三种类型饮用水对小鼠胆固醇及脂肪细胞的影响

为探讨不同类型饮用水对小鼠胆固醇水平及脂肪细胞的影响,将60只健康3月龄清洁级ICR小鼠按体重随机分为3组,分别为自来水组、纯净水组、矿泉水组,每组20只,雌雄各半。采用自由饮水方式分别饮用相应类型的饮水,连续90 d。测定小鼠血清总胆汁酸(TBA)、总胆固醇(TC)、甘油三酯(TG)和钙离子、镁离子水平及肝脏超氧化物岐化酶(SOD)活力、丙二醛(MDA)含量,并计数单位视野脂肪细胞数目。分别向自来水、纯净水、高偏硅酸天然矿泉水中滴加三油酸甘油酯或胆固醇混合振荡,观察其乳化差异。结果显示,与自来水组比较,纯净水组雌性小鼠血镁离子含量降低(P0.05);纯净水组雌性小鼠肝脏SOD活力低于自来水组、矿泉水组(P0.05);纯净水组单位视野脂肪细胞数目高于自来水组、矿泉水组(P0.05)。纯净水乳化脂类能力强于矿泉水、自来水(P0.05),尤其是乳化胆固醇能力。提示与饮用自来水、矿泉水相比,长期饮用纯净水会引起小鼠脂肪细胞形态变小,推测其可能与体内胆固醇水平降低有关。     

三种饮用水体内外抗氧化能力比较

目的探究不同饮用水体内外抗氧化能力差异及可能机制。方法测定纯净水、自来水及矿泉水的水质情况:钙、镁、氯化物、硫酸盐及硝酸盐含量;通过羟自由基、超氧阴离子自由基、DPPH自由基清除实验检测3种饮用水体外抗氧化能力;取60只清洁级ICR小鼠随机分为3组,每组20只,雌雄各半,分别用纯净水(对照组)、自来水及矿泉水喂养,90 d后测定小鼠脑、心脏、肝脏、肾脏的总抗氧化能力(T-AOC)、抑制羟自由基能力、丙二醛(MDA)含量及过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、总超氧化物歧化酶(T-SOD)活性。结果 3种饮用水钙、镁含量:矿泉水自来水纯净水,而氯化物、硫酸盐及硝酸盐含量:自来水矿泉水纯净水。自来水、矿泉水羟自由基清除率[分别为(45.60±6.69)、(55.78±3.85)%]和超氧阴离子自由基清除率[分别为(16.62±7.50)、(17.24±6.46)%],明显高于纯净水(38.37±5.13)%和(0.26±4.29)%,且矿泉水羟自由基清除率还明显高于自来水,差异均有统计学意义(P0.05)。自来水组、矿泉水组肾脏T-AOC[分别为(4.33±1.28)、(4.43±0.74)U/mg prot]、抑制羟自由基能力[分别为(51.43±15.27)、(59.13±10.74)U/mg prot]、CAT[分别为(134.78±22.34)、(156.46±19.81)U/mg prot]、GSH-Px[分别为(92.53±14.88)、(97.16±19.86)U/mg prot]明显升高而MDA含量[分别为(1.75±0.26)、(1.63±0.20)nmol/mg prot]明显降低,相比于纯净水组[依次为(2.20±0.37)、(29.22±5.72)、(75.59±6.84)、(44.93±12.82)U/mg prot和(2.20±0.27)nmol/mg prot],且矿泉水组T-SOD[(148.31±21.47)U/mg prot]还明显高于纯净水组[(113.99±15.25)U/mg prot],差异均有统计学意义(P0.05)。结论自来水或矿泉水的体外及肾脏抗氧化能力优于纯净水,其中矿泉水可能更优。     

微营养素提高衰老小鼠雄激素作用的研究

目的研究微营养素对提高衰老小鼠雄激素和抗氧化作用。方法将3月龄的ICR雄性小鼠60只,按体重随机分成2个组,即正常对照组(12只)、衰老模型组(48只),2个月后,将致衰造模成功的ICR雄性小鼠分组按血清雄激素水平分为模型对照组、微营养素组、雄激素组、微营养素 雄激素组4组,每组各12只。饲养1个月后取血清及小鼠肺、心、脑、肝脏,测定睾酮水平、谷胱甘肽过氧化物酶(GSH.Px)活性、超氧化物歧化酶(SOD)酶活性。结果各试验组雄激素水平在实验后较实验前均有升高,其中微营养组和微营养 雄激素组与对照组比较有显著性差异(P<0.05)。微营养素组小鼠的GSH.Px活性较模型对照组均有升高,且肺、心、脑GStH-Px活力与模型对照组组比较具有显著性差异(P<0.05);微营养素组在心、脑、肺组织SOD活力明显高于模型对照组(P<0.05)。结论微营养素可以明显提高致衰小鼠的雄激素水平。对致衰小鼠GSH-Px活力和SOD活力也有升高作用,具有较强的抗氧化作用。     

鹰嘴豆蛋白酶解物对D-半乳糖衰老小鼠抗氧化能力的影响

目的研究不同剂量鹰嘴豆蛋白酶解物(CPH)对D-半乳糖致衰小鼠血清、心脏和肝脏抗氧化能力的影响。方法D-半乳糖连续颈部注射制作亚急性衰老的小鼠模型,采用生物化学方法检测各组小鼠血清、心脏和肝组织匀浆中超氧化物岐化酶(SOD)、谷胱苷肽过氧化物酶(GSH-Px)的活力及丙二醛(MDA)的含量。结果D-半乳糖致衰小鼠SOD活力、GSH-Px活力均明显下降,MDA含量明显上升,与正常小鼠比较差异显著;不同剂量的鹰嘴豆蛋白酶解物灌胃给药后均能提高小鼠血清、肝脏和心脏组织中的SOD和GSH-Px,同是降低血清、心脏和肝脏组织中MDA浓度;其效果与VE效果相当。结论鹰嘴豆蛋白酶解物能显著提高亚急性衰老小鼠的抗氧化能力,尤以高剂量组效果最好,具有一定延缓衰老的作用。     

亚慢性钐暴露对小鼠睾丸组织抗氧化能力的影响

目的 探讨亚慢性钐暴露对小鼠睾丸组织抗氧化能力的影响.方法 将50只初断乳的清洁级ICR雄性小鼠随机分成5组,分别为对照(蒸馏水)组和5、50、500、2000 mg/L硝酸钐染毒组,每组10只.采用自由饮水方式进行染毒,连续染毒90d.检测睾丸匀浆中氧化损伤指标超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、总抗氧化能力(T-AOC)活力和丙二醛(MDA)含量.结果 与对照组比较,2000 mg/L硝酸钐染毒组小鼠睾丸匀浆中SOD、GSH-Px活力以及500、2000 mg/L硝酸钐染毒组小鼠睾丸匀浆中T-AOC活力均明显下降,500、2000 mg/L硝酸钐染毒组小鼠睾丸匀浆中MDA含量明显上升,差异有统计学意义(P＜0.05).结论 亚慢性钐暴露对小鼠睾丸抗氧化能力具有一定的抑制作用.     

汉防己甲素对急性百草枯中毒致肺损伤的实验治疗研究

目的 探讨汉防己甲素(TET)对急性百草枯中毒所致肺损伤的拮抗作用.方法 雄性Wistar大鼠随机分为对照组(7只)、未治疗组(32只)和治疗组(32只).治疗组与未治疗组大鼠用百草枯(15 mg/kg)一次性腹腔注射染毒.治疗组于百草枯染毒后6 h经口给予汉防己甲素30 mg/kg,1次/d;未治疗组给予等体积的生理盐水;对照组一次性腹腔注射等体积生理盐水.分别测定不同处理后3、7、14和21 d时大鼠血浆和肺匀浆中丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力,并观察肺组织结构改变.结果 染毒3 d时,未治疗组血浆及匀浆中MDA含量分别为(3.65±0.44)nmol/ml、(9.54±0.92)nmol/mgpro,均高于对照组,差异有统计学意义(P<0.01);未治疗组3 d时血浆和3、7 d时匀浆中GSH-Px活力与对照组相比明显降低,差异有统计学意义(P<0.05);未治疗组3 d时血浆和14 d时匀浆中的SOD活力与对照组相比明显降低.差异有统计学意义(P<0.05);各时点治疗组血浆、匀浆中MDA含量与未治疗组比较,差异无统计学意义(P>0.05).3 d时治疗组血浆SOD活力与未治疗组相比明显增高,差异有统计学意义(P<0.01).治疗组血浆中GSH-Px活力虽均高于未治疗组,但差异均无统计学意义(P>0.05).治疗组肺纤维组织积分均低于未治疗组,差异有统计学意义(P<0.01).结论 TET对急性百草枯中毒大鼠血浆中SOD和GSH-Px活力降低有一定的拮抗作用,可减轻肺纤维化.     

1,2,4-三氯苯对小鼠心脏、肝脏和肾脏抗氧化系统的影响

目的探讨1,2,4-三氯苯(1,2,4-TCB)对小鼠心脏、肝脏和肾脏抗氧化系统的影响。方法经皮下注射染毒,分为1 382.2、2 764.4、4 146.6 mg/kg低、中、高3个剂量,测定心、肝、肾脏中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、总巯基(T-SH)、非蛋白巯基(NP-SH)、蛋白巯基(P-SH)及脂质过氧化物(LPO)的含量。结果心脏检测示低剂量组NP-SH含量显著高于对照组;肝脏检测示中、高剂量组LPO含量显著增高,GSH-Px活力和NP-SH含量显著低于对照组,高剂量组SOD活力增高,与对照组相比差异有显著性;肾脏检测示3个剂量组GSH-Px活力有所降低,与对照组相比差异有显著性,低剂量组NP-SH含量显著低于对照组。结论1,2,4-TCB可使小鼠心、肝和肾脏脂质过氧化作用增强,并相应地引起抗氧化酶活力和抗氧化物质含量的变化。     

银耳多糖对D-半乳糖所致衰老小鼠抗氧化能力的影响

目的探讨银耳多糖（TP）对D-半乳糖所致衰老模型小鼠抗氧化能力的影响。方法ICR小鼠腹腔注射D-半乳糖建立衰老模型,同时给予不同剂量的TP,8周后获取小鼠心、脑,测定超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活力以及丙二醛（MDA）的含量。结果TP各剂量组SOD和GSH-Px活力显著高于对照组（P〈0．05）,且高剂量TP组SOD、GSH-Px活力均高于低剂量和中剂量TP组（P〈0．05）;中、高剂量TP组MDA含量低于对照组（P〈0．05）且高剂量1]P组MDA含量低于低剂量TP组（P〈0．05）。结论TP对衰老模型小鼠抗氧化能力具有一定的正性调节作用。     

1,2,4三氯苯对小鼠抗氧化能力的影响

目的：通过测定1,2,4－三氯苯（1,2,4－TCB）染毒小鼠全血及组织中超氧化物歧化酶（Superoxide Dismutase,SOD)及谷胱甘肽过氧化物酶（Glutahione Peroxidase,GSH-Px）活力的变化,探讨三氯苯对 氧化能力的影响。采用经后肢皮下注射染毒法,于小鼠染毒24小时后采集血样,摘取肝、肾、心和脑并制成匀浆,分别测定全血及组织中SOD和GSH-Px活力的变化。结果：在肝脏高剂量组和脑高、中、低剂量组SOD活力显著升高,在全血高、中、低剂量组、肝脏的高和中剂量组,肾脏的高、中、低剂量组GSH-Px活力均显著降低,脑的高剂量组GSH-Px活力显著升高。结论,1,2,4－TCB能导致肝脏和脑中SOD活力及脑中GSH-Px活力代偿性升高,血液,肝脏和肾脏GSH-Px活力显著下降。     

PM_(2.5)诱导小鼠肺氧化应激损伤及硒的拮抗作用

目的探讨不同剂量PM_(2.5)诱导小鼠肺氧化应激及硒的保护作用。方法将清洁级昆明小鼠50只随机分为对照组、低剂量组(30μl 0.2μg/μl PM_(2.5)悬液)、中剂量组(30μl 1.2μg/μl PM_(2.5)悬液)、高剂量组(30μl 2.3μg/μl PM_(2.5)悬液)、硒+高剂量组,每组10只,其中对照组气管滴注生理盐水,各染毒组气管滴注不同浓度PM_(2.5),硒+高剂量组在进行硒预处理(35μg/kg)后气管滴注30μl 1.2μg/μl PM_(2.5)悬液。24 h后处死动物,取血清、肺泡灌洗液及肺组织,检测超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)、谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)水平。结果染毒后,中、高剂量组小鼠血清中GSH、SOD及GSH-Px水平低于对照组,高剂量组MDA、GSSG/GSH值高于对照组;硒预处理后,SOD活力高于高剂量组,差异有统计学意义(P0.05)。高剂量组小鼠肺灌洗液中SOD、GSH及GSH-Px水平低于对照组,各剂量组MDA含量高于对照组;硒预处理后,SOD活力高于高剂量组,MDA含量低于高剂量组,差异有统计学意义(P0.05)。中、高剂量组小鼠肺组织匀浆中GSH、GSH-Px水平低于对照组,GSSG/GSH值高于对照组,高剂量组SOD活力低于对照组;硒预处理后,GSH、SOD、GSH-Px水平高于高剂量组,GSSG/GSH值低于高剂量组,差异有统计学意义(P0.05)。结论不同剂量的PM_(2.5)可诱导小鼠出现不同程度的氧化应激,硒可在一定程度上拮抗其造成的氧化应激。     

白藜芦醇对铅诱导小鼠脂质过氧化的拮抗作用

目的探讨白藜芦醇对铅暴露引起的氧化损伤的拮抗作用。方法铅染毒动物模型用含铅(醋酸铅0.5%)饮用水构建。60只健康雄性昆明种小鼠随机分为6组,每组10只:正常对照组,铅染毒组,铅染毒+白藜芦醇低、中、高剂量干预组,白藜芦醇组。检测小鼠血铅和组织铅含量及肝、肾组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性和丙二醛(MDA)的含量和抗氧化能力指数。结果与铅染毒组相比,白藜芦醇处理组肝、肾组织中SOD、CAT和GSH-Px活性均上升(P<0.01),MDA含量降低(P<0.01)。白藜芦醇使用剂量在800～1 200mg/kg时能够显著地提高机体抗氧化酶的活力,增强机体的抗氧化能力。铅染毒小鼠血浆、肝组织及肾组织中ORAC值均有一定程度的减小,给予白藜芦醇可以拮抗铅毒性引起的ORAC值的下降。结论白藜芦醇通过提高抗氧化酶活性,以减轻铅毒引起的脂质过氧化损伤,提高小鼠机体的抗氧化能力,而实现保护肝、肾组织的作用。     

Effect of dietary n-3 and n-6 oils with and without food restriction on activity of antioxidant enzymes and lipid peroxidation in livers of cyclophosphamide treated autoimmune-prone NZB/W female mice

OBJECTIVE: Cyclophosphamide (CTX), an alkylating agent, is extensively used in the treatment of lupus nephritis, but its administration has been associated with free radical mediated oxidative stress. The present study was designed to investigate the effect of dietary corn oil (CO), fish oil (FO) and food restriction (FR) on the activities of hepatic antioxidant enzymes, fatty acid composition and lipid peroxidation following CTX administration in autoimmune-prone NZB/W female mice. METHODS: Autoimmune-prone NZB/W female mice were fed either ad libitum (AL) or food restricted (60% of AL intake), semipurified diets containing 5% CO or 5% FO supplemented with equal levels of antioxidants and injected with either phosphate buffered saline (PBS), or CTX (50 mg/kg body weight) every 10 days. Proteinuria was measured biweekly. The treatment was stopped at 10 months and diets were continued until the mice were killed at 12 months. Fatty acid composition, activity of antioxidant enzymes and lipid peroxidation were analyzed in liver homogenates, and anti-DNA antibodies were analyzed in the serum. RESULTS: Mice in the FO/AL dietary group exhibited significantly higher liver catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities compared to the CO/AL dietary group. CTX significantly decreased SOD and GSH-Px activity in the FO/AL group and CAT and GSH-Px in the CO/AL group. In AL fed mice given CTX, activities of CAT, GSH-Px and GST were significantly higher in mice fed FO diets than in mice fed CO diets. FR increased the activity of enzymes in both the CO and FO diet groups. In FR mice, CTX decreased CAT and GSH-Px activity in both the CO and FO dietary groups, but glutathione S-transferase (GST) only in the CO group. The decrease in SOD activity was not significant in either of the restricted groups. CTX significantly increased generation of thiobarbituric acid reactive substances (TBARS) in both AL groups. FR significantly decreased lipid peroxidation in both the CO and FO groups, with or without CTX. CTX decreased serum anti-DNA antibody levels in both the CO and FO dietary groups. FR also decreased antibody titer in both the CO and FO dietary groups, and it was decreased further with CTX treatment. FO fed animals had higher levels of n-3 fatty acids, whereas CO fed animals had high levels of n-6 fatty acids. CTX significantly increased 20:4 and decreased 18:1 in CO/AL fed animals, whereas it increased 18:1 and decreased 22:6 in FO/AL fed animals. CONCLUSIONS: Results obtained in the present study suggests that FO and, more significantly, FO combined with FR can have a beneficial effect in hepatic tissues subjected to CTX induced oxidative stress by regulating the activity of antioxidant enzymes. In addition, the study also indicates that n-3 and n-6 dietary lipids are susceptible to lipid peroxidation, particularly in the presence of a prooxidant like CTX, and that FR is beneficial in decreasing lipid peroxidation. The study also suggests that FO and CTX can have additive effects in preventing kidney disease in NZB/W mice.     

Antioxidant defense mechanisms in the male rat: Interaction with alcohol,copper, and type of dietary carbohydrate

The activities of enzymes participating in cellular protection against free radical reactions were measured in hepatic tissues from copper-adequate and copper-deficient rats fed fructose or starch-based diets. Half of the rats consumed 20% ethanol in their drinking water. The consumption of ethanol depressed growth rate, reduced hematocrit, and hepatic copper concentration. Feed efficiency was greatly depressed by ethanol. Mortality due to copper deficiency occurred in fructose-fed rats and in starch-fed rats that drank ethanol. Ethanol had no effect on superoxide dismutase (SOD), glutathione peroxidsase (GSH-Px), or catalase. In contrast, copper deficiency reduced SOD and fructose feeding depressed catalase activity. GSH-Px was not affected by either the type of dietary carbohydrate, copper, or ethanol. Taken together, these data suggest that additional mechanisms to antioxidant defense systems are responsible for the metabolic changes that occur during the interactions between ethanol low copper and dietary carbohydrates.     

大骨节病区粮和腐植酸的过氧化损伤效应及微量元素硒、锌的作用的实验观察

应用大骨节病区粮和腐植酸喂养大鼠6周:动物血液和各组织的GSH-Px活力显著降低,但对SOD活力没有大的影响;腓肠肌的GSH-Px活力明显低于心肌和肝脏,其活力降低也最为显著;饮水中加0.2ppm硒能显著升高血液和各组织GSH-Px活力,而2.5ppm锌对SOD、GSH-Px活力和LPO量都无大的影响。说明病区粮,腐植酸引起的动物过氧化损伤效应中,主要是GSH-Px活力降低所致,与SOD的关系不大。     

邻苯二甲酸二异丁酯对小鼠抗氧化酶活性及DNA损伤影响的研究

目的对邻苯二甲酸二异丁酯(DiBP)引起机体组织氧化损伤进行初步研究,借此探讨邻苯二甲酸二异丁酯对自由基氧化损伤的作用机制。方法将60只昆明小鼠在实验动物房内适应3天,按体重随机分为5组:1个对照组和4个不同剂量的DiBP组(Ⅰ组:50mg/kg,Ⅱ组:250mg/kg,Ⅲ组:500mg/kg,Ⅳ组:1000mg/kg)。其中,对照组给予玉米油溶剂灌胃,而各DiBP组给予相应剂量的邻苯二甲酸二异丁酯玉米油溶液灌胃,实验连续进行8周,普通饲料喂养,自由饮水。实验结束后,拔眼球取血分离淋巴细胞,进行彗星实验;测定肝脏组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛(MDA)、8-羟基脱氧鸟苷(8-OHdG)的含量。结果各DiBP组小鼠的肝SOD和GSH-Px酶活性比对照组显著较低(P0.05);MDA含量在DiBPⅢ和Ⅳ组显著高于对照组(P0.05),DiBPⅡ组的8-OHdG含量亦显著高于对照组(P0.01);各DiBP组小鼠的DNA出现氧化损伤,与对照组相比,差异具有显著性(P0.05)。结论在本实验条件下,邻苯二甲酸二异丁酯能够导致实验小鼠机体组织发生氧化应激,从而引起机体抗氧化系统酶活性的改变以及机体组织不同程度的氧化应激损伤。     

Melatonin improved the disturbances in hepatic prooxidant and antioxidant balance and hepatotoxicity induced by a high cholesterol diet in C57BL/6J mice

We examined the effect of melatonin in prooxidant and antioxidant state in the liver of C57BL/6J mice fed on a high cholesterol (HC) diet. Mice were fed with normal mice chow containing 1.5% cholesterol and 0.5% cholic acid for 4 months without and with melatonin (10 mg/L in drinking water) treatment. HC diet was observed to increase malondialdehyde (MDA) and diene conjugate (DC) levels in the liver. This diet lowered glutathione (GSH), alpha-tocopherol, and total ascorbic acid levels as well as glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in the liver, but hepatic superoxide dismutase (SOD) activity remained unchanged. Although melatonin treatment did not affect these parameters in mice fed a normal diet, it reduced hepatic MDA and DC levels in mice fed an HC diet. Hepatic alpha-tocopherol and ascorbic acid levels increased, but hepatic GSH levels remained unchanged in the melatonin-treated HC group as compared to the HC group. Melatonin treatment was found to increase liver GSH-Px and GST activities in mice fed an HC diet. However, SOD activity did not alter in the liver of hypercholesterolemic mice following melatonin treatment. In addition, the histopathological lesions observed in the cholesterol-plus-melatonin group were less severe than those seen in the cholesterol group. According to these observations, we can say that melatonin treatment has an ameliorating effect on the disturbances in prooxidant and antioxidant balance and histopathological lesions in the liver of mice following cholesterol feeding.     

In vivo antioxidant activity of methanol extract from quinoa fermented with Rhizopus oligosporus

Previously, this author reported that the fermentation of quinoa with Rhizopus oligosporeus increased antioxidant activity, and the antioxidant activity of the 80% methanol extract of the fermented quinoa (Q-tempeh) was higher than the other extracts with n-hexane and water in vitro. In this paper, to clarify a beneficial effect of the fermentation of quinoa with R. oligosporus, the antioxidant activity of 80% methanol extract of Q-tempeh was investigated in rats ex vivo and in vivo. In the ex vivo experiment, the 80% methanol extract from Q-tempeh increased both activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the liver, and accelerated the production of 12-hydroxyeicosatetraenoic acid (12-HETE) in the lung. In rats fed vitamin E-free diets with 80% methanol extract of Q-tempeh, the alpha-tocopherol concentration, thiobarbituric acid-reactive substance (TBARS) value, and activities of GSH-Px and SOD in serum showed a similar concentration to those of the control rats fed a vitamin E-supplemented diet. However, the hepatic GSH-Px and SOD activities were higher than those in the control rats. On the other hand, in rats fed a vitamin E-free diet with the 80% methanol extract of quinoa, the serum alpha-tocopherol level was lower, and both TBARS values of serum and liver were higher than those in the control rats. From these results, the 80% methanol extract of Q-tempeh was inferred to be an active superoxide scavenger and peroxide reducer in vivo.     

T-2毒素对低硒大鼠关节软骨抗氧化酶活性及基因表达的影响

目的研究T-2毒素对低硒(Se)大鼠关节软骨抗氧化酶及基因表达的影响。方法新生断乳雄性健康SD大鼠,平均体重60~80g,随机分成两大组即常规组和低Se组喂养30 d,低Se动物模型建造成功后再分成常规组、低Se组、常规+低T-2组、常规+高T-2组、低Se+低T-2组、低Se+高T-2组,再T-2毒素灌胃饲养30 d后,观察低Se、T-2毒素及二者共同作用对各组大鼠关节软骨丙二醛(MDA)含量、总抗氧化能力(T-AOC)、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)活性及SOD、CAT、GSH-Px mRNA表达的影响。结果与常规组相比,各组大鼠关节软骨中MDA含量升高,T-AOC、SOD、CAT和GSH-Px活性下降,均有统计学意义(P<0.05);低Se+低T-2组、低Se+高T-2组与低Se组相比,MDA含量升高,T-AOC、SOD、CAT和GSH-Px活性下降(P<0.05);与常规组相比,各组大鼠关节软骨SOD、CAT、GSH-Px mRNA表达降低(P<0.05)。结论低Se或单纯T-2毒素均可减弱大鼠关节软骨抗氧化酶活性,低Se与T-2毒素对机体抗氧化功能有协同作用。     

Antioxidant enzyme response to selenium deficiency in rat myocardium.

Influences of dietary selenium (Se) deficiency, physical training and an acute bout of exercise on myocardial antioxidant enzyme activity, lipid peroxidation and related biochemical properties were investigated in post-weanling male Sprague-Dawley rats. An experimental group was fed a diet containing less than 0.01 mg Se/kg and had free access to distilled water (Se-D), whereas control rats were supplemented with 0.5 mg Se/l in drinking water (Se-A). Se deficiency depleted heart mitochondrial and cytosolic Se-dependent glutathione peroxidase activity to 24 and 3%, respectively, of those in Se-A rats. Heart mitochondrial superoxide dismutase (Mn SOD) activity was 24% higher (p less than 0.05) in Se-D than in Se-A rats. Cytosolic (copper-zinc) SOD and catalase activities were not altered, whereas glutathione S-transferase activity was significantly decreased in Se-D (p less than 0.01). Myocardial antioxidant enzyme activities were not affected by either training or an acute exercise bout. Heart lipid peroxidation and activities of several enzymes in substrate metabolism were also unaffected by Se or exercise. It is concluded that rat heart has sufficient reserve of antioxidant enzyme capacity in coping with oxidative stress imposed by Se deficiency or exercise. The adaptation of Mn SOD may reveal its potential role in myocardial antioxidant defense.     

干酪乳杆菌Zhang对大鼠抗氧化能力的影响

目的研究两株干酪乳杆菌对大鼠的抗氧化作用。方法将分离自酸马奶的两株干酪乳杆菌:Zhang及MG1-4以活菌制剂的形式灌服大鼠28 d,测定大鼠肝脏组织匀浆和血清SOD、GSH-Px活力和MDA的含量。结果干酪乳杆菌Zhang可使大鼠肝脏组织匀浆中的SOD活力非常显著提高,使大鼠血清中的GSH-Px活力非常显著提高,使大鼠肝脏组织匀浆中的MDA浓度非常显著降低(P。干酪乳杆菌Zhang的抗氧化能力高于MG1-4的。结论干酪乳杆菌Zhang具有提高大鼠体内的抗氧化作用。