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1.
Fukada S Shimada Y Morita T Sugiyama K 《Bioscience, biotechnology, and biochemistry》2006,70(10):2403-2409
The hyperhomocysteinemia induced by a dietary addition of 1% methionine was significantly suppressed by the concurrent addition of 1% glycine or 1.4% serine to the same degree. The methionine-induced increase in the hepatic concentration of methionine metabolites was significantly suppressed by glycine and serine, but the hepatic cystathionine beta-synthase activity was not enhanced by these amino acids. When the methionine-supplemented diet was changed to the methionine plus glycine or serine diet, the plasma homocysteine concentration rapidly decreased during and after the first day. The hyperhomocysteinemia induced by an intraperitoneal injection with methionine was also suppressed by concurrent injection with glycine or serine, although the effect of serine was significantly greater than that of glycine. These results indicate that glycine and serine were effective for suppressing methionine-induced hyperhomocysteinemia: serine and its precursor glycine are considered to have elicited their effects mainly by stimulating cystathionine synthesis by supplying serine, another substrate for cystathionine synthesis. 相似文献
2.
Rats were fed diets supplemented with 1% L-methionine with and without 2.5% various amino acids for 7 d to determine what amino acids other than glycine, serine, and cystine can suppress methionine-induced hyperhomocysteinemia. L-Glutamic acid, L-histidine, and L-arginine significantly suppressed methionine-induced enhancement of plasma homocysteine concentrations, but the mechanisms underlying the effect of these amino acids are thought not to be identical. 相似文献
3.
The present study was designed to investigate the antioxidant effect of curcumin on methionine-induced hyperlipidemia and hyperhomocysteinemia in Wistar rats (200-250 g) of either sex. The vehicle control rats were treated with 1% Tween 80 in normal saline (2 ml/kg, po) for 30 days. Hyperlipidemia and hyperhomocysteinemia was induced by methionine administration (1 g/kg, po) for 30 days. A significant increase in total cholesterol, triglycerides, low density lipoprotein cholesterol (LDL-C) and homocysteine levels in serum and thiobarbituric acid reactive substances (TBARS) levels in heart homogenates were observed with a concomitant decrease in serum high density lipoprotein (HDL-C) levels in pathogenic control (i.e. group II) rats, as compared to vehicle control (i.e. group I) rats. Further, curcumin (200 mg/kg, p.o.) treatment in methionine treated rats for 30 days significantly decreased the total cholesterol, triglycerides, LDL-C and homocysteine levels in serum and TBARS levels in heart homogenates and increased serum HDL-C levels, as compared to pathogenic control (i.e. group II) rats. The results of biochemical observations were supplemented by histopathological examination of rat's aortic section. The results of test drug were comparable to that obtained with folic acid (100 mg/kg, p.o.). The results suggest that curcumin has significant antihyperlipidemic and antihyperhomocysteinemic effect against methionine-induced hyperlipidemia and hyperhomocysteinemia in rats. 相似文献
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Methionine (1g/kg, po) administration to pathogenic control rats for 30 days significantly increased the levels of homocysteine, total cholesterol (TC), low density lipoprotein (LDL-C), very low density lipoprotein (VLDL-C) and triglycerides (TGs) and decreased the levels of high density lipoprotein (HDL-C) in serum. Hematological observations of the peripheral blood smears of pathogenic rats fed with methionine also showed crenation of RBCs cell membrane and significant increase in total leukocyte count, differential leukocyte count and platelet counts with significant decrease in the mean hemoglobin levels as compared to vehicle control rats. Administration of atorvastatin (0.2 mg/kg/po) to hyperhomocysteinemic rats significantly decreased the levels of homocysteine, TC, TGs, LDL-C and VLDL-C and increased the levels of HDL-C in serum. The present results provide clear evidence that oral treatment with atorvastatin exhibit homocysteine and lipid lowering activity and also reversal of hematological changes induced by methionine in albino rats. 相似文献
5.
Effects of dietary eritadenine on the liver microsomal Delta6-desaturase activity and its mRNA in rats 总被引:1,自引:0,他引:1
Shimada Y Yamakawa A Morita T Sugiyama K 《Bioscience, biotechnology, and biochemistry》2003,67(6):1258-1266
Eritadenine, a hypocholesterolemic factor of Lentinus edodes mushroom, has a wide range of effects on lipid metabolism such as an increase in the liver microsomal phosphatidylethanolamine (PE) concentration, a decrease in the liver microsomal Delta6-desaturase activity, and an alteration of the fatty acid and molecular species profile of liver and plasma lipids. In this study, the time-dependent effects of dietary eritadenine on several variables concerning lipid metabolism were investigated in rats to clarify the sequence of metabolic changes caused by eritadenine, with special interest in the association of the liver microsomal phospholipid profile and the activity of Delta6-desaturase. The effect of dietary eritadenine on the abundance of mRNA for Delta6-desaturase was also investigated. When the time required for a half-change of variables was estimated during the first 5 days after the change from the control diet to the eritadenine-supplemented (50 mg/kg) diet, the change rates of the variables were fastest in the following order: alteration of the liver microsomal phospholipid profile>decrease in liver microsomal Delta6-desaturase activity>alteration of the fatty acid and molecular species profiles of microsomal and plasma phosphatidylcholine (PC)>decrease in the plasma cholesterol concentration. There was a significant correlation between the Delta6-desaturase activity and liver microsomal PE concentration, but not PC concentration, or the proportion of PC and PE or the PC/PE ratio. The suppression of Delta6-desaturase activity by dietary eritadenine was accompanied by a significant reduction in the abundance of mRNA for the enzyme. These results suggest that dietary eritadenine might suppress the activity of liver microsomal Delta6-desaturase by altering the microsomal phospholipid profile, as represented by an increase in PE concentration, and that the effect of eritadenine is mediated by the regulation of gene expression. 相似文献
6.
The present study was aimed to find out the protective effect of ethanolic extract of E. ribes fruits on homocysteine, lactate dehydrogenase (LDH) and lipid profile in serum, lipid peroxidation (LPO) and non-enzymatic antioxidant glutathione (GSH) levels in brain homogenates and histopathological examination of brain tissue in methionine (1 g/kg body weight, orally for 30 days) induced hyperhomocysteinemic rats. A significant increase in homocysteine, LDH, total cholesterol, triglycerides, low density lipoprotein (LDL-C) and very low density lipoprotein (VLDL-C) levels was observed in serum. Increased LPO levels in brain homogenates with reduced serum high density lipoprotein (HDL-C) levels and decreased GSH content were other salient features observed in methionine treated pathogenic control rats. Administration of ethanolic E. ribes extract (100 mg/kg body weight, orally) for 30 days to methionine-induced hyperhomocysteinemic rats produced a significant decrease in the levels of homocysteine, LDH, total cholesterol, triglycerides, LDL-C, VLDL-C in serum and LPO levels in brain homogenates with significant increase in serum HDL-C levels and GSH content in brain homogenates, when compared with pathogenic control rats. Biochemical observations were further substantiated with histological examination of brain. Degenerative changes of neuronal cells in methionine treated rats were minimized to near normal morphology by ethanolic E. ribes extract administration as evident by histopathological examination. The results provide clear evidence for the first time, that ethanolic E. ribes extract treatment enhances the antioxidant defense against methionine-induced hyperhomocysteinemia and oxidative stress in brain. 相似文献
7.
Effects of dietary eritadenine on liver microsomal delta6-desaturase activity and the fatty acid profile of phosphatidylcholine, cholesteryl esters, and triglycerides of liver microsomes or plasma were investigated in rats fed different fats (palm oil, olive oil, and safflower oil). The activity of delta6-desaturase was influenced by both dietary fat types and eritadenine. In rats fed control diets, delta6-desaturase activity was higher in the order of the palm oil, olive oil, and safflower oil groups. In rats fed eritadenine-supplemented diets, the enzyme activity was markedly decreased to a constant level irrespective of dietary fat type. The 20:4n-6/18:2n-6 ratio of phosphatidylcholine and cholesteryl esters, as compared with triglycerides, was highly sensitive to eritadenine. The results suggest that the activity of delta6-desaturase is regulated by dietary fats and eritadenine independently, and that the effect of eritadenine is stronger than that of dietary fats. 相似文献
8.
Taurine protected myocardial mitochondria injury induced by hyperhomocysteinemia in rats 总被引:4,自引:0,他引:4
Summary. Taurine can protect against cardiovascular diseases, whereas elevated levels of plasma homocysteine are associated with atherosclerotic and thromboembolic cardiovascular diseases. To illustrate the effects of taurine on hyperhomocysteinemia, we observed the myocardial mitochondria dysfunction in the rats with hyperhomocysteinemia induced by diet methionine loading, and the therapeutic effect of taurine. A methionine diet increased plasma homocysteine concentration (133.51±27.91mol/L vs 12.31±2.58mol/L in control, P<0.01), stimulated the production of reactive oxygen species (ROS) in the myocardial mitochondria, and inhibited the activities of mitochondrial Mn-superoxide dismutase and catalase. The 45Ca uptake and Ca2+-ATPase activity in the myocardial mitochondria were significantly lowered in rats with hyperhomocysteinemia. Taurine supplements effectively attenuated the hyperhomocysteinemia-induced ROS production and inhibition of Mn-superoxide dismutase and catalase activities in the myocardial mitochondria, and increased its 45Ca uptake and Ca2+-ATPase activity. Thus, taurine antagonizes the oxidative stress injury in the myocardial mitochondria induced by the hyperhomocysteinemia. 相似文献
9.
The effect of the ginseng root powder on avian hepatic cholesterol biosynthesis and serum lipoprotein cholesterol levels were examined. Lohman strain broiler females were fed for 4 weeks a corn-based diet (control) or an experimental diet in which 0.25% Korean ginseng was incorporated (treatment). B.-hydroxy-B-methylglutaryl-CoA) HMG-CoA reductase activity was significantly lower (P < 0.01) in the treatment group (47% of control activity). Ginseng treatment affected a lowering of the serum total cholesterol level (83% of control, (P < 0.05) and of serum low density lipoprotein cholesterol level (77% of control, P < 0.05). The mechanism of the hypocholesterolemic action of ginseng involves the suppression of cholesterol biosynthesis. 相似文献
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W McVaugh B Lawrence A Kulkarni R Pizzini C Van Buren F Rudolph I Wolinsky N Dafny 《Life sciences》1989,44(14):977-983
It has been demonstrated in a murine model that a defined diet (Purina Basal Diet 5755) has immunosuppressive effects similar to cyclosporin A (CsA). It was also shown that CsA treatment in opiate dependent rats can attenuate the severity of opiate withdrawal. In this study, an opiate dependence model was established in Balb/c mice to assess the effects of the 5755 diet and CsA on morphine withdrawal - a CNS mediated phenomenon. Three groups of mice were used; a chow-fed control group (Purina 5008), a chow fed CsA treated group, and a group maintained on the 5755 diet. Morphine dependence was established by subcutaneous implantation of a 100 mg morphine base pellet under ether anesthesia. Seventy-two hours after pellet implantation, withdrawal was precipitated by a single injection of the opiate antagonist naloxone (2 mg/kg ip). Two indicators of withdrawal were assessed; jumping and diarrhea. The data demonstrated that both CsA and the 5755 diet resulted in significant attenuation of withdrawal symptoms with the 5755 diet being the most effective of the two. These findings suggest that immune modulation elicited by the 5755 diet and CsA treatment has a direct impact on the CNS opioid function. 相似文献
14.
目的:在大鼠血管钙化模型上,探讨高同型半胱氨酸血症对血管钙化的影响及其作用机制.方法:用维生素D3加尼古丁诱导大鼠血管钙化模型,并给以高蛋氨酸饮食六周诱导大鼠高同型半胱氨酸血症,用高效液相色谱法检测血浆总同型半胱氨酸(Hcy)水平;采用血管组织vonKossa染色、钙含量测定、碱性磷酸酶(ALP)活性和骨钙素(OC)含量测定以判断血管钙化程度,同时测定血浆脂质共轭烯(Diene键)含量反映其脂质过氧化水平.结果:钙化组大鼠血管yon Kossa染色可见大量黑色颗粒沉积,其血管的钙含量,碱性磷酸酶活性及骨钙素含量分别较对照组增加8.09倍、45.57%和2.81倍(P<0.01).高蛋氨酸饮食的钙化组大鼠血管内钙含量较单纯钙化组增高了34.29%,而碱性磷酸酶活性及骨钙素含量则较单纯的钙化组降低29.13%和74.69%(P<0.01).钙化组大鼠血浆脂质共轭烯含量与对照组比较无显著性差异,单纯高蛋氨酸饮食和钙化加高蛋氨酸饮食大鼠血浆脂质共轭烯含量较对照组增加了1.93和2.89倍(P<0.01),而钙化加高蛋氨酸饮食大鼠血浆脂质共轭烯含量较单纯高蛋氨酸饮食大鼠又增加了32.90%(P<0.01).结论:高同型半胱氨酸血症可以促进血管的钙化,可能与其所致的脂质过氧化程度增强有关. 相似文献
15.
P K Duitsman H W Chen L R Cook S Hendrich 《Prostaglandins, leukotrienes, and essential fatty acids》1992,47(1):63-68
Groups of eight weanling female F344/N rats were fed semipurified diets that supplied 0, 50, 500, 5000, or 15,000 mg alpha-tocopherol acetate/kg diet, with and without 0.05% phenobarbital (PB) for 9 weeks. Both plasma and hepatic alpha-tocopherol levels, measured by HPLC, strongly correlated with alpha-tocopherol intake (r greater than 0.73, p less than 0.0001). Phenobarbital both depleted hepatic alpha-tocopherol and increased plasma alpha-tocopherol significantly. Although treatment with PB for 9 weeks significantly increased GST activity, PB did not affect hepatic prostaglandin (PG)F2 alpha status, as determined by radioimmunoassay. PGF2 alpha was significantly greater (by 52%) in rats fed no alpha-tocopherol than in rats fed 15,000 mg alpha-tocopherol acetate/kg diet. Hepatic PGF2 alpha status was correlated inversely but weakly with dietary alpha-tocopherol (r = -0.24, p less than 0.05). Hepatic PGF2 alpha status was not correlated with hepatic or plasma alpha-tocopherol status. This finding suggests either that there is a small depletion-resistant subcellular alpha-tocopherol pool which regulates PGF2 alpha production or that alpha-tocopherol alters PGF2 alpha production in vivo by an indirect mechanism. 相似文献
16.
Suppression of N-nitrosodiethylamine induced hepatocarcinogenesis by silymarin in rats 总被引:4,自引:0,他引:4
Ramakrishnan G Raghavendran HR Vinodhkumar R Devaki T 《Chemico-biological interactions》2006,161(2):104-114
Antioxidants are one of the key players in tumorigenesis, several natural and synthetic antioxidants were shown to have anticancer effects. In the present investigation the efficacy of silymarin on the antioxidant status of N-nitrosodiethylamine (NDEA) induced hepatocarcinogenesis in Wistar albino male rats were assessed. The animals were divided into five groups. The animals in the groups 1 and 3 were normal control and silymarin control, respectively. Groups 2, 4 and 5 were administered with 0.01% NDEA in drinking water for 15 weeks to induce hepatocellular carcinoma (HCC). Starting 1 week prior to NDEA administration group 4 animals were treated with silymarin in diet for 16 weeks, 10 weeks after NDEA administration group 5 animals were treated with silymarin and continued till the end of the experiment period (16 weeks). After the experimental period the body weight, relative liver weight, number of nodules, size of nodules, the levels of lipid peroxidation, glutathione (GSH), and the activities of antioxidant enzymes were assessed in both haemolysate and liver tissue. In group 2 hepatocellular carcinoma induced animals there was an increase in the number of nodules, relative liver weight. The levels of lipid peroxides were elevated with subsequent decrease in the body weight, (glutathione) GSH, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD). In contrast, silymarin + NDEA treated groups 4 and 5 animals showed a significant decrease in the number of nodules with concomitant decrease in the lipid peroxidation status. The levels of GSH and the activities of antioxidant enzymes in both haemolysate and liver were improved when compared with hepatocellular carcinoma induced group 2 animals. The electron microscopy studies were also carried out which supports the chemopreventive action of the silymarin against NDEA administration during liver cancer progression. These findings suggest that silymarin suppresses NDEA induced hepatocarcinogenesis by modulating the antioxidant defense status of the animals. 相似文献
17.
Lee EW He P Kawagishi H Sugiyama K 《Bioscience, biotechnology, and biochemistry》2000,64(9):2001-2004
Six species of edible mushroom were found to suppress D-galactosamine-induced enhancement of plasma alanine and aspartate aminotransferase activities when powdered mushrooms were added to the diet (5%) and fed to rats for 2 wk. Grifola frondosa exhibited the most potent effect in a dose-dependent manner. A significant effect was observed only from the water-soluble low-molecular-weight fraction of G. frondosa. The results indicate that several mushrooms possess a protective effect against liver injury induced by D-galactosamine. 相似文献
18.
The effect of gamma-butyrolactone (GBL) on voluntary ethanol intake was studied in a group of Wistar rats in which a stable preference had been induced by exposure to increasing ethanol concentrations. These rats drank 60% of their daily fluid intake as 15% ethanol solution, corresponding to about 6 g ethanol/kg/day. GBL, injected intraperitoneally at the dose of 200 mg/kg, twice daily for 3 consecutive days, decreased ethanol intake by about 80% on the days of treatment, but did not reduce total fluid intake. Ethanol intake remained significantly reduced up to the 5th day following cessation of GBL administration. GBL, up to a concentration of 10(-3) M, inhibited neither alcohol-dehydrogenase nor aldehyde-dehydrogenase in rat liver homogenates, nor dopamine-beta-hydroxylase in homogenates of adrenal medulla or hypothalamus of rats. It is suggested that inhibition of firing in dopaminergic neurons mediates the suppressant effect of GBL on ethanol preference. 相似文献
19.
Homocysteine (Hcy), an independent risk factor for atherosclerosis, undergoes auto-oxidation and generates reactive oxygen species, which are thought to be main cause of Hcy neurotoxicity. However, the mechanisms leading to neurodegenerative disorders are poorly understood because studies that have investigated the potential neurotoxicity of hyperhomocysteinemia in vivo are scarce. The purpose of this study was to test whether daily administration of methionine, which induces hyperhomocysteinemia, causes glial hyperactivity, and also to investigate the protective effects of melatonin on the brain tissue against oxidative stress of Hcy in rats. There was a significant development of oxidative stress as indicated by an increase in malondialdehyde + 4-hydroxyalkenals in hippocampus and cortex of hyperhomocysteinemic rats, whereas significant reduction was found in the activity of glutathione peroxidase (GSH-Px). Co-treatment with melatonin inhibited the elevation of lipid peroxidation and significantly increased GSH-Px activity in the brain regions studied. Western blot analysis revealed an increase in glial fibrillary acidic protein (GFAP) contents both in hippocampus and frontal cortex (p < 0.001) of hyperhomocysteinemic rats compared to the controls. Administration of melatonin significantly decreased GFAP contents in hippocampus and cortex (p < 0.05). S100B contents increased only in frontal cortex in hyperhomocysteinemic rats compared to the control (p < 0.01) and was inhibited by melatonin treatment (p < 0.01). The present findings show that Hcy can sensitize glial cells, a mechanism which might contribute to the pathogenesis of neurodegenerative disorders, and further suggest that melatonin can be involved in protecting against the toxicity of Hcy by inhibiting free radical generation and stabilizing glial cell activity. 相似文献
20.
Homocysteine (Hcy), an independent risk factor for atherosclerosis, undergoes auto-oxidation and generates reactive oxygen species, which are thought to be main cause of Hcy neurotoxicity. However, the mechanisms leading to neurodegenerative disorders are poorly understood because studies that have investigated the potential neurotoxicity of hyperhomocysteinemia in vivo are scarce. The purpose of this study was to test whether daily administration of methionine, which induces hyperhomocysteinemia, causes glial hyperactivity, and also to investigate the protective effects of melatonin on the brain tissue against oxidative stress of Hcy in rats. There was a significant development of oxidative stress as indicated by an increase in malondialdehyde + 4-hydroxyalkenals in hippocampus and cortex of hyperhomocysteine mic rats, whereas significant reduction was found in the activity of glutathione peroxidase (GSH-Px). Co-treatment with melatonin inhibited the elevation of lipid peroxidation and significantly increased GSH-Px activity in the brain regions studied. Western blot analysis revealed an increase in glial fibrillary acidic protein (GFAP) contents both in hippocampus and frontal cortex (p < 0.001) of hyperhomocysteinemic rats compared to the controls. Administration of melatonin significantly decreased GFAP contents in hippocampus and cortex (p < 0.05). S100B contents increased only in frontal cortex in hyperhomocysteinemic rats compared to the control (p < 0.01) and was inhibited by melatonin treatment (p < 0.01). The present findings show that Hcy can sensitize glial cells, a mechanism which might contribute to the pathogenesis of neurodegenerative disorders, and further suggest that melatonin can be involved in protecting against the toxicity of Hcy by inhibiting free radical generation and stabilizing glial cell activity. 相似文献