莲心碱对实验性高脂血症大鼠血脂及脂质过氧化的影响

本文研究莲心碱对实验性高脂血症大鼠血脂和抗氧化能力的影响.将32只大鼠随机分为4组,对照组饲喂基础饲料;诱导组饲喂高脂饲料;试验组给予高脂饲料+莲心碱灌胃2.5和5.0 mg·kg-1.测血清中血脂和丙二醛(MDA)水平,以及谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性;取肝脏测绝对和相对肝重及MDA含量.结果表明莲心碱可显著降低实验性高脂血症大鼠血清中总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平和动脉粥样硬化指数;显著升高血清高密度脂蛋白胆固醇、GSH-Px和SOD水平;同时还可显著降低血清和肝脏中MDA的含量;其绝对和相对肝重均低于诱导组.     

锰,硒对离体大鼠工作心脏心肌收缩功能的影响

我们曾通过对比观察证明,饲喂低硒饲料两个月与注射黄嘌呤-黄嘌呤氧化酶3d对大鼠的影响相似,均能使心肌收缩功能减弱、谷胱甘肽过氧化物酶(GSH-Px)活性降低、脂质过氧化物(LPO)含量增多、电子自旋共振谱线面积增大。本实验沿用相同的低硒饲料与硒、锰添加量,在离体鼠心肌上,观     

硒的抗自由基损伤作用

用黄嘌呤-黄嘌呤氧化酶体系或低硒饲料诱发自由基损伤。在培养的鼠心肌细胞上,硒能使受损心肌细胞的自由基含量、超微结构、动作电位、膜输入阻抗恢复正常;在离体灌流的鼠心上,硒能改善受损心脏的心肌收缩性能;硒能使受损鼠的心硒含量与肝谷胱甘肽过氧化物酶(GSH_(ps))活力回升、肝过氧化脂质(LPO)含量下降。上述结果提示硒保护作用的基本机制可能与增强GSH_(px)活力、促进自由基清除有关。     

富硒大豆多肽对高脂致大鼠脂肪肝和抗氧化功能的影响

目的：探讨富硒大豆多肽改善高脂所致脂肪肝大鼠肝抗氧化功能的影响及机制。方法：将40只Wistar大鼠分成4组（n=10）,分别饲喂标准饲料＋水（NC）、标准饲料＋富硒大豆多肽液（SeN）、高脂饲料＋水（HC）、高脂饲料＋富硒大豆多肽液（SeH）,10周后处死,用苏丹Ⅲ染色肝脏组织切片观察脂肪变性程度,免疫组织化学方法测定肝组织葡萄糖调节蛋白78（GRP78）表达情况,并分析其肝功能、血脂及血清和肝匀浆中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）含量的变化情况。结果：HC组在血清TC、TG水平、肝脏脂肪化程度、GRP78表达情况都明显高于NC、SeN、SeH组（P〈0.01）。SeH组血清和肝组织中MDA含量较HC组降低（P〈0.01）,GSH-Px、SOD活性升高。NC和SeN两组各项指标之间无明显差异。结论：富硒大豆多肽能有效提高脂肪肝大鼠肝内抗氧化酶活性,抑制脂质过氧化反应,降低肝组织内GRP78表达。     

萝卜过氧化物酶对小鼠机体抗氧化作用的研究

目的 探索新的抗氧化剂.方法 研究萝卜过氧化物酶(POD)对小鼠肝、脾和肾脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)的影响.结果 用不同剂量的POD处理后,可以提高肝、脾和肾的SOD、GSH-Px的活性,减低丙二醛的含量.结论 萝卜过氧化物酶可以提高机体的抗氧化能力.     

纳米硒对氟胁迫下鲤鱼肝抗氧化功能及组织结构的影响

为探讨纳米硒(nano selenium, NSe)对氟暴露下鲤鱼肝脏的抗氧化功能和组织结构的保护作用,将750条鲤鱼随机分为5个组,分别为对照组(CK)、氟胁迫组(FS)和纳米硒低、中、高剂量组(NSe L、NSeM、NSeH),NSe L、NSeM、NSeH组在基础饵料中分别添加0.1、0.5、1.0 mg·kg^-1的纳米硒,FS和 NSe组用100 mg·L^-1氟溶液进行胁迫,试验时间为30 d.结果表明：与CK组比较,氟暴露降低了鲤鱼肝组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH Px)的活性,增加了丙二醛(MDA)含量,肝脏的组织结构受到一定程度的损伤;与FS组比较,NSe增强了鲤鱼肝组织中SOD、CAT和GSH-Px活性,降低了MDA含量,缓解了氟胁迫对鲤鱼肝脏组织结构的损伤.表明饵料中添加纳米硒可在一定程度上改善氟胁迫所造成的鲤鱼抗氧化能力的下降和组织结构的损伤.     

六妙散对氟中毒大鼠自由基及肾功的影响

目的:观察投氟后不同给药组的大鼠血清中肌酐(creatimine Cr)、尿素氮(Urearutrogen BUN)、丙二醛(MDA)、超氧化物歧化酶(SOD)等水平变化。方法:48只SD大鼠,随机分为四组。给大鼠饮水投氟(每升水含氟150mg)10周,检测不同组大鼠血清中Cr、BUN、MDA、SOD的水平变化。结果:高氟组随着大鼠体内氟含量的蓄积,血清中的MDA有明显的上升趋势。血清中SOD的含量逐渐降低。与高氟组比较给予药物六妙散干扰组血清中MDA、SOD有明显差异。Cr、BUN含量高氟组与六妙散干扰组比较,数据有明显差异(P<0.05)六妙散组对氟中毒大鼠的肾功有明显的保护作用。结论:六妙散影响了氟中毒大鼠血清中MDA、SOD的含量,对氟中毒造成的肾损伤有保护作用。     

顺铂诱导肾损伤过程中肾皮质脂质过氧化的变化

目的:探讨顺铂肾损伤过程中肾皮质脂质过氧化与肾小管结构改变的关系.方法:雌性Wistar大鼠随机分为生理盐水组、顺铂Ⅰ组、顺铂Ⅱ组、顺铂Ⅲ组,均为尾静脉注射给药,每天一次,连续五天.第六天取血测肌酐(Scr)、尿素氮(BUN)含量,取肾皮质测丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-Px)活性,同时进行肾小管上皮细胞碱性磷酸酶组织化学染色和组织病理学观察.结果:顺铂组Scr、BUN明显升高,肾皮质MDA含量升高,SOD与GSH-Px活性降低,与对照组相比均有显著差异(P＜0.05),且肾皮质SOD活性、GSH-Px活性与Scr、BUN含量呈明显负相关(P＜0.05),肾皮质MDA含量与Scr、BUN含量呈明显正相关(P＜0.05).酶组化显示肾小管上皮细胞碱性磷酸酶大量丢失,病理切片结果显示肾皮质部分肾小管上皮细胞变性、坏死.结论:顺铂引起肾皮质组织的破坏与肾皮质脂质过氧化增强有关,且随剂量增加肾皮质损伤加重.     

红葡萄酒对大鼠肝脏抗氧化酶和脂质过氧化的影响

选用雄性SD大鼠,分别灌胃红葡萄酒、酒精及水。实验90 d中每隔30 d处死一批动物,测定大鼠肝脏匀浆组织中的超氧化物歧化酶(Superoxide dismutase SOD)、过氧化氢酶(Catalase CAT)、谷胱甘肽过氧化物酶(Glutathione peroxidase GSH-Px)活性和脂质过氧化产物丙二醛(Malondialdehyde MDA)含量变化。观察摄入红葡萄酒后大鼠肝脏抗氧化酶活性变化及对肝脏脂质过氧化的影响。结果表明,红葡萄酒能提高SOD活性,且SOD活性与灌胃时间、剂量有一定关系;长期红葡萄酒和酒精摄入可诱导CAT活性增强,加剧肝脏的脂质过氧化(LPO)作用;红葡萄酒组、酒精组0.63、1.25 g/kg剂量GSH-Px活性均明显升高(P<0.05),酒精组1.88 g/kg剂量有极显著性差异(P<0.01);试验初期,红葡萄酒大剂量显著降低肝脏中MDA的含量。试验中期,红葡萄酒中大剂量显著降低MDA含量。试验末期,红葡萄酒大剂量和酒精中大剂量显著升高肝脏中MDA含量。     

基于不同饲料的洋虫水提液对小鼠的抗衰老作用

为了评价洋虫Martianus dermestoides成虫和幼虫水提液的抗衰老作用,用高级饲料红花、枸杞、大枣、核桃仁的混合饲料)、大米、麦麸饲料饲养洋虫成虫和幼虫,并用幼虫水提液对D-半乳糖致衰老小鼠灌胃, 测定小鼠血清中超氧化物歧化酶(SOD)、 谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶（CAT)的活力及丙二醛（MDA)含量。结果表明：3种饲料饲养的洋虫成虫水提液均能提高小鼠血清中SOD,GSH-Px和CAT活力(P<0.05或P<0.01),且显著降低MDA含量(P<0.05);高级饲料组作用优于大米及麦麸饲料组,但三者差异不显著。高级饲料饲养组,其幼虫水提液对小鼠血清中SOD和CAT活力作用显著强于成虫水提液（P<0.05);对GSH-Px活力及MDA含量影响差异不显著。揭示洋虫成虫和幼虫水提液均有一定的抗氧化作用,是一种有效的抗衰老保健食品,且幼虫抗氧化作用优于成虫,饲料种类对洋虫的抗氧化作用无显著影响。     

Protective effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation and antioxidant enzymes in diabetic rat liver

The aim of this study was to examine the effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the liver of streptozotocin (STZ)-induced diabetic rats. Twenty-seven rats were randomly divided into three groups: group I, control non-diabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 8); group III, STZ-induced, CAPE-treated diabetic rats (n = 10), which were intraperitoneally injected with CAPE (10 microM kg(-1) day(-1)) after 3 days followed by STZ treatment. The liver was excised after 8 weeks of CAPE treatment, the levels of malondialdehyde (MDA) and the activities of SOD, CAT, and GSH-Px in the hepatic tissues of all groups were analyzed. In the untreated diabetic rats, MDA markedly increased in the hepatic tissue compared with the control rats (p < 0.0001). However, MDA levels were reduced to the control level by CAPE. The activities of SOD, CAT, and GSH-Px in the untreated diabetic group were higher than that in the control group (p < 0.0001). The activities of SOD and GSH-Px in the CAPE-treated diabetic group were higher than that in the control group (respectively, p < 0.0001, p < 0.035). There were no significant differences in the activity of CAT between the rats of CAPE-treated diabetic and control groups. Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats of untreated diabetic group (p < 0.0001). There were no significant differences in the activity of GSH-Px between the rats of untreated diabetic and CAPE-treated groups. It is likely that STZ-induced diabetes caused liver damage. In addition, LPO may be one of the molecular mechanisms involved in STZ-induced diabetic damage. CAPE can reduce LPO caused by STZ-induced diabetes.     

Comparison of selenium level and glutathione peroxidase activity in tissues of vitamin B6-deficient rats fed sodium selenite or DL-selenomethionine

The effect of vitamin B₆ on the levels of tissue selenium (Se) and glutathione peroxidase (GSH-Px) was studied. Male Wistar 4-week-old rats were fed a vitamin B₆-Se-deficient basal diet for 2 weeks, then divided into 10 groups of five or six rats and fed their respective diets for 4 weeks. The experimental design was a 2×2×2 factorial with two levels of vitamin B₆, two forms of Se, and two levels of Se, plus two extra groups (vitamin B₆-supplemented and deficient without Se). Vitamin B₆ was 0 and 250 μg pyridoxine-HCl/100 g of diet; Se forms were Na₂SeO₃ and DL-selenomethionine; Se levels were 0.5 and 5.0 mg Se/kg of diet. Regardless of form or level of Se, vitamin B₆-deficient rats had lower body weights and organ weights than vitamin B₆-supplemented rats. At 5.0 mg Se/kg of diet, Na₂SeO₃ caused a further depression. Vitamin B₆ deficiency resulted in a higher Se level and GSH-Px activity in plasma of rats fed selenomethionine. However, Se content an GSH-Px activity in erythrocytes were significantly elevated in vitamin B₆-supplemented rats compared with vitamin B₆-deficient rats. Se levels in muscle and heart were significantly lower in vitamin B₆-deficient groups fed Na₂SeO₃ than in vitamin B₆-supplemented groups. Vitamin B₆-deficient rats fed selenomethionine had higher Se levels in muscle, heart, spleen, liver, and kidneys than vitamin B₆-supplemented rats. Activity of GSH-Px in muscle, heart, and spleen was significantly lower in vitamin B₆-deficient groups than in vitamin B₆-supplemented groups, regardless of form of Se. A significant decrease of GSH-Px in liver was observed in vitamin B₆-deficient rats fed selenomethionine compared with vitamin B₆-supplemented rats, whereas no significant decrease was observed in those fed Na₂SeO₃. These results suggest that vitamin B₆ is involved in the distribution and transportation of Se in body and the metabolism of selenomethionine in liver.     

Lipid peroxidation and activity of antioxidant enzymes in diabetic rats

We hypothesized that oxygen free radicals (OFRs) may be involved in pathogenesis of diabetic complications. We therefore investigated the levels of lipid peroxidation by measuring thiobarbituric acid reactive substances (TBARS) and activity of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)] in tissues and blood of streptozotocin (STZ)-induced diabetic rats. The animals were divided into two groups: control and diabetic. After 10 weeks (wks) of diabetes the animals were sacrificed and liver, heart, pancreas, kidney and blood were collected for measurement of various biochemical parameters. Diabetes was associated with a significant increase in TBARS in pancreas, heart and blood. The activity of CAT increased in liver, heart and blood but decreased in kidney. GSH-Px activity increased in pancreas and kidney while SOD activity increased in liver, heart and pancreas. Our findings suggest that oxidative stress occurs in diabetic state and that oxidative damage to tissues may be a contributory factor in complications associated with diabetes.     

Effects of fluoride on hepatic antioxidant system and transcription of Cu/Zn SOD gene in young pigs

Thirty-two barrows (Duroc x Landrace x Yorkshire) were randomly divided into four groups, each of which included eight pigs. The groups received the same basal diet supplemented with 0, 100, 250 and 400mg/kg fluoride, respectively. The malondialdehyde (MDA) and glutathione (GSH) levels, antioxidant enzymes activities and zinc/copper superoxide dismutase (Cu/Zn SOD) mRNA content in the liver were determined to evaluate the fluoride hepatic intoxication. Results showed the increased lipid peroxides (LPO) level and the reduced GSH content, along with a concomitant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px). Moreover, the level of hepatic Cu/Zn SOD mRNA was also significantly reduced. We suggest the mechanism of fluoride injuring the liver as follows: fluoride causes a decrease in Cu/Zn SOD mRNA and the reduced activities of antioxidant enzymes, leads to the declined ability of scavenging free radicals with excessive production of LPO, which seriously damages the hepatic structure and function.     

Effect of sex and time of sampling on selenium and glutathione peroxidase activity in tissues of mature rats

Sprague-Dawley rats were used to investigate variations in measures of glutathione peroxidase (GSH-Px) and selenium (Se) concentration resulting from diurnal cycles and sex. Mature rats (equal numbers of males and females) were killed at 4 h intervals over a 48 h period (0200, 0600, 1000, 1800 and 2200 h each day). Selenium and GSH-Px were measured in plasma, erythrocytes, and liver and kidney cytosols. Selenium concentrations did not vary diurnally, but plasma GSH-Px activities were higher during the light than dark periods. Males had greater plasma GSH-Px activities and Se concentrations (42 EU and .45 mg/kg, respectively) than females (35 EU and .41 mg/kg respectively). GSH-Px activities were also higher in male kidney cytosols than females (117 and 76 EU, respectively). Selenium and GSH-Px activities, however, were lower in male liver cytosols (.48 mg/kg and 272 EU) than females (1.19 mg/kg and 795 EU, respectively). These data suggest that Se is distributed differently in male and female rats and the difference in Se distribution is accomplished by differences in GSH-Px activities.     

Effects of dietary vitamin E and selenium on antioxidative defense mechanisms in the liver of rats treated with high doses of glucocorticoid

The aim of this work was to determine the effects of dietary intake vitamin E and selenium (Se) on lipid peroxidation as thiobarbituric acid reactive substances (TBARS) and on the antioxidative defense mechanisms in the liver of rats treated with high doses of prednisolone. Two hundred fifty adult male Wistar rats were randomly divided into five groups. The rats were fed a normal diet, but groups 3, 4, and 5 received a daily supplement in their drinking water of 20 mg vitamin E, 0.3 mg Se, and a combination of vitamin E and Se, respectively, for 30 d. For 3 d subsequently, the control group (group 1) was treated with a placebo, and the remaining four groups were injected intramuscularly with 100 mg/kg body weight (BW) prednisolone. After the last administration of prednisolone, 10 rats from each group were killed at 4, 8, 12, 24, and 48 h and the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) enzymes and the levels of glutathione (GSH) and TBARS in their livers were measured. GSH-Px, SOD, and CAT enzyme activities and GSH levels in prednisolone-treatment group (group 2) began to decrease gradually at 4 h, falling respectively to 38%, 55%, and 40% of the control levels by 24 h, and recovering to the control levels at 48 h. In contrast, prednisolone administration caused an increase in the hepatic TBARS, reaching up to four times the levels of the control at 24 h. However, supplementation with vitamin E and Se had a preventive effect on the elevation of the hepatic TBARS and improved the diminished activities of the antioxidative enzymes and the levels of GSH. Therefore, the present study demonstrates the effectiveness of vitamin E and Se in reducing hepatic damage in glucocorticoid-treated rats and suggests that reductions in increased TBARS as a result of prednisolone may be an important factor in the action of vitamin E and Se.     

Effect of dietary fluoride on selenite toxicity in the rat

Three factorial experiments were conducted to determine if high dietary fluoride (F) would inhibit selenite toxicity in rats. Initially, three levels of selenite (0.05, 3, and 5 mg/kg diet) were matched against three levels of F (2, 75, and 150 mg/kg diet). Fluoride failed to prevent the depressive effect of selenite on 8-wk food intake and body wt gain. Selenium (Se) concentration of plasma and kidney and enzymatic activity of whole blood glutathione peroxidase (GSH-Px) were also unaffected by F. Liver Se concentration, however, was slightly (12%) but significantly (p<0.025) reduced when the highest F and Se levels were combined. Fluoride (150 mg/kg) appeared to reduce liver selenite toxicity (5 mg/kg). Therefore, further study focused on liver histology with treatments that eliminated the middle levels of selenite and F. Fluoride prevented the hepatic necrosis seen in selenite-toxic rats. Similar histological lesions were not observed for kidney or heart. Fluoride partially (26%) but significantly (p<0.025) reduced thiobarbituric-reactive substances in selenite-toxic rats, but there was no F effect on intracellular distribution of liver Se, glutathione levels in liver and kidney, or on liver xanthine oxidase activity. Overall, the protective effect of F on selenite toxicity appears to be confined to liver pathology. The exact mechanism for this effect, however, remains unclear. Oregon Agricultural Experiment Station Technical Paper No. 9728.     

The effects of some antioxidant vitamin- and trace element-supplemented diets on activities of SOD, CAT, GSH-Px and LPO levels in chicken tissues

The effect of diets containing antioxidant vitamins and trace elements on chicken tissue activities of SOD, CAT, GSH-Px and of LPO levels was investigated. Chickens, 45 weeks of age were divided into six groups: control group, Cu group (13.2 mg Cu kg(-1) diet); Se group (0.07 mg Se kg(-l) diet); vitamin E group (70 mg DL-alpha-tocopherol acetate kg(-1) diet) and a constant level vitamin C, 200 mg kg(-1) diet); vitamin A group (240 mg retinol acetate kg(-1) diet) and vitamin C group (500 mg ascorbic acid kg(-1) diet). Significant variation of these antioxidant enzyme activities and LPO levels according to gender was demonstrated statistically. In the Cu group, CuZnSOD activity in the liver, erythrocyte, kidney and heart significantly increased by 75, 40, 12, 12% respectively (P<0.05). MnSOD activity in the heart, liver, kidney and brain of the vitamin C and in the heart of Cu group were found to be increased by approximately 15%, while in liver tissue of the Cu group it was reduced by 19% (P<0.05). GSH-Px activities in the Se, vitamin E and C groups were significantly increased, conversely LPO levels decreased (P<0.001). CAT activities in the liver and heart of the vitamin C group were significantly decreased (by 32%), but in kidney tissue only that of the Cu group was increased from 30.2 +/- 4.767 to 144.49 +/- 6.93 U mg(-1) P<0.001. The resistance to stress of the vitamin E and C groups, which had significantly increased activities of antioxidant enzymes and decreased lipid peroxide levels, were determined in 60% moisture medium at 45 degrees C.     

Effect of 3-(1<Emphasis Type="Italic">H</Emphasis>-Pyrrol-2-yl)-1<Emphasis Type="Italic">H</Emphasis>-Indazole on the Antioxidant Status of Rats

The influence of injection periods of 3-(1H-pyrrol-2-yl)-1H-indazole regarding vitamins A, E, C, selenium (Se), malondialdehyde (MDA) levels, and glutathione peroxidase (GSH-Px) activity in rats has been investigated. The substance was given by subcutaneous injection at 20 mg/kg every other day for a total of 15 injections. At the end of the treatment, Se levels in serum were determined by fluorimetry, and those of vitamins A, E, C, and malondialdehyde in serum, liver, and kidney were determined by high-performance liquid chromatography. GSH-Px activities in erythrocytes were determined spectrophotometrically. Vitamins A, E, C, and Se levels were generally lower than in the controls, while GSH-Px activity at the third injection period was maximally increased, with the activities after the other injection periods being higher than in the control group. In addition, vitamins A, E, and C levels were generally lower than the control groups, while serum, liver, and kidney MDA levels gradually increased depending on injection periods. On the other hand, GSH-Px activity was higher than in the control group. Thus, the results show that while vitamins A, E, C, and Se levels decreased, MDA levels and GSH-Px activities increased after administration of 3-(1H-pyrrol-2-yl)-1H-indazole to the rats. These findings might be related to the increased amount of free radicals caused by 3-(1H-pyrrol-2-yl)-1H-indazole injection.