with LDL (60μg/ml) of increasing oxidation grade. Cell proliferation and DNA synthesis were determined by cell count and [³H]-thymidine uptake, respectively. Results Vitamin C alone or in combination with E increased significantly cell number and [³H]-thymidine uptake in HUAEC. The combination exhibited the strongest effect. In contrast, cell number and [³H]-thymidine uptake in HUASMC were significantly decreased in the presence of vitamin C, vitamin E or its combination. OxLDL (60 μg/ml) inhibited cell number and [³H]-thymidine uptake in HUAECs, the latter in an oxidation-grade dependent manner. In HUASMC oxLDL promoted a higher cell number and [³H]-thymidine uptake. If induced by minimally oxLDL, this reduc-tion or increase could be partially reversed by vitamin C alone or in combination with vitamin E. Conclusion Vitamin C and E, alone or in combination, modulate proliferation and DNA synthesis of human arterial endothelial and muscle cells and this modulation is antagonistic. Thus, vitamin C and E may act “preventive” on atherosclerotic plaque formation in two steps: first reendothelialisation is promoted, then HUASMC growth is inhibited. Received: 23 August 2001, Accepted: 8 January 2002     

Chronic vitamin E inadequacy and thermally treated oils affect the synthesis of hepatic metallothionein isoforms

Summary Background: Metallothionein (MT)^# synthesis can be stimulated in many organs not only by various metals such as cadmium, zinc, and copper, but also by many nonmetalic compounds or experimental conditions such as oxidative stress. The latter lead to the hypothesis that MT is induced in response to free radicals formed in tissues and lipid peroxidation. Aims of the study: Whether the relationship between lipid peroxidation amd MT synthesis is a common phenomenon also valid for lipid peroxidation induced by dietary factors such as chronic vitamin E inadequacy and autoxidation products of polyenoic fatty acids derived from thermally oxidized oil was investigated in the presence study. Methods: The relationship between the induction of metallothionein isoforms I and II (MT-I and MT-II) in response to diet-induced lipid peroxidation using a rat model system in which lipid peroxidation was examined in vivo by chronic vitamin E inadequacy or by administration of lipid peroxidation products from a thermally treated polyenoicrich oil with either basal (dietary zinc concentration: 48 mg/kd; experiment 1) or Zn-stimulated MT levels (dietary zinc concentration: 305 mg/kd; experiment 2) was studied. In both experiments, growing male rats were fed diet containing either a fresh or a thermally treated soybean oil with deficient of sufficient amounts of vitamin E (14 and 11 vs. 648 and 560 mg α-tocopherol equivalents per kg diet) over 40 days according to a bifactorial experimental design. Plasma and liver concentrations of tocopherols and hepatic levels of thiobarbituric acid-reacitve substances (TBARS) were measured by high performance liquid chromatography. MT isoform concentrations in rat liver were isolated and quantified by ion-exchange high performance liquid chromatography and atomic absorption spectrometry. Results: Irrespective of the zinc supply, rats receiving inadequate amounts of vitamin E with the diet had markedly lower plasma and liver concentrations of α-tocopherol and total tocopherols than vitamin E-sufficient rats. ANOVA also revealed an interaction between the diet factors vitamin E and oil on tocopherols in plasma and liver of rats from both experiments. In experiment 1, where rats received normal amounts of dietary zinc, ingestion of the thermally treated oil impaired the tocopherol status compared to the treatment with the fresh oil, although this effect was only obvious in the vitamin E-deficient groups. In experiment 2, where rats received excessive amounts of zinc, the thermally treated oil did not contribute to a reduction of the tocopherol status in plasma and liver. In both experiments a significant increase in TBARS level, indicative of lipid peroxidation, was observed in the liver at chronic vitamin E inadequacy, but no effect of the oil was observed. Here, we show that the dietary treatment had some effects on the synthesis of liver metallothionein isoforms. In groups, receiving normal amounts of zinc, there was a significant interaction between the dietary treatments on the levels of MT-I and MT-II in liver. Chronic vitamin E inadequacy which was accompanied by diminisched tocopherol levels in liver induced the synthesis of MT-I and MT-II. When vitamin E inadequacy was combined with the ingestion of a thermally treated polyenoic acid-rich oil hepatic levels of MT-I and MT-II remained low. In experiment 2, where rats were fed the high zinc diet, vitamin E inadequacy caused an increase of hepatic MT-I level just as in experiment 1, although this MT stimulating effect was irrespective of the oil. For MT-II there was a 43% increase in the vitamin E-deficient group fed the fresh oil compared to all the other groups, although this effect was not statistically significant. The liver MT isoform response to stress was similar in rats with basal MT levels and Zn-induced liver MT levels. The failing effect of the thermally treated oil on MT levels which were stimulated by vitamin E deficiency in experiment 2 was possibly due to the low oxidation grade of the thermally treated oil. Conclusion: The present results are strongly indicative of an apparent induction of MT isoform synthesis in response to an impaired antioxidant defence system in the lipid regions of liver cells induced by vitamin E inadequacy. In contrast, thermally treated polyenoic-rich oils with a certain oxidation grade seem to restrain the induction of MT isoform synthesis under the present experimental conditions. Received: 10 January 2000, Accepted: 27 April 2000     

吞噬细胞介导的不同脂肪乳剂的脂质过氧化以及维生素E的抗氧化作用

评估维生素E在体外的抗氧化、预防脂质过氧化的作用,比较各种不同类型脂肪乳剂对氧自由基产生及脂质过氧化的影响。取18倒健康志愿静脉血,采用Boyum法提取多核白细胞(PMN)并在体外培养PMN。实验分单纯PMN组,Intralipid组(100％LCT),Vasolipid组(50％LCT,50％MCT)Structolipid组(63％LCT,37％MCT)。各组均分为静止和刺激(用热灭活白色粘株菌刺激PMN)两种状态。采用NBT还原试验测定氧自由基产生量。根据以上分组在体外孵育PMN,并再分为添加Vit E组和无Vit E组。采用比色法-LPO-586测定脂质过氧化的终产物Malonaldehyde(MDA)和4-hydroxyalkenal来计算脂质过氧化程度。刺激组的氧自由基产生量明显高于静止组(0．795±0．180vs.0.405±0．090,P<0．001)。脂肪乳剂可明显降低各组的NBT值,脂肪乳剂浓度与NBT值之间呈负线性相关(r=-0．83,P<0．001)。三组不同脂肪乳剂之间,其NBT值无统计学差异(P>0.05)。刺激组的脂质过氧化产物明显高于静止组(3．15±1.12vs1．34±0．72,P<0.001)。各脂肪乳剂组的脂质过氧化产物明显高于单纯PMN组,而Intratipid组脂质过氧化值高于Vasolipid组和Structolipid组,差异有显性。隧着PMN孵育时间的延长,各组的脂质过氧化值增加,6小时后接近最大值。在体外,维生素E可明显抑制脂质过氧化的产生,8μg／d的维生素E可抑制70-80％PMN所致的脂质过氧化。脂肪乳剂在体外可增加由吞噬细胞介导的脂质过氧化,所增加的脂质过氧化可通过添加维生素E而得到有效的抑制。     

2,3,7,8-四氯二苯-p-二英对雌性小鼠血浆维生素A、E的影响

目的了解2,3,7,8-四氯二苯-p-二(口恶)英(TCDD)对雌鼠血浆维生素A、E水平的影响.方法将实验昆明种雌性小鼠24只,随机分为染毒高(100 μg/kg)、中(10 μg/kg)、低(1 μg/kg)剂量和空白对照4组,腹腔注射染毒.48 h后对实验小鼠取血,离心后取上层血浆,用无水乙醇沉淀蛋白,加环己烷萃取后,使用荧光分光光度仪在不同波长下测定其荧光值,计算出维生素A、E浓度,进行统计分析.结果对照及染毒剂量低、中、高4组中小鼠血浆维生素A的平均水平差异无显著性(P＞0.05);血浆维生素E的平均水平差异有显著性(P＜0.05),对照组与低剂量组之间维生素E的浓度水平差异无显著性,但与中、高剂量组之间维生素E的浓度水平差异都有显著性(P＜0.05).结论在此实验条件下,尚不能够认为TCDD对雌鼠血浆维生素A的水平有影响,但对维生素E的水平有一定影响.     

铁负荷对大鼠脂质过氧化作用影响及抗氧化维生素对其抑制作用

目的研究铁负荷对大鼠脂质过氧化的影响及具有抗氧化作用的维生素 (维生素E和 β 胡萝卜素 )对铁负荷所产生影响的作用。方法将 80只雄性Wistar大鼠按体重随机分为 8组 ,前 4组给予的饲料铁浓度分别为 5 0、2 0 0、3 5 0和 5 0 0mg kg饲料。后 4组饲料铁浓度分别与前 4组相同 ,但同时在饲料中补充抗氧化剂(维生素E 10 0mg kg饲料、β 胡萝卜素 2 5mg kg .BW) ,喂养 8周。实验结束时 ,测定血清铁、血脂 (总胆固醇、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇 )、维生素E、维生素A ,血清丙二醛、氧化性低密度脂蛋白 ,超氧化物歧化酶和谷胱甘肽过氧化物酶。结果铁负荷具有增加血清丙二醛、氧化性低密度脂蛋白及低密度脂蛋白胆固醇水平的趋势 ,5 0 0mg kg饲料组显著 ;各组谷胱甘肽过氧化物酶活性应激性增加 ,VE、VA含量下降。加入维生素类抗氧化剂可使丙二醛、氧化性低密度脂蛋白及低密度脂蛋白胆固醇降低 ,高密度脂蛋白胆固醇升高 ,超氧化物歧化酶降低。结论铁负荷可促进体内脂质过氧化反应 ,以十倍生理剂量最为显著 ,同时抗氧化酶类活性增加 ,以维持机体动态平衡 ;维生素类抗氧化剂可能通过非酶促反应体系发挥作用 ,抑制上述改变