Creatine and Antioxidant Treatment Prevent the Inhibition of Creatine Kinase Activity and the Morphological Alterations of C6 Glioma Cells Induced by the Branched-Chain α-Keto Acids Accumulating in Maple Syrup Urine Disease

Accumulation of the branched-chain alpha-keto acids (BCKA), alpha-ketoisocaproic acid (KIC), alpha-keto-beta-methylvaleric acid (KMV), and alpha-ketoisovaleric acid (KIV) and their respective branched-chain alpha-amino acids (BCAA) in tissues and biological fluids is the biochemical hallmark of patients affected by the neurometabolic disorder known as maple syrup urine disease (MSUD). Considering that brain energy metabolism is possibly altered in MSUD, the objective of this study was to determine creatine kinase (CK) activity, a key enzyme of energy homeostasis, in C6 glioma cells exposed to BCKA. The cells were incubated with 1, 5, or 10 mM BCKA for 3 h and the CK activity measured afterwards. The results indicated that the BCKA significantly inhibited CK activity at all tested concentrations. Furthermore, the inhibition caused by the BCKA on CK activity was totally prevented by preincubation with the energetic substrate creatine and by coincubation with the N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, indicating that deficit of energy and nitric oxide (NO) are involved in these effects. In contrast, other antioxidants such as glutathione (GSH) and trolox (soluble Vitamin E) were not able to prevent CK inhibition. In addition, we observed that the C6 cells changed their usual rounded morphology when exposed for 3 h to 10 mM BCKA and that creatine and L-NAME prevented these morphological alterations. Considering the importance of CK for brain metabolism homeostasis, it is conceivable that inhibition of this enzyme by increased levels of BCKA may contribute to the neurodegeneration of MSUD patients.     

ω3 fatty acid desaturases from microorganisms: structure, function, evolution, and biotechnological use

The biosynthesis of very-long-chain polyunsaturated fatty acids involves an alternating process of fatty acid desaturation and elongation catalyzed by complex series of enzymes. ω3 desaturase plays an important role in converting ω6 fatty acids into ω3 fatty acids. Genes for this desaturase have been identified and characterized in a wide range of microorganisms, including cyanobacteria, yeasts, molds, and microalgae. Like all fatty acid desaturases, ω3 desaturase is structurally characterized by the presence of three highly conserved histidine-rich motifs; however, unlike some desaturases, it lacks a cytochrome b5-like domain. Understanding the structure, function, and evolution of ω3 desaturases, particularly their substrate specificities in the biosynthesis of very-long-chain polyunsaturated fatty acids, lays the foundation for potential production of various ω3 fatty acids in transgenic microorganisms.     

Identification and characterization of new Δ-17 fatty acid desaturases

ω-3 fatty acid desaturase is a key enzyme for the biosynthesis of ω-3 polyunsaturated fatty acids via the oxidative desaturase/elongase pathways. Here we report the identification of three ω-3 desaturases from oomycetes, Pythium aphanidermatum, Phytophthora sojae, and Phytophthora ramorum. These new ω-3 desaturases share 55 % identity at the amino acid level with the known Δ-17 desaturase of Saprolegnia diclina, and about 31 % identity with the bifunctional Δ-12/Δ-15 desaturase of Fusarium monoliforme. The three enzymes were expressed in either wild-type or codon optimized form in an engineered arachidonic acid producing strain of Yarrowia lipolytica to study their activity and substrate specificity. All three were able to convert the ω-6 arachidonic acid to the ω-3 eicosapentanoic acid, with a substrate conversion efficiency of 54–65 %. These enzymes have a broad ω-6 fatty acid substrate spectrum, including both C18 and C20 ω-6 fatty acids although they prefer the C20 substrates, and have strong Δ-17 desaturase activity but weaker Δ-15 desaturase activity. Thus, they belong to the Δ-17 desaturase class. Unlike the previously identified bifunctional Δ-12/Δ-15 desaturase from F. monoliforme, they lack Δ-12 desaturase activity. The newly identified Δ-17 desaturases could use fatty acids in both acyl-CoA and phospholipid fraction as substrates. The identification of these Δ-17 desaturases provides a set of powerful new tools for genetic engineering of microbes and plants to produce ω-3 fatty acids, such as eicosapentanoic acid and docosahexanoic acid, at high levels.     

Differential effect of valproate and its Delta2- and Delta4-unsaturated metabolites, on the beta-oxidation rate of long-chain and medium-chain fatty acids

Overall fatty acid oxidation rates were investigated in rat hepatocytes using [9,10-3H]-palmitic, [9,10-3H]-oleic, [9,10-3H]-myristic and [2,3-3H]-phenylpropionic acids. The effect of both valproate (VPA) (0-10 mM) and two of its unsaturated metabolites, Delta2(E)-VPA and Delta4-VPA (0-10 mM), on the overall 3H2O production rate was studied. The results give evidence of a general inhibitory effect of VPA on the beta-oxidation rate of all the tested substrates. Similar effects were observed with both VPA metabolites but these effects appeared to be dependent on the chain length of the substrate. When the effect on the oxidation of the medium-chain fatty acid 3-phenylpropionate (PPA) was studied, Delta2(E)-VPA at 0.5 mM caused a 94% inhibition of the overall beta-oxidation rate. However, with long-chain substrates, 0.5 mM Delta(4)-VPA was a more potent inhibitor (20-30% of control activity) than 0.5 mM Delta(2E)-VPA (60-80% of control activity). Our results suggest that VPA and/or its metabolites inhibit fatty acyl-CoA metabolism within the mitochondrion by two different mechanisms. The first mechanism involves CoASH sequestration, which affects the oxidation rate of all fatty acids with different chain length. The second mechanism is more specific in nature and involves selective inhibition of particular enzymes implicated in fatty acid beta-oxidation.     

Uridine Prevents Fenofibrate-Induced Fatty Liver

Uridine, a pyrimidine nucleoside, can modulate liver lipid metabolism although its specific acting targets have not been identified. Using mice with fenofibrate-induced fatty liver as a model system, the effects of uridine on liver lipid metabolism are examined. At a daily dosage of 400 mg/kg, fenofibrate treatment causes reduction of liver NAD⁺/NADH ratio, induces hyper-acetylation of peroxisomal bifunctional enzyme (ECHD) and acyl-CoA oxidase 1 (ACOX1), and induces excessive accumulation of long chain fatty acids (LCFA) and very long chain fatty acids (VLCFA). Uridine co-administration at a daily dosage of 400 mg/kg raises NAD⁺/NADH ratio, inhibits fenofibrate-induced hyper-acetylation of ECHD, ACOX1, and reduces accumulation of LCFA and VLCFA. Our data indicates a therapeutic potential for uridine co-administration to prevent fenofibrate-induced fatty liver.     

Continuum solvent model studies of the interactions of an anticonvulsant drug with a lipid bilayer

Valproic acid (VPA) is a short, branched fatty acid with broad-spectrum anticonvulsant activity. It has been suggested that VPA acts directly on the plasma membrane. We calculated the free energy of interaction of VPA with a model lipid bilayer using simulated annealing and the continuum solvent model. Our calculations indicate that VPA is likely to partition into the bilayer both in its neutral and charged forms, as expected from such an amphipathic molecule. The calculations also show that VPA may migrate (flip-flop) across the membrane; according to our (theoretical) study, the most likely flip-flop path at neutral pH involves protonation of VPA pending its insertion into the lipid bilayer and deprotonation upon departure from the other side of the bilayer. Recently, the flip-flop of long fatty acids across lipid bilayers was studied using fluorescence and NMR spectroscopies. However, the measured value of the flip-flop rate appears to depend on the method used in these studies. Our calculated value of the flip-flop rate constant, 20/s, agrees with some of these studies. The limitations of the model and the implications of the study for VPA and other fatty acids are discussed.     

RESPIRATION AND PROTEIN SYNTHESIS IN ESCHERICHIA COLI MEMBRANE-ENVELOPE FRAGMENTS : II. Effects of Fatty Acids and Albumin on Respiration

Fatty acids inhibited the ability of Escherichia coli membrane-envelope fragments to catalyze the oxidation of succinate and nicotinamide adenine dinucleotide, reduced form (NADH) and also inhibited the response of the Clark oxygen electrode to nonenzymatic oxygen uptake. In all cases, unsaturated fatty acids were much more inhibitory than saturated fatty acids. Albumin afforded complete protection from inhibition in the nonenzymatic oxygen-uptake experiments but only partial protection for the respiratory activities of the membrane fragments. The succinoxidase activity was totally inhibited by bovine serum albumin at concentrations that inhibited succinate dehydrogenase only slightly and NADH oxidase not at all. The E. coli acellular preparation showed no dehydrogenase or oxidase activity for any of the fatty acids under a variety of conditions. These conditions included variations of pH, concentration of fatty acids, and the presence or absence of albumin, CoA, ATP, NAD, cysteine, succinate, and carnitine. It thus appears that E. coli grown in the absence of fatty acid can not use fatty acids as an energy source.     

Effect of Long Chain Fatty Acids on Bacterial Respiration and Amino Acid Uptake

S ummary . Long chain fatty acids stimulated oxygen uptake by Gram positive bacteria at bactericidal and protoplast lytic concentrations and produced inhibition at higher levels. The order of activity between individual acids and effects of reversal agents on respiratory activity corresponded to those which produced bactericidal activity. Protoplasts were more susceptible to inhibition than whole cells. Gram negative bacteria were inhibited to a limited extent at high fatty acid concentrations, but spheroplasts were highly sensitive. Fatty acids inhibited amino acid uptake both aerobically and anaerobically at sub-bactericidal levels. The effects were reversed by metal cations, and reflected the activity of dinitrophenol and sodium azide. The susceptibility of organisms to inhibition was of the same order as the sensitivity to other antibacterial effects. The probable mode of action of the fatty acids is discussed in terms of the interference with energy metabolism within the bacterial cell.     

Eicosapentaenoic acid ablates valproate-induced liver oxidative stress and cellular derangement without altering its clearance rate: dynamic synergy and therapeutic utility

The omega-3 fatty acid eicosapentaenoic acid (EPA) is a superb nature's medicine, with still unfolding health benefits. Because hepatotoxicity is a prominent adverse drug reaction, we currently attempted a new approach in which EPA was challenged to both alleviate hepatotoxicity and provide synergy with anticonvulsant effects of valproate (VPA). Besides, we verified whether EPA may kinetically modulate the clearance rate of VPA. VPA (500mg/kg p.o., for 2weeks) caused rat hepatotoxicity that was manifested as notable (2- to 4-fold) rise in serum liver enzymes (GGT, ALT, and ALP), increased hepatic levels of lipid peroxides and TNF-α (3- and 7-fold) and activity of myeloperoxidase (MPO, 4-fold), lowering of serum albumin (42%), and depletion of liver reduced glutathione (GSH, 36%). Furthermore, histopathologic examination revealed hepatocellular degeneration, focal pericentral necrosis, infiltration of inflammatory cells, and steatosis. Joint treatment with EPA (300mg/kg) blunted the oxidative stress, TNF-α levels and MPO activity, while enhanced levels of serum albumin and hepatic GSH. EPA also ameliorated most of the hepatocellular anomalies evoked by VPA. Additionally, in a mouse PTZ convulsion model, EPA markedly augmented the anticonvulsant effects of VPA far beyond their single responses. On the other hand, pharmacokinetic analyses revealed that joint EPA administration had no effect on serum VPA concentrations. Collectively, results demonstrate for the first time that the ω-3 FA (EPA) markedly alleviated VPA-induced hepatotoxicity, oxidative stress, and inflammation, while enhanced its anticonvulsant effects without altering its clearance. Therapeutically, these protective and synergy profiles for EPA foster a more safe and efficacious drug combination regimen than VPA.     

Dietary omega-3 and omega-6 polyunsaturated fatty acids modulate hepatic pathology

Recent evidence has suggested that dietary polyunsaturated fatty acids (PUFAs) modulate inflammation; however, few studies have focused on the pathobiology of PUFA using isocaloric and isolipidic diets and it is unclear if the associated pathologies are due to dietary PUFA composition, lipid metabolism or obesity, as most studies compare diets fed ad libitum. Our studies used isocaloric and isolipidic liquid diets (35% of calories from fat), with differing compositions of omega (ω)-6 or long chain (Lc) ω-3 PUFA that were pair-fed and assessed hepatic pathology, inflammation and lipid metabolism. Consistent with an isocaloric, pair-fed model we observed no significant difference in diet consumption between the groups. In contrast, the body and liver weight, total lipid level and abdominal fat deposits were significantly higher in mice fed an ω-6 diet. An analysis of the fatty acid profile in plasma and liver showed that mice on the ω-6 diet had significantly more arachidonic acid (AA) in the plasma and liver, whereas, in these mice ω-3 fatty acids such as eicosapentaenoic acid (EPA) were not detected and docosahexaenoic acid (DHA) was significantly lower. Histopathologic analyses documented that mice on the ω-6 diet had a significant increase in macrovesicular steatosis, extramedullary myelopoiesis (EMM), apoptotic hepatocytes and decreased glycogen storage in lobular hepatocytes, and hepatocyte proliferation relative to mice fed the Lc ω-3 diet. Together, these results support PUFA dietary regulation of hepatic pathology and inflammation with implications for enteral feeding regulation of steatosis and other hepatic lesions.     

Brain and systemic glucose metabolism in the healthy elderly following fish oil supplementation

Cerebral metabolic rate of glucose (CMRg) is lower in individuals affected by cognitive decline and dementia, especially in Alzheimer's disease. However, as yet there is no consensus as to whether CMRg decreases during healthy aging. Epidemiological studies show that weekly consumption of fish abundant in ω3 fatty acids has a protective effect on cognition during aging. Thus, the primary objective of this human study was to use positron emission tomography analysis with (18)F-fluorodeoxyglucose to evaluate whether supplementation with a fish oil rich in ω3 fatty acids increases cerebral glucose metabolism in young or elderly adults. Healthy young (23±5y old; n=5) and elderly (76±3y old; n=6) women and men were included in the study. Semi-quantitative expression of the data as 'standardized uptake values' showed that elderly participants had significantly lower cerebral glucose metabolism compared with the young group. However, when expressed quantitatively a CMRg, there was no effect of age or ω3 supplementation on glucose metabolism in any of the brains regions studied. Higher plasma triglyceride levels and higher plasma insulin levels were associated with lower CMRg in several regions, suggesting that a trend towards the metabolic syndrome may be associated with cerebral hypometabolism. We conclude that under these experimental conditions, ω3 supplementation did not affect brain glucose metabolism in the healthy elderly. Future studies in this area should address whether glucose intolerance or other conditions linked to the metabolic syndrome impact negatively on brain glucose metabolism and cognition.     

Long chain omega-3 fatty acids: Micronutrients in disguise

Considerable information has accumulated to show that DHA and EPA have unique roles that differ from other n-3 fatty acids and the n-6 fatty acids, with increasing understanding of the mechanisms through which these fatty acids reduce risk of disease. DHA and EPA regulate hepatic lipid and glucose metabolism, but are present in foods of animal origin, which are generally high in protein with variable triglycerides and low carbohydrate. Biological activity at intakes too low to provide significant amounts of energy is consistent with the definition of a vitamin for which needs are modified by life-stage, diet and genetic variables, and disease. Recent studies reveal that DHA may play a central role in co-coordinating complex networks that integrate hepatic glucose, fatty acid and amino acid metabolism for the purpose of efficient utilization of dietary protein, particularly during early development when the milk diet provides large amounts of energy from fat.     

“自我剪切”2A肽介导的Δ-12和ω-3脂肪酸脱氢酶以及过氧化氢酶在转基因小鼠肌肉表达研究

哺乳动物因为缺乏Δ-12和ω-3脂肪酸脱氢酶,不能自身合成必需的多不饱和脂肪酸．目前,通过转基因技术在哺乳动物体内表达ω-3脂肪酸脱氢酶,能将长链的n-6多不饱和脂肪酸转化成n-3多不饱和脂肪酸,造成体内长链的n-6多不饱和脂肪酸含量显著减低．本研究通过自我剪切2A肽介导Δ-12和ω-3脂肪酸脱氢酶(FAT-2和FAT-1)以及人过氧化氢酶(human catalase,hCAT)在小鼠的肌肉同时表达．结果表明,转基因小鼠肌肉中长链n-3多不饱和脂肪酸含量提高2.6倍,长链n-6多不饱和脂肪酸含量没有显著变化,而n-6/n-3比例显著降低(P < 0.01)．同时蛋白质印迹检测到人过氧化氢酶hCAT在小鼠的肌肉组织中表达,且过氧化氢酶活性比野生型小鼠显著提高(P < 0.01)．     

Fenproporex Increases Locomotor Activity and Alters Energy Metabolism,and Mood Stabilizers Reverse These Changes: a Proposal for a New Animal Model of Mania

Fenproporex (Fen) is converted in vivo into amphetamine, which is used to induce mania-like behaviors in animals. In the present study, we intend to present a new animal model of mania. In order to prove through face, construct, and predictive validities, we evaluated behavioral parameters (locomotor activity, stereotypy activity, and fecal boli amount) and brain energy metabolism (enzymes citrate synthase; malate dehydrogenase; succinate dehydrogenase; complexes I, II, II–III, and IV of the mitochondrial respiratory chain; and creatine kinase) in rats submitted to acute and chronic administration of fenproporex, treated with lithium (Li) and valproate (VPA). The administration of Fen increased locomotor activity and decreased the activity of Krebs cycle enzymes, mitochondrial respiratory chain complexes, and creatine kinase, in most brain structures evaluated. In addition, treatment with mood stabilizers prevented and reversed this effect. Our results are consistent with the literature that demonstrates behavioral changes and mitochondrial dysfunction caused by psychostimulants. These findings suggest that chronic administration of Fen may be a potential animal model of mania.     

Structural and functional changes in heart mitochondria from sucrose-fed hypertriglyceridemic rats

In the heart of sugar-induced hypertriglyceridemic (HTG) rats, cardiac performance is impaired with glucose as fuel, but not with fatty acids. Accordingly, the glycolytic flux and the transfer of energy diminish in the HTG heart, in comparison to control heart. To further explore the biochemical nature of such alteration in the HTG heart, the components of the non-glycolytic energy systems involved were evaluated. Total creatine kinase (CK) activity in the myocardial tissue was depressed by 30% in the HTG heart whereas the activity of the mitochondrial CK (mitCK) isoenzyme fraction that is functionally associated with oxidative phosphorylation decreased in isolated HTG heart mitochondria by 45%. Adenylate kinase (AK) was 20% lower in the HTG heart. In contrast, respiratory rates with 2-oxoglutarate (2-OG) and pyruvate/malate (pyr) were significantly higher in HTG heart mitochondria than in control mitochondria. 2-OG dehydrogenase activity was also higher in HTG mitochondria. Respiration with succinate was similar in both groups. Content of cytochromes b, c + c1 and a + a3, and cytochrome c oxidase activity, were also similar in the two kinds of mitochondria. A larger content of saturated and monounsaturated fatty acids was found in the HTG mitochondrial membranes with no changes in phospholipids composition or cholesterol content. Mitochondrial membranes from HTG hearts were more rigid, which correlated with the generation of higher membrane potentials. As the mitochondrial function was preserved or even enhanced in the HTG heart, these results indicated that deficiency in energy transfer was associated with impairment in mitCK and AK. This situation brought about uncoupling between the site of ATP production and the site of ATP consumption (contractile machinery), in spite of compensatory increase in mitochondrial oxidative capacity and membrane potential generation.     

Influence of dietary selenium and vitamin E on the levels of fatty acids in brain and liver tissues of lambs

In this study, the effects of dietary vitamin E, selenium, and their combination on the levels of fatty acid composition of the brain and liver tissues were examined. In brain tissue, the amounts of most fatty acids increased in vitamin E, combination and selenium groups compared with control group values. While the proportions of myristic, pentadecanoic, palmitic, linoleic, and total saturated fatty acids were decreased in vitamin E, Se and combination groups, eicosapentaenoic, total unsaturated and MUFA were increased in the same groups. In addition, the proportions arachidonic, eicosapentaenoic, total unsaturated, ω6 and MUFA in the combination group were higher than in the control group. In liver tissue, the amounts of myristic, pentadecanoic, palmitic, eicosedienoic, eicosapentaenoic, docosahexaenoic, ω3 and PUFA were higher in the combination group than in the control group. Also the proportions of eicosapentaenoic, docosahexaenoic acids in supplemented groups were higher than those in the control group. We conclude that dietary vitamin E and selenium have an influence on the levels of fatty acids in the brain and liver. Copyright © 1999 John Wiley & Sons, Ltd.     

Evaluation of energy metabolism on the myocardium analyzing of creatine kinase isoenzymes in rats]

The purpose of this study is to evaluate the efficiency of energy metabolism in the myocardium by means of the activities of creatine kinase (CK) and CK isoenzyme following age-related change in the heart and experimental heart failure. Wistar strain male rats aged from 3 weeks to 57 weeks after birth were used. The main experimental results obtained are as follows. (1) There were differences in the compositions of CK isoenzyme of the ventricular, atrial, and papillar muscles. No apparent variation, however, was noted among the basal portions of the left and right ventricular muscles, free wall of the left ventricle, and apex. (2) Compositions of CK isoenzyme analyzed from the ventricle and atrium were clearly different. The level of CK-B subunit activity of the ventricular muscle was highest level in the 5-week-old rat, and subsequently dropped significantly in the 24-week-old rat. Thereafter, the level gradually increased with aging. Dramatic change in the energy metabolism in the myocardium occurred in rats more than 3 weeks old. (3) Decrease in activity of m-CK but increase in activity of succinate dehydrogenase analyzed from the ventricular muscle of experimental heart failure induced by monocrotaline was recognized. From these results, the author assumed that the trend of the composition of CK isoenzyme is one of the indices in the determination of the regulation of energy metabolism of the myocardium.     

Metabolic syndrome: a brain disease

Recent research indicates an association between brain dysfunction and the pathogenesis of metabolic syndrome. To investigate this, we created a Medline search (up to December 2011) of articles in PubMed. The results indicated that refined carbohydrates, saturated and total fat, high levels of ω-6 fatty acids, and low levels of ω-3 fatty acids and other long chain polyunsaturated fatty acids (PUFA), all in conjunction with sedentary behaviour and mental stress can predispose to inflammation. Increased sympathetic activity, with increased secretion of catecholamine, cortisol, and serotonin can cause oxidative stress, which may damage the arcuate nucleus as well as the hypothalamus and macrophages, and the liver may release pro-inflammatory cytokines. These, in conjunction with an underlying deficiency in long chain PUFA, may damage the arcuate nucleus as well as neuropeptide-Y and pro-opiomelanocortin neurons and insulin receptors in the brain, especially during fetal life, infancy, and childhood, resulting in their dysfunction. Of the fatty acids in the brain, 30%-50% are long chain PUFA, which are incorporated in the cell membrane phospholipids. Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus, may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.     

Effects of boiling,deep‐frying,and microwave treatment on the proximate composition of rainbow trout fillets: changes in fatty acids,total protein,and minerals

This study was conducted to investigate the differences in the proximate composition (moisture, fat, protein and ash), cholesterol content, energy, mineral composition (Na, Ca, Mg, K, P, Fe and Zn) and fatty acid profile of rainbow trout, Oncorhynchus mykiss, after frying, boiling, or microwaving. Results showed that all cooking methods reduced moisture and increased total protein, fat and ash contents. Also all minerals increased significantly during the microwave and frying methods. Statistical results showed that the major fatty acids among the saturated and monounsaturated fatty acids in each fish were palmitic (C16:0) and oleic (C18:1) acids, respectively. In addition, linoleic acid (C18:2) was predominant in the n‐6 polyunsaturated fatty acids (PUFA) in both cooked and raw trout. The EPA (eicosapentaenoic acid; C20:5 ω3) and DHA (docosahexaenoic acid; C22:6 ω6) acids were the major fatty acids among total n‐3 acids in fish samples. The fatty acids profile of the cooked fish showed a saturated (SFA) and monounsaturated (MUFA) decrease and an increase in PUFA contents. However, the ω‐3 fatty acids content increased in microwaved samples but decreased in the fried samples. Moreover, the PUFA/SFA and Hypocholesterolaemic/Hypercholesterolaemic (HH) ratios increased in both fried and microwaved trout, whereas significant increases in ω3/ω6 as well as EPA + DHA/C16 content were observed only in microwaved samples. A significant increase in energy content was observed in all cooked samples, whereas the cholesterol decreased. Research results show that microwaving is recommended as the best cooking method for a healthy consumption of rainbow trout.     

植物提取物槲皮素调节小鼠的能量代谢和氧化应激

为了探讨植物提取物槲皮素对负重游泳小鼠的能量代谢和氧化应激的影响,本研究将45只SPF级雄性昆明小鼠随机分为正常对照组、游泳组和槲皮素组,每组15只。槲皮素组小鼠喂养2 g/kg的槲皮素饲料,其他组小鼠喂养标准饲料,共喂养14 d。然后将游泳组和槲皮素组小鼠按照体重的3%进行负重游泳1 h,测定各组小鼠的血糖、乳酸、尿素氮、游离脂肪酸、琥珀酸脱氢酶、三磷酸腺苷、丙二醛、谷胱甘肽过氧化物酶和总抗氧化活性。结果显示,负重游泳后,槲皮素组血清乳酸和尿素氮水平显著低于游泳组,并且槲皮素组游离脂肪酸水平显著高于游泳组。负重游泳后,游泳组小鼠的肝脏和肌肉组织中的琥珀酸脱氢酶含量均显著降低,槲皮素组小鼠游泳后未见明显降低。负重游泳后,游泳组小鼠肌肉组织中的ATP酶活性显著降低,槲皮素组小鼠游泳后未见明显降低。负重游泳后,槲皮素组的丙二醛含量显著低于游泳组。游泳组和槲皮素组小鼠负重游泳后的谷胱甘肽过氧化物酶含量均显著降低,槲皮素组小鼠的谷胱甘肽过氧化物酶含量未见明显降低。游泳组小鼠血清总抗氧化活性显著低于对照组,而槲皮素组与对照组无显著差异。本研究初步表明,槲皮素可调节负重游泳小鼠的能量代谢来起到抗疲劳作用,主要机制与增加脂肪动员、抑制蛋白质分解和加强三羧酸循环有关。另外,槲皮素可通过抑制脂质过氧化、清除超氧阴离子自由基来防止运动过程中的氧化应激损伤。