碘氟联用对大鼠红细胞膜磷脂和脂肪酸的影响

目的研究高氟及碘氟联用对大鼠红细胞膜磷脂和脂肪酸组成的影响。方法选用SD大鼠，饮用加氟(150mg／L)及同时分别加入不同浓度碘化钾(0．003，0．03，3mg／L)溶液共5个月，用高效液相色谱法测定大鼠红细胞膜磷脂和肪肪酸含量。结果高碘高氟组大鼠血液红细胞膜磷脂含量下降；高氟组大鼠血液红细胞膜的不饱和脂肪酸下降，饱和脂肪酸含量上升，中等浓度的碘起到毒性协同作用。结论长期摄入过量氟导致血液红细胞膜磷脂、脂肪酸组成改变，不饱和脂肪酸减少，这可能与自由基水平升高所造成的脂质过氧化增强有关；一定浓度的碘可能对氟中毒大鼠血液中红细胞膜磷脂脂肪酸组成的影响有协同作用。     

慢性氟中毒大鼠脑组织辅酶Q含量的改变

以小剂量（６６．３ｍｇ／Ｌ）和大剂量（２２１ｍｇ／Ｌ）的含氟水饲养Ｗｉｓｔａｒ纯系小鼠，实验期分别为３个月、５个月和７个月，用来复制不同程度病理损害的慢性氟中毒动物模型。用高效液相色谱方法测定各组动物脑组织中胆固醇、多萜醇和辅酶Ｑ含量。实验结果显示，慢性氟中毒大鼠脑组织中胆固醇和多萜醇含量与正常对照组相比，未见异常改变。染氟动物脑组织中辅酶Ｑ含量在氟中毒早期均有所降低，而在氟中毒后期明显增加。辅酶Ｑ含量变化可能与氟诱发的自由基水平改变有关     

慢性氟中毒对大鼠脑组织脂质过氧化水平和抗氧化能力的影响

目的研究氟在大鼠脑组织中的蓄积及其对脂质过氧化水平和抗氧化能力的影响。方法用氟化钠对大鼠进行亚慢性染毒,测定大鼠脑组织中氟浓度和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（SOD）、谷胱甘肽过氧化物氧化酶（GSH-Px）的活力。结果大鼠脑组织中氟浓度与染毒剂量呈正相关,高剂量组脑组织氟浓度明显高于低剂量组和对照组（P〈0．01）。脂质过氧化产物MDA含量在三组问差异有统计学意义（P〈0．01）,高剂量组MDA含量高于低剂量组,低剂量组高于对照组。抗氧化酶SOD和GSH-Px的活力三组间差异有统计学意义（P〈0．01）。但在组间比较时发现,低剂量组与对照组间差异没有统计学意义（P〉0．05）。高剂量组与低剂量组、对照组间差异有统计学意义（P〈0．01）。脑组织中氟浓度与MDA含量之间呈明显正相关（r=0．731,P〈0．01）,而与SOD和GSH．Px的相关性不明显（r分别为0．234和0．148,P〉0．05）,MDA与SOD和GSH-Px呈明显负相关（r分别为一0．571和0．591,P〈0．01）。结论氟可透过血脑屏障在大鼠脑内蓄积。过量的氟接触将导致机体抗氧化系统紊乱,脂质过氧化程度加剧,造成脑组织氧化性损伤。     

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     

硫芥中毒复合烫伤早期大鼠血浆MDA和SOD的变化

目的探讨硫芥中毒合并烫伤对大鼠血浆丙二醛和过氧化物岐化酶的影响.方法分别注射0.2 LD50、0.4 LD50、0.6 LD50剂量的硫芥,以测定剂量-效应关系.大鼠以92℃热水致伤18 s,建立硫芥中毒合并大鼠深Ⅱ度烫伤模型,同时注射硫芥0.6 LD50.伤后1 h、2 h、6 h、12 h、24 h取心脏血,常规方法测定血浆丙二醛含量和过氧化物岐化酶活性.结果单纯硫芥中毒和单纯烫伤均可引起丙二醛含量升高,6 h开始下降.伤后2 h丙二醛含量随硫芥剂量的增大而增加.过氧化物岐化酶活性在接触硫芥和烫伤后均显著降低.硫芥-烫伤复合伤动物血浆丙二醛含量和过氧化物岐化酶活性变化比单纯损伤强烈.结论硫芥中毒复合烫伤导致的脂质过氧化反应比单纯中毒或单纯烫伤严重.     

大鼠肾脏某些金属含量对铅致脂质过氧化的影响

大鼠经饮水连续染铅（醋酸铅１５００ｍｇ／Ｌ蒸馏水）。分别在第１、２、４、６、８周末处死动物，取肾脏进行脂质过氧化相关指标及铅、锌、铜含量测定。结果表明，铅使丙二醛的生成量显著增加，且不受还原性谷胱甘肽含量的影响。超氧物歧化物酶活力表现为先受抑后升高再正常的变化过程，与组织中锌含量先降低后正常的状况一致。提示：铅可能通过取代酶活性中心的锌而抑制其活力，进而引起脂质过氧化。     

甲基汞在脑组织中的积累和脂质过氧化作用

[目的]通过对SD大鼠进行腹腔注射氯化甲基汞,研究不同时间、不同剂量氯化甲基汞在大鼠脑组织中的积累情况和对大鼠脑组织的脂质过氧化作用及两者之间可能存在的关系.[方法]将SD大鼠在不同剂量(0,0.05,0.5,5mg/kg)下分别暴露20min和24h.处死后测定脑组织汞含量、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量.[结果]20min时,0.5mg/kg剂量下脑组织汞含量为(0.0173±0.0230)μg/g,表明甲基汞已到达脑组织;20min时,各剂量下各脂质过氧化指标与对照组相比均未见显著差异.24h时,5mg/kg剂量下,GSH-Px活性为(19.13±4.49)U/mgprot,SOD活性为(89.09±13.55)U/ml,MDA含量为(3.53±0.70)nmol/ml,与对照相比差异显著,表明已有脂质过氧化发生.[结论]甲基汞对脑组织有极大的亲合性,在0.5mg/kg剂量下,20min即可迅速穿过血脑屏障进入脑组织并逐渐积累.脂质过氧化作用是在甲基汞积累到一定程度后发生,可能与组织中汞的含量有一定关系.     

外源性脂肪酸对结肠癌细胞生长的影响及其可能机制

目的：探讨八种外源性脂肪酸对人结肠癌细胞生长的影响及其作用机制。方法：体外实验中应用MTT法观察外源性脂肪酸对细胞生长的影响，并对细胞脂质过氧化反应产物丙二醛含量进行了测定。结果：多不饱和脂肪酸可抑制结肠癌细胞生长，饱和及单不饱和脂肪酸作用不明显，八种脂肪酸对正常成纤维细胞没有明显抑制作用。多不饱和脂肪酸可引起细胞内丙二醛含量升高。结论：多不饱和脂肪酸可选择性抑制肿瘤细胞生长，脂质过氧化反应增强，可能是其主要作用机制。     

多元抗氧化营养胶囊对自然衰老大鼠抗氧化功能的研究

目的:探讨多元抗氧化营养胶囊对自然衰老大鼠的抗氧化作用。方法:将40只Wistar老年雄性大鼠根据其血清丙二醛(MDA)含量分层随机分成4个组,每组10只,根据样品的人体推荐量设147、73、37 mg/kg BW(分别相当于人体推荐用量的20、10、5倍)3个剂量实验组,同时设一个阴性对照组。阴性对照组给予等体积的玉米胚芽油,每天灌胃一次,连续灌胃60 d。60 d后处死动物,留取血液和肝、脑组织,测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和过氧化脂质含量(以MDA计)、脂褐质(Lip)含量。结果:多元抗氧化营养胶囊能降低大鼠的血清及肝组织匀浆液中过氧化脂质含量和肝组织匀浆液中的脂褐质含量,提高大鼠的血清和脑组织匀浆液中SOD及GSH-Px活力,对大鼠的体重无不良影响。结论:多元抗氧化营养胶囊具有抗氧化的功能。     

明矾对大鼠脑组织脂质过氧化及金属元素影响

目的研究明矾对大鼠脑组织脂质过氧化和铜、锰、铁、锌含量影响,探讨明矾对大鼠脑神经损伤机制。方法 32只Wistar大鼠,随机分为4组,在大鼠饲料中加入不同剂量明矾,染毒30 d,测定大鼠脑组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,采用原子吸收分光光度法测定铝、铜、锰、铁、锌含量。结果低、中、高剂量组大鼠脑组织中MDA含量分别为(1.64±0.25),(2.10±0.36),(2.33±0.27)nmol/mgprot,明显高于对照组(1.16±0.26)nmol/mgprot(P0.01);与对照组比较,高剂量组SOD活性明显下降(P0.05),中、高剂量组GSH-Px活性下降(P0.05);低、中、高剂量组大鼠脑组织中铝含量分别为(2.19±0.39),(2.48±0.33),(3.52±0.41)g/g,明显高于对照组(P0.01),各剂量组大鼠脑组织中铜、锰、铁、锌含量与对照组比较呈降低趋势。结论明矾在一定程度上影响大鼠脑组织脂质过氧化水平,可能是明矾引起大脑神经损伤的机制之一。     

Effect of fish oil pretreatment on isoproterenol-induced changes in myocardial membrane phospholipids

OBJECTIVE: In the present study, the protective effect of fish oil treatment on the fatty acid composition in isoproterenol (IPH)-induced myocardial infarction was studied in male albino Wistar rats. METHODS: Rats were injected for 2 consecutive days with IPH (60 mg/kg body weight) at 24-h intervals to induce myocardial infarction. Fish oil was administered orally at a dose of 0.05 mL/d for 45 d, after which serum and heart tissue were assayed for lipid profile, lipoprotein changes, and myocardial membrane phospholipid fatty acid composition. RESULTS: Biochemical assessment of myocardial infarction was done by measuring the activities of creatinine kinase and lactate dehydrogenase, which were significantly elevated in the rats administered with IPH. Further, the administration of IPH modified the fatty acid composition and analysis of fatty acids showed there was an increase in the omega-3/omega-6 ratio in phospholipid pool. In addition, increased levels of total cholesterol, free cholesterol, ester cholesterol, phospholipids, triacylglycerols and free fatty acid was observed in serum and heart tissue of IPH-induced rats. The fish oil treatment for a period of 45 d decreased the levels of cardiac markers (creatinine kinase and lactate dehydrogenase) and reversed the biochemical lesions induced by IPH. CONCLUSION: Our study suggests that fish oil treatment has a hypolipidemic effect and has potential use in the treatment of myocardial infarction.     

Olive oil feeding up-regulates uncoupling protein genes in rat brown adipose tissue and skeletal muscle

BACKGROUND: Some nutrients, such as carotenoids, retinoic acid, and certain types of fatty acids, increase thermogenic capacity. OBJECTIVE: The influence of 4 dietary lipid sources (olive oil, sunflower oil, palm oil, and beef tallow) on the content of uncoupling proteins 1, 2, and 3 (UCP1, UCP2, and UCP3) and their messenger RNA (mRNA) expression in several tissues of rats was compared. DESIGN: Wistar rats were randomly divided into 4 groups and fed ad libitum diets containing 40% of energy as fat. UCP1, UCP2, and UCP3 mRNA and protein were assessed by Northern blot and Western blot, respectively. Oxygen consumption in tissues was measured by polarography. Total-body oxygen consumption was assessed in an open-circuit chamber system. Circulating fuels (fatty acids and glucose) and hormones (triiodothyronine, thyroxine, corticosterone, and insulin) were measured. RESULTS: Olive oil feeding induced the highest UCP1, UCP2, and UCP3 mRNA expression in interscapular brown adipose tissue. An analogous effect was observed in gastrocnemius muscle UCP3 mRNA. No significant differences were observed in perirenal white adipose tissue UCP2 mRNA. Changes in mRNAs were not accompanied by close changes in the protein content of UCPs and were not associated with changes in adipose tissue oxygen consumption. Nevertheless, total-body oxygen consumption was higher in rats fed olive oil than in those fed the other 3 diets. No significant differences were found in body and tissue weights or in serum indexes. CONCLUSION: Olive oil induced an up-regulating effect on UCP mRNA that was probably not mediated by systemic metabolic changes, but rather related to a local effect on interscapular brown adipose tissue and skeletal muscle.     

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.     

Protective role of Phaseolus vulgaris on changes in the fatty acid composition in experimental diabetes

The present investigation was carried out to evaluate the effect of Phaseolus vulgaris, an indigenous plant used in Unani and Ayurvedic medicine in India, on blood glucose, plasma insulin, cholesterol, triglycerides, free fatty acids, phospholipids, and fatty acid composition of total lipids in liver, kidney, and brain of normal and streptozotocin (STZ) diabetic rats. The results show that there was a significant increase in tissue cholesterol, triglycerides, free fatty acids, and phospholipids in STZ diabetic rats. The analysis of fatty acids showed that there was a significant increase in the concentrations of palmitic acid (16:1), stearic acid (18:0), and oleic acid (18:1) in liver, kidney, and brain, whereas the concentrations of linolenic acid (18:3) and arachidonic acid (20:4) were significantly decreased. Oral administration of the aqueous extract of P. vulgaris pods (200 mg/kg of body weight) for 45 days to diabetic rats decreased the concentrations of lipids and fatty acids, viz., palmitic, stearic, and oleic acids, whereas linolenic and arachidonic acids were elevated. Similarly, the administration of P. vulgaris pod extract (PPEt) to normal animals resulted in a significant hypolipidemic effect. These results suggest that PPEt exhibits hypoglycemic and hypolipidemic effects in STZ diabetic rats. It also prevents the fatty acid changes produced during diabetes. The effect of PPEt at 200 mg/kg of body weight was better than that of glibenclamide.     

褪黑素对细菌脂多糖导致的宫内感染脑损伤的保护作用

目的:研究褪黑素(melatonin,MT)对宫内感染胎鼠脑组织自由基的影响,探讨MT对宫内感染胎鼠脑组织的保护作用。方法:通过给孕鼠腹腔注射细菌脂多糖(lipopolysaccharide,LPS),造成宫内感染脑瘫动物模型,并行MT干预。选用妊娠第19天SD大鼠随机分为空白对照组、宫内感染组和MT处理组,宫内感染组孕鼠缓慢腹腔注射LPS500μg/kg,MT处理组孕鼠腹腔注射LPS 500μg/kg+MT 10 mg/kg。将各大组孕鼠根据注药后观察时间不同,平均分为注药后2 h、6 h、12 h 3小组,各小组4只孕鼠。各小组于相应的时间点迅速处死,于冰盒上剖腹取胎鼠脑组织,分别测定脑组织匀浆的超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)含量,HE染色观察组织病理变化,并比较各组之间的差异。结果:宫内感染组较空白对照组胎鼠脑组织中SOD、GSH-Px活力下降,MDA含量上升;同时随着感染时间的延长,上述改变亦趋于明显,差异有统计学意义。与宫内感染组相比,MT处理组能提高胎鼠脑组织中SOD、GSH-Px活力,降低MDA含量。结论:宫内感染胎鼠脑组织在宫内已出现自由基蓄积而自身清除力不足,导致胎鼠脑组织损伤,并随着感染时间的延长而脑损伤逐渐加重。褪黑素能对宫内感染胎鼠脑损伤有抗氧化和较强的自由基清除作用,有神经保护作用。     

Pork with a high content of polyunsaturated fatty acids lowers LDL cholesterol in women

BACKGROUND: Animal products contribute significantly to the saturated fat and cholesterol content of the American diet. Contrary to dietary advice, consumers have not limited their consumption of animal products. Thus, an alternative approach might be to modify the fatty acid composition of animal products. OBJECTIVE: We tested the hypothesis that modified pork with a high content of polyunsaturated fatty acids (PUFAs) and a low content of saturated fatty acids (SFAs) would lower plasma LDL-cholesterol concentrations in women. DESIGN: Twenty women aged 19-24 y completed a crossover study with 2 diets. Nutritionally complete diets containing 42% of energy from fat differed only in the inclusion of either standard or modified pork. Venous blood samples were collected at weeks 0, 4, and 8. RESULTS: The diet containing modified pork significantly lowered total plasma (P < 0.0076) and LDL (P < 0.0382) cholesterol. The modified diet also resulted in an increase in the PUFA and a decrease in the SFA and monounsaturated fatty acid contents of the cholesteryl ester, free fatty acid, phospholipid, and triacylglycerol lipid classes in both plasma and erythrocytes. Plasma concentrations of glucose, insulin, triacylglycerol, and free fatty acids did not change significantly. CONCLUSIONS: Consumption of pork with a high PUFA content resulted in a decrease in the subjects' total plasma and LDL cholesterol and shifted the fatty acid composition from SFAs to PUFAs in the plasma and erythrocytes. Modification of the fatty acid composition of animal foods will be a useful approach to lowering the saturated fat consumption of Americans.     

Effects of alpha-ketoglutarate on antioxidants and lipid peroxidation products in rats treated with ammonium acetate

The effects of alpha-ketoglutarate (alpha-KG) on hyperammonemia induced by ammonium acetate were studied biochemically in experimental rats. The levels of circulatory urea and non-protein nitrogen increased significantly in rats treated with ammonium acetate and decreased significantly in rats treated with alpha-KG and ammonium acetate. In liver and kidney tissues, similar patterns of alterations across groups were observed in the levels of thiobarbituric acid-reactive substances and lipid profile variables (free fatty acids, triacylglycerols, phospholipids, and cholesterol). Further, enzymatic (superoxide dismutase, catalase, and glutathione peroxidase) and non-enzymatic (reduced glutathione) antioxidants in both tissues decreased significantly in rats treated with ammonium acetate and increased significantly in rats treated with alpha-KG and ammonium acetate. The biochemical alterations during alpha-KG treatment might have been due to 1) the detoxification of excess ammonia, 2) participation in the non-enzymatic oxidative decarboxylation during hydrogen peroxide decomposition, and 3) enhancement of the proper metabolism of fats that could suppress oxygen radical generation and thus prevent lipid peroxidative damages in rats.     

The influence of dietary medium and long chain triglycerides on growth performances and fat deposition in growing rats.

The present study was undertaken to investigate the effects of dietary medium and long chain triglycerides (MCT and LCT) on fat deposition and fatty acid composition of adipose tissues of rats. Twenty-seven Wistar strain male rats were divided into three groups and fed semisynthetic experimental diets: Basal (AIN 76), MCT (basal+C8:0 10%), LCT (basal+corn oil 10%). Feed intake was measured every day and body weight was measured once a week. At the beginning, 4th and 8th week of experimental feeding, 3, 12, 12 rats were slaughtered, respectively. Liver, perirenal and epididymal adipose tissue pads were weighted and their fatty acid composition was determined. Chemical composition of wholebody carcass was measured. Body weight gain was greater in rats fed the LCT diet than in rats fed the basal and MCT diets. Feed intakes were decreased in rats fed the MCT and LCT diets compared to that of the basal group. Subsequently, when compared to the basal group rats, feed efficiencies in rats fed the MCT and LCT diets were improved at the level of 6 and 14% for 4 weeks, and then 17 and 24% for 8 weeks, respectively. The weight of perirenal and epididymal adipose tissue pads tended to be larger in rats fed the MCT and LCT diets than in the basal group, although not significant. There were not significant differences in wholebody composition among the three groups. But it appeared that in rats fed the MCT diet, moisture content tended to be decreased and crude protein content increased compared to the LCT group rats. Fatty acid composition of the rats fed the LCT diet showed a good reflection of dietary fatty acid composition. Unlike LCT, little of medium chain fatty acid (MCFA) itself were incorporated into liver or adipose tissues. However, it seems that fat deposition of the MCT group was accomplished not by incorporation of dietary fatty acids but by de novo fatty acids synthesis.