碘氟联用对大鼠脑细胞膜磷脂和脂肪酸组成的影响

目的　研究不同浓度碘和高浓度氟联合作用对大鼠脑细胞膜磷脂和脂肪酸组成的影响。方法　给大鼠饮用高浓度的氟化钠 (15 0mg L) ,同时分别加入低、中、高浓度碘化钾(0 0 0 3、0 0 3和 3mg L)的溶液共 5个月 ,然后用液相色谱法分离和测定大鼠脑细胞磷脂和脂肪酸组成。结果　实验各组中各种磷脂含量无显著变化。高浓度氟和高浓度碘加氟 (15 0mg L + 3mg L)可使大鼠脑细胞膜脂肪酸构成比发生了明显的变化 ,饱和脂肪酸中的月桂酸(C12 :0 )显著增加 (P <0 0 5 ) ,不饱和脂肪酸中的亚油酸 (C18:2 )显著减少 ;中浓度碘对氟的这种作用有明显的拮抗作用 ,而高浓度时则反而有协同毒性作用。结论　氟中毒所致大鼠脑细胞膜脂肪酸组成的变化可能与氟致脂质过氧化作用有关 ,而 0 0 3mg L的碘化钾是本实验条件下拮抗氟中毒对大鼠脑细胞脂肪酸组成的最佳浓度     

花生油、茶油、牛油对大鼠脂质过氧化、膜磷脂脂肪酸组成及膜流动性的影响

用含11％花生油、茶油、牛油的饲料分别饲养SD大鼠，观察其血清和心、肝、脑丙二醛（MDA）、血清和肝超氧化物歧化酶（SOD）水平、生物膜磷脂脂肪酸组成及膜流动性的改变。结果发现：花生油组心线粒体及牛油组RBC膜磷脂脂肪酸含量与摄入脂肪酸呈正相关（r分别为0.6275和0.6967，P＜0.01）。喂饲花生油引起生物膜磷脂多不饱和脂肪酸含量增加，膜流动性增高，血清和肝SOD水平较低（分别为3.76±1.61mg／L、616±163μg／g），血清MDA较高（8.70±1.71μmol／L），提示脂质过氧化程度较高。喂饲茶油引起膜磷脂单不饱和脂肪酸含量增加，膜流动性和血清SOD（5.66±2.00mg／L）较高，血清及脑MDA较低（5.92±1.15μmol／L，2.45±0.44μmol／g），提示脂质过氧化程度较低。喂饲牛油引起膜磷脂饱和脂肪酸含量增加，膜流动性较低，血清及肝SOD较高（5.79±0.56mg／L，886±99μg／g），血清MDA较低（7.04±1.66μmol／L），脑MDA较高（3.96±1.68μmol／g），脂质过氧化程度介于花生油组与茶油组之间。     

氧化应激在亚慢性氟中毒大鼠肝脏损伤中的作用

目的 探讨氧化应激在亚慢性氟中毒大鼠肝脏损伤中的作用。方法 在饮水中加入50，100，和150mg／L氟化钠(NaF)喂饲大鼠3个月，制备亚慢性氟中毒模型。测定染氟各组大鼠肝脏脂质过氧化产物丙二醛(MDA)的含量及抗氧化酶超氧化物歧化酶(S0D)、谷胱甘肽过氧化物酶(GSH—Px)的活力，同时检测血清中谷丙转氨酶(SG-PT)、谷草转氨酶(SGOT)的活性。结果 150mg/L染氟组大鼠肝脏MDA含量显高于对照组(P＜0．01)；100，150mg／L染氟组大鼠肝脏S0D活力显下降(P＜0．05)；随染氟剂量增加，GSH—PX活力有下降趋势；150mg／L染氟组SGPT活性显高于对照组(P＜0．01)，100，150mg/L染氟组SGOT活性显高于对照组(P＜0．01)，MDA与SGPT之间存在显正相关(r＝0．460，P＝0．007)。结论 氟中毒大鼠肝脏内氧化系统与抗氧化系统失衡，氧化应激引起的氧化损伤作用可能是氟致大鼠肝毒性的重要原因之一。     

荔枝种仁油对大鼠血脂水平的影响

用高压液相色谱法测定了荔枝种仁油的脂肪酸组成并研究了其对高脂大鼠血脂水平的影响。结果表明，荔枝种仁油含有５０．３％的不饱和脂肪酸和３０．８５％的环丙烷基长链脂肪酸；可以显著降低高脂大鼠血总胆固醇浓度和低密度脂蛋白胆固醇浓度，同时增加高密度脂蛋白胆固醇含量，使高密度脂蛋白胆固醇／总胆固醇含量比值极显著提高。提示荔枝种仁油对改善血脂水平，防止心血管疾病，可能具有良好的保健作用。     

碘、氟对大鼠子代脑发育形态学改变联合作用的研究

目的　观察碘、氟对大鼠子代脑发育形态学方面是否存在联合作用。方法　将实验用Wistar成年大鼠雌 1 6只 ,雄 8只 ,按饮水中不同碘、氟或碘 +氟浓度分为 8组 ,即 :碘、氟为 0 (对照组 ,采用重蒸水 ) ,碘 0 5、 1 0、 2 0mg/L ,氟 50mg/L ,碘 +氟 0 5+ 50、 1 0 + 50、 2 0 + 50mg/L。喂养 90d后相同浓度组雌、雄按 2∶1合笼交配 ,交配后 2 1～ 2 8d母鼠产仔 ,哺乳 5d后将各组仔鼠断头处死。取其脑组织进行大脑重量、光镜 (观察大脑皮质神经细胞密度及未分化神经母细胞占细胞总数百分比 )、电镜 (观察神经元发育情况 )等形态学指标检查。结果　仔鼠大脑重量及光镜指标经 2× 4析因方差分析均表明各组之间差异有显著性 (P <0 0 0 1 )。其中氟 50mg/L、碘 2 0mg/L及碘 +氟 2 0+ 50mg/L组各项指标都提示仔鼠大脑发育状况次于其余各组。电镜检查发现氟 50mg/L及碘 +氟 2 0 + 50ml/L组神经元发育及超微结构形态有轻微变性改变。结论　长期饲以高氟及高碘饮水的大鼠均可影响其子代大脑发育 ,且高碘、高氟对仔鼠大脑发育的危害存在协同作用     

鱼油豆油对大鼠线粒体磷脂脂肪酸组成的影响

方法：大鼠分别饲以低硒和补硒饲料３０天，补加油类之后（５０ｇ／ｋｇ饲料）继续饲养３０天。结果：线粒体膜磷脂中脂肪酸组成可反映大鼠饮食中脂肪酸的组成，磷脂酰胆碱（ＰＣ）和磷脂酰乙醇胺（ＰＥ）中Ｃ２０∶５和Ｃ２２∶６含量鱼油组明显高于豆油组，而且鱼油中Ｃ２２∶６比Ｃ２０∶５优先结合掺入磷脂中。ＰＣ中Ｃ２０∶４豆油组明显高于鱼油组。ω６／ω３比值降低。豆油和鱼油均使线粒体Ｃａ２＋－ＡＴＰａｓｅ活性下降，但对线粒体钙有不同的影响。补硒对脂肪酸组成，Ｃａ２＋－ＡＴＰａｓｅ影响不大，但加速钙的释放。结论：鱼油具有防治心血管疾病的作用，其作用基础可能在于Ｃ２０∶５和Ｃ２２∶６掺入细胞膜磷脂中，影响了脂肪酸组成，并对其功能产生影响     

兔和大鼠吸入全氟异丁烯后血液氟离子浓度的变化

目的了解家兔及大鼠吸入全氟异丁烯（PnB）后血液中氟离子（FL）浓度的变化。方法家兔6只，雌雄各半；大鼠48只，雌雄各半，随机均分为8组。在动物动态染毒装置中，家兔头部暴露染毒20min，染毒浓度为（0．300±0．005）mg／L；大鼠头部暴露8min，染毒浓度为（0．150±0．005）mg／L。测定家兔染毒前和染毒后0…3612、24h时血液中P浓度；分别测定大鼠染毒前和染毒后0、0.5、1．0、1．5、2．0、2．5、3．0h时血液中F^-浓度。结果与染毒前比较，家兔及大鼠染毒后即刻血液中P浓度明显升高，差异有统计学意义（P〈0．01）。大鼠染毒后0．5和1．0h血液中F^-浓度仍明显高于染毒前，差异有统计学意义（P〈0．05）；至染毒后1．5h血液中F^-浓度与染毒前基本一致。结论PFIB被动物吸入后迅速与体内物质作用，产物中有可解离出F^-的产物，血液中肿农度升高可为临床提供诊断依据。     

昆山市饮用水中氟含量的调查分析

天然水中氟化物的含量一般为0．2mg／L，流经含氟矿层的地下水有时高达2～5mg／L。一般认为饮用水适宜的氟含量为0．5～1．0mg／L。氟含量过高，将使儿童产生氟斑牙，超过5mg／L时，可引起人体和家畜的氟骨症；氟含量过低，被认为是诱发龋齿的重要因素。因此，在国内外对供水的脱氟和加氟已作为饮水卫生的重要措施。我国规定生活饮用水中氟含量限值为1．0mg／L^[1]。昆山地处长江三角洲，为冲积平原，无含氟矿层。传统经济为农业和养殖业，化工企业只有零星几家，     

膳食维生素E对大鼠红细胞膜丙二醛和唾液酸含量的影响

维生素Ｅ（ＶＥ）可以保护细胞膜免受脂质过氧化损害，唾液酸是细胞膜上的多糖残基。为了探讨膳食ＶＥ对细胞膜唾液酸（ＳＡ）的影响，对ＳＤ大鼠饲以含不同ＶＥ水平的饲料，并对大鼠进行冷暴露刺激，检测了大鼠红细胞膜ＳＡ的丙二醛（ＭＤＡ）含量。实验结果表明：低ＶＥ膳食（饲料ＶＥ含量为３０ｍｇ／ｋｇ）摄入组大鼠在冷暴露时死亡率明显高于高ＶＥ膳食（饲料ＶＥ含量为２３０ｍｇ／ｋｇ）组大鼠；冷暴露１０天后，大鼠红细胞膜ＳＡ含量降低；高ＶＥ膳食组大鼠ＳＡ含量明显高于低ＶＥ组；冷暴露对红细胞膜ＭＤＡ含量无明显影响；膜ＭＤＡ含量和ＳＡ含量间无明显相关关系。说明ＶＥ可以提高大鼠红细胞膜ＳＡ含量，但此结果尚不能用降低ＬＰＯ作用来解释。     

2,4,6-三氯苯酚对Vero细胞状态及质膜组分的影响

目的研究有机化学污染物对Vero细胞状态及质膜组分的影响,以阐明Vero细胞变形的分子机制,为建立一种基于Vero细胞变形的微量化学污染物生物毒性定量分析方法提供理论基础。方法选取了典型污染物2,4,6-三氯苯酚(2,4,6-trichlorophenol,TCP)为研究对象,采用流式细胞术分析了不同浓度(0、1、5、20、50mg/L)TCP对Vero细胞状态的影响。采用两相分配法提取了具有活力的细胞质膜,运用膜组分分析技术研究了不同浓度(0、25、50、75、100、125mg/L)TCP对Vero细胞状态和细胞膜结构、组分的影响。结果与对照(0mg/L)相比,1、5、20、50mg/L的TCP就可导致Vero细胞的变形。随着TCP染毒浓度的升高,活细胞数呈下降趋势,死细胞数呈升高趋势。污染物在导致细胞凋亡与坏死前,先致Vero细胞膜的损伤。随着TCP浓度的升高,变形Vero细胞质膜中蛋白和磷脂含量呈下降趋势,蛋白/磷脂比值呈升高趋势。结论 TCP对Vero细胞质膜中蛋白和磷脂含量以及蛋白/磷脂比值的影响可能导致细胞膜刚性结构的变化,进而导致细胞形态异常。     

Dietary linoleic acid modulates liver plasma membrane unsaturated fatty acid composition,phosphatidylcholine and cholesterol content,as well as glucagon stimulated adenylate cyclase activity

Male Sprague-Dawley rats were fed diets containing 20% (w/w) fat in which linoleic acid was substituted for saturated fatty acids. High or low levels of dietary linoleic acid were fed for 24 days. Liver plasma membranes were isolated for analysis of lipid composition and glucagon stimulated adenylate cyclase activity. Dietary saturated fatty acid content did not affect the saturated fatty acid composition of membrane phospholipids. Increase in dietary linoleic acid increased content of linoleic acid homologues in phosphatidylcholine. Diets low in linoleic acid increased total phosphatidylcholine and cholesterol levels in the plasma membrane, increasing glucagon stimulated and fluoride stimulated adenylate cyclase activity. These observations imply that change in glucagon stimulated adenylate cyclase activity resulted from transitions in membrane phospholipid content of linoleic acid and its homologous fatty acids or from associated changes in membrane phospholipid class content.     

Dietary trans fatty acids alter diaphragm phospholipid fatty acid composition, triacylglycerol content and glucose transport in rats

The present study evaluates the effect of dietary trans fatty acids on diaphragm phospholipid fatty acid composition, intramyocellular triacylglycerol content and insulin-stimulated glucose uptake in comparison with dietary saturated fatty acids. Male weanling WNIN rats were divided into three groups and fed for 3 months on one of the following diets containing 10 % oil differing in fatty acid composition: control diet, saturated fatty acid diet and trans fatty acid diet. Dietary trans fatty acids increased the intramyocellular triacylglycerols and decreased the ratio of 20 : 4n-6 to 18 : 2n-6 and long-chain PUFA levels (20 %) in diaphragm phospholipids, indicating inhibition of PUFA biosynthesis. However, saturated fatty acids decreased both 18 : 2n-6 and 20 : 4n-6 without change in the ratio. Trans fatty acid-induced alterations in diaphragm phospholipid fatty acid composition and intramyocellular triacylglycerol content were associated with decreased insulin-stimulated glucose transport in the diaphragm. These observations suggest that dietary trans fatty acids decrease diaphragm insulin sensitivity, possibly due to increased intramyocellular triacylglycerol accumulation and decreased long-chain PUFA in phospholipids.     

Phospholipid fatty acid composition and diamine oxidase activity of intestinal mucosa from rats treated with irinotecan hydrochloride (CPT-11) under vegetable oil-enriched diets: comparison between perilla oil and corn oil

BACKGROUND: Irinotecan hydrochloride (CPT-11), a topoisomerase I inhibitor highly effective for various cancers, has its dosage limited by diffuse mucosal damage with increased prostaglandin (PG) E(2). However, an analysis of intestinal phospholipid fatty acid composition after CPT-11 treatment has not been reported. This study aimed to evaluate intestinal phospholipid fatty acid composition in relation to intestinal mucosal integrity and plasma and mucosal PGE(2) levels after CPT-11 treatment. The effect of dietary vegetable oil supplementation, perilla oil vs corn oil, was also evaluated. METHODS: Intestinal phospholipid fatty acid composition, PGE(2) level, mucosal diamine oxidase (DAO) activity, diarrhea, and blood tests were evaluated in rats injected with CPT-11 under a conventional diet. The same parameters were compared among 3 different dietary vegetable oil supplementations: perilla oil, corn oil, and a 1:3, respectively, mixture with a semisynthetic diet during 14 days. RESULTS: CPT-11 treatment caused severe diarrhea, and intestinal mucosal fatty acid composition changed with increased PGE(2) level and decreased DAO activity. Decreases in eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and EPA/arachidonic acid (AA) ratio in colonic mucosa were observed. Perilla oil increased omega-3 polyunsaturated fatty acids, alpha-linolenic acid, EPA, and EPA/AA ratio and decreased plasma PGE(2). But the amounts used were not enough to attenuate intestinal damage from CPT-11 treatment. CONCLUSIONS: CPT-11 induced changes of intestinal mucosal fatty acid composition with increased PGE(2) level and decreased intestinal integrity; perilla oil shows the possibility of being able to attenuate those changes.     

Effect of chronic consumption of ethanol and vitamin E on fatty acid composition and lipid peroxidation in rat heart tissue.

Lipid peroxidation products and the fatty acid composition of phospholipids were studied in the hearts of rats chronically consuming ethanol supplemented with large amounts of vitamin E. Ethanol representing 36% of the total calories was ingested for 7 weeks in a modified Lieber-DeCarli liquid diet that contained vitamin E at 30 IU/L in the control or 172 IU/L in the supplemental dietary group. Ethanol and/or vitamin E did not change the absolute content (micrograms per mg of phospholipids) of the main fatty acids (C18:0, C18:2, and C20:4) of heart phospholipids but increased the amount of the minor C20-C22 fatty acids. Cardiac phospholipid levels increased in rats chronically consuming excess vitamin E and/or alcohol. Chronic ethanol consumption caused elevations of the relative content (percent of total fatty acids) of tri-, tetra-, and hexaenoic acids and peroxidizability index (PI) of the cardiac phospholipids. Supplementation with vitamin E blocked this ethanol-induced shift in the fatty acid profile toward unsaturation and decreased the PI. Ethanol enhanced accumulation of vitamin E in heart tissue by 30% irrespective of the vitamin E content in the diet. Enrichment of the diet with vitamin E coincided with the low levels of fluorescent products in heart lipids. A positive correlation (r = 0.36; p = 2%) was found between vitamin E and diene conjugates in the heart cells. Thus, vitamin E has a stabilizing effect on heart phospholipids by preventing changes in their fatty acid composition and peroxidative deterioration.     

Accumulation of linoleic and gamma-linolenic acids in tissue lipids of pyridoxine-deficient rats

Young male Sprague-Dawley rats were fed diets containing added pyridoxine . HCl at 22 mg/kg (control), 0 mg/kg or 88 mg/kg for 6 weeks. In comparison with control or pyridoxine-supplemented (+PN) rats, growth of the pyridoxine-deficient (-PN) rats was significantly less after 2 weeks. After 6 weeks, liver weight was higher but thymus and epididymal fat weights, in relation to body weight, were significantly lower in -PN compared to control rats. In -PN rats, phospholipid levels of linoleic and gamma-linolenic acids were increased, but arachidonic acid was decreased compared to controls in plasma, liver, thymus and skin. In liver triglycerides from -PN rats, all essential fatty acids (n3 and n6) were increased compared to both control and +PN rats. The n3 essential fatty acids were significantly increased in plasma, liver, and thymus phospholipids in the +PN compared to control rats. These results support previous reports of an effect of pyridoxine on essential fatty acid metabolism and suggest that both linoleic desaturation and gamma-linolenic acid elongation may be impaired in -PN rats. In addition, the accumulation of essential fatty acids in the liver triglycerides of -PN rats suggests that essential fatty acid turnover between triglyceride and phospholipid may be influenced by pyridoxine.     

共轭亚油酸对动脉粥样硬化老龄大鼠血脂和血浆脂肪酸的影响

目的:研究共轭亚油酸(CLA)对动脉粥样硬化(AS)老龄大鼠血脂和血浆脂肪酸组成的影响。方法:先用高脂饲料喂养SD老龄大鼠,建立AS模型后分别添加不同剂量的CLA,研究CLA对AS大鼠血脂和血浆脂肪酸含量和组成的影响。结果:CLA添加组均能改变实验大鼠血脂和血浆脂肪酸的含量,血脂中甘油三酯的含量有显著性改变,对照组为1.15mmol/L,CLA添加组分别为0.97、0.91和0.92mmol/L,HDL-C/LDL-C的比值均有所降低;总饱和脂肪酸(SFA)的含量CLA添加组比对照组显著降低,对照组为46.15%,CLA添加组分别为42.33%、41.34%和39.07%,;总单不饱和脂肪酸(MUFA)、总CLA和总n-6多不饱和脂肪酸(PUFA)的含量CLA添加组比对照组升高;M/P/S的比值CLA添加组与对照组相比MUFA和PUFA含量明显升高;n-3PUFA/n-6PUFA的比值,CLA添加组比对照组低。结论:CLA可以改善AS大鼠血脂和血浆脂肪酸的含量和组成,具有一定的抗AS作用。     

The effect of fish oil supplementation on brain DHA and EPA content and fatty acid profile in mice

Supplementation with omega-3 (n-3) fatty acids may improve cognitive performance and protect against cognitive decline. However, changes in brain phospholipid fatty acid composition after supplementation with n-3 fatty acids are poorly described. The purpose of this study was to feed increasing n-3 fatty acids and characterise the changes in brain phospholipid fatty acid composition and correlate the changes with red blood cells (RBCs) and plasma in mice. Increasing dietary docosahexaenoic (DHA) and eicosapentaenoic acid (EPA) did not alter brain DHA. Brain EPA increased and total n-6 polyunsaturated fatty acids decreased across treatment groups, and correlated with fatty acid changes in the RBC (r?>?0.7). Brain cis-monounsaturated fatty acids oleic and nervonic acid (p?p?相似文献   

Mitochondrial function in rats is affected by modification of membrane phospholipids with dietary sardine oil

Phospholipids of heart and liver of rats fed a diet containing sardine oil had more omega 3 polyunsaturated fatty acids and less omega 6 polyunsaturated fatty acids than those of rats fed corn oil, whereas there was little difference in the fatty acid composition of brain phospholipids. The mass of phospholipid classes in rat heart mitochondria was not changed, but their fatty acid compositions were altered. Modification of the fatty acid compositions of mitochondrial phosphatidylcholine and phosphatidylethanolamine reached a plateau after 10 d of feeding, but that of cardiolipin continued for 30 d. The O2 consumption rate of rat heart mitochondria decreased as the fatty acid composition of the phospholipids changed. This may be due to the reduction of the activity of cytochrome c oxidase, which requires cardiolipin for its activity. However, F1F0-ATPase, which also requires cardiolipin, was activated under the same conditions.