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1.
滕旭  武文琦  周显青 《动物学报》2006,52(6):1107-1112
为研究维生素C多聚磷酸酯对小鼠肝脏脂质抗氧化物酶基因转录的影响,将24只3-4周龄、体重为16-22g的健康雄性小鼠随机分为4组,分别在饵料中添加0、500、2500和5000mg/kg的35%维生素C多聚磷酸酯,喂食4周后取其肝脏,用Trizol法抽提总RNA,利用RT-PCR方法对小鼠肝脏超氧化物歧化酶基因、过氧化氢酶基因和谷胱甘肽过氧化物酶基因的mRNA进行分析。结果表明,维生素C多聚磷酸酯对小鼠肝脏抗氧化物酶基因的转录有显著性影响(P<0·05)。维生素C多聚磷酸酯添加量为2500和5000mg/kg的两组,过氧化氢酶基因的mRNA水平明显高于对照组;维生素C多聚磷酸酯添加量为2500和5000mg/kg的两组超氧化物歧化酶基因的mRNA水平明显高于对照组,其中5000mg/kg组的mRNA水平明显高于其它三组;维生素C多聚磷酸酯添加量为5000mg/kg组,谷胱甘肽过氧化物酶基因的转录活性明显高于其它三组(P<0·05)。研究结果表明:高剂量的维生素C多聚磷酸酯能促进小鼠抗氧化物酶基因的转录活性,但促进不同抗氧化物酶基因转录所需的维生素C多聚磷酸酯的量不同。  相似文献   

2.
维生素C多聚磷酸酯对小鼠抗热应激能力的影响   总被引:3,自引:1,他引:2  
周显青  乔欣 《动物学研究》2004,25(5):447-451
为研究维生素C多聚磷酸酯对小鼠抗热应激能力的影响 ,将 4 8只 3~ 4周龄、体重为 16~ 2 9g的健康雄性小鼠随机分为 4组 (对照组、Ⅰ、Ⅱ和Ⅲ组 ) ,在其饵料中分别添加 0、 5 0 0、 2 5 0 0和 5 0 0 0mg/kg的35 %维生素C多聚磷酸酯。喂食 4周后 ,每组取一半小鼠处死取其肝脏 ,另一半置于 (35± 1)℃条件下 ,2 4h后作同样处理。用硫代巴比妥酸分光光度法测肝脏脂质过氧化物 (LPO)的含量 ,用亚硝酸盐形成法测超氧化物歧化酶 (SOD)的活性 ,用分光光度法测过氧化氢酶 (CAT)和谷胱甘肽过氧化物酶 (GSH Px)的活性。经热应激与未经热应激相比 ,LPO :对照组和Ⅰ组显著升高 ,而Ⅱ和Ⅲ组无显著差异。SOD和GSH Px :对照组显著下降 ,其他 3组无显著差异 ;其中SOD :Ⅱ和Ⅲ组显著高于对照组和Ⅰ组 ,GSH Px :Ⅲ组显著高于其他 3组。CAT :对照组和Ⅰ组显著降低 ,而Ⅱ和Ⅲ组无显著差异 ;Ⅱ和Ⅲ组显著高于对照组和Ⅰ组。表明热应激促进了小鼠肝脏LPO的产生 ,抑制了抗化物酶的活性 ;而维生素C多聚磷酸酯对热应激造成的不利影响有缓解作用。  相似文献   

3.
把实验小鼠分成2、6和10只3个密度组,饲养一周后取肝脏,采用硫代巴比妥酸法、比色法和亚硝酸盐形成法分别测定脂质过氧化物、过氧化氢酶和超氧化物歧化酶。6只组和10只组小鼠肝脏脂质过氧化物显著高于2只组;10只组过氧化氢酶活性显著低于2只组,说明拥挤降低小鼠肝脏中过氧化氢酶的活性,使脂质过氧化物含量增加,从而对机体造成过氧化损伤。  相似文献   

4.
为了探讨维生素E对急性2,3,7,8-四氯代二苯并二噁英(TCDD)染毒小鼠肝脏细胞色素P450酶(CYP450)基因和抗氧化物酶基因转录的影响,我们设计了对照组、TCDD(30μg/kg)染毒组和染毒同时给予100mg/kg维生素E组(实验组)3组实验。用Real—Time PCR法检测小鼠细胞色素P450酶1A1、1A2、181、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)基因表达的变化。结果显示:1)急性TCDD染毒小鼠肝脏细胞色素P450酶1A1、1A2、181mRNA水平与对照组相比明显升高,100mg/kg的维生素E具有部分拮抗肝脏细胞色素P450酶1A1、1A2、181 mRNA水平升高的作用;2)急性TCDD染毒小鼠肝脏SOD和GSH-PX mRNA水平呈现降低的趋势,CAT的mRNA水平明显降低,染毒并给予100mg/kg维生素E,SOD和CATmRNA水平与染毒组相比明显升高,GSH.PxmRNA水平也有升高的趋势。上述结果表明:TCDD能影响或部分影响小鼠肝脏细胞色素P450酶1A1、1A2、181、SOD、CAT、GSH-Px的基因转录,而维生素E能在一定程度上缓解TCDD的作用[动物学报54(6):1038—1043,2008]。  相似文献   

5.
本文观察了用抗氧化剂维生素E预处理后,三氯乙烯(3000mg/kg B-W-) 一次性经口染毒24h 大鼠肝脏的超氧化物歧化酶、谷胱甘肽过氧化物酶等抗氧化酶活力及丙二醛含量的变化,结果表明三氯乙烯染毒组肝脏中丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均高于对照组(P< 0-01) ;而维生素E干预组的丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均分别低于三氯乙烯染毒组(P< 0-01) ,说明三氯乙烯急性染毒可引起肝脏脂质过氧化反应及肝损害,肝脏超氧化物歧化酶活力升高可能是机体受自由基及脂质过氧化反应刺激而诱导产生的一种适应性反应,维生素E对三氯乙烯所致的肝损害有一定的保护作用。  相似文献   

6.
本文观察了用抗氧化剂维生素E预处理后,三氯乙烯(3000mg/kg B.W.)一次性经口染毒24h大鼠肝脏的超氧化物歧化酶、谷胱甘肽过氧化物酶等抗氧化酶活力及丙二醛含量的变化,结果表明三氯乙烯染毒组肝脏中丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均高于对照组(P<0.01);而维生素E干预组的丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均分别低于三氯乙烯染毒组(P<0.01),说明三氯乙烯急性染毒可引起肝脏脂质过氧化反应及肝损害,肝脏超氧化物歧化酶活力升高可能是机体受自由基及脂质过氧化反应刺激而诱导产生的一种适应性反应,维生素E对三氯乙烯所致的肝损害有一定的保护作用。  相似文献   

7.
硒和维生素E对皱纹盘鲍血清抗氧化酶活力的影响   总被引:11,自引:3,他引:8  
利用双因素实验设计研究了在饲料中添加维生素E(VE) (0 ,5 0IU/kg)和硒 (Se) (0 ,0 2 ,0 6 ,1 5mg/kg)对皱纹盘鲍 (HaliotisdiscushannaiIno)血清中过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD)、依赖硒的谷胱甘肽过氧化物酶(GPX)、谷胱甘肽还原酶 (GR)、谷胱甘肽转移酶 (GST)这 5种抗氧化酶活力的影响。结果表明 :Se对皱纹盘鲍血清 5种抗氧化酶活力都有显著影响 (P <0 0 5 ) ,而VE仅对GPX和GR的活力有显著影响 (P <0 0 5 )。VE和Se对CAT、GRX和GR的活力的影响具有显著的交互作用。GPX/SOD、GR/GPX、CAT/SOD这 3个抗氧化的重要指标都表明 ,当饲料中含有 4 5 0IU/kg的VE时 ,添加 0 6mg/kg的硒能使皱纹盘鲍血清中的抗氧化物酶系统总体达到相对平衡 ,从而能有效地抵抗氧化损害。  相似文献   

8.
维生素C对凡纳滨对虾生长及抗病力的影响   总被引:8,自引:2,他引:6  
以不同水平维生素C 2 磷酸酯 (添加量分别为 0、75、15 0、30 0和 6 0 0mg/kg)的饲料喂养凡纳滨对虾 10周 ,研究维生素C 2 磷酸酯对凡纳滨对虾生长及抗病力的影响。结果显示 :在养殖前 4周 ,饲料中添加维生素C 2 磷酸酯显著促进凡纳滨对虾的生长 ,然而对对虾的成活以及饲料利用不产生影响 (P >0 0 5 ) ;而到实验后期添加维生素C 2 磷酸酯不能促进凡纳滨对虾的生长 ,却显著提高凡纳滨对虾的成活率 (P <0 0 5 )。维生素C 2 磷酸酯对对虾体水分、脂肪、蛋白质和维生素C在肝胰脏中的积累量的影响显著 (P <0 0 5 ) ,对对虾体灰分影响不显著 (P >0 0 5 )。维生素C 2 磷酸酯对对虾血清中超氧化物歧化酶活力无显著影响 ,饲料中未添加维生素C或过量添加 (超过 30 0mg/kg饲料 )均导致血清中酚氧化酶活力、血细胞总数和溶菌酶活力的显著下降。以生长、成活和酚氧化酶活力为指标 ,饲料中维生素C 2 磷酸酯的适宜添加量为 15 0mg/kg。  相似文献   

9.
目的:对铁过量引发肝脏损伤的小鼠应用不同剂量的富硒酵母所起到的保护作用进行研究。方法:利用腹腔注射方法,向小鼠体内注射过量的铁元素,经过6周的诱导之后导致小鼠肝脏受损,然后给予小鼠不同剂量的富硒酵母进行治疗。分别观察每组小鼠肝脏内丙二醛、超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶的含量和活性,以及对细胞凋亡所造成的影响。结果:本次实验当中,与对比组相比,采取每天给予40药物治疗的研究Ⅱ组小鼠肝组织中的丙二醛含量明显下降,同时也使得超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶的活性明显提高,减少细胞凋亡情况;而采用每天给予20或60的研究Ⅰ组和Ⅲ组肝组织内的丙二醛含量明显提升,同时也使得超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶的活性明显降低,增加了细胞凋亡情。结论:富硒酵母的药效具有一定的浓度指向,应该根据实际治疗目的选择不同的药物浓度,这样才能够有效提升治疗效果。  相似文献   

10.
研究旨在探讨饲料中添加还原型谷胱甘肽(Glutathione, GSH)对黄颡鱼幼鱼(Pelteobagrus fulvidraco)组织谷胱甘肽含量、免疫及抗氧化性能的影响。选用初始体重为(1.32±0.01) g的黄颡鱼800尾, 随机分为5组, 每组4个重复, 每个重复40 尾鱼, 分别投喂基础饲料和添加100、300、500和700 mg/kg GSH的试验饲料, 饲养56d后采样分析, 并采用氯化铵进行96h氨氮应激试验。结果表明: 除100 mg/kg组外, 饲料中添加GSH显著提高黄颡鱼肝脏、血清GSH含量(P<0.05), 当GSH添加量≥300 mg/kg时, 肝脏和血清GSH含量均呈现稳定状态。随着饲料中谷胱甘肽水平的增加, 血清免疫和肝脏抗氧化指标均呈现先升高后降低的趋势, 其中300和500 mg/kg组溶菌酶与碱性磷酸酶活性、300 mg/kg组免疫球蛋白M与补体4含量、500 mg/kg组酸性磷酸酶活性与对照组相比显著升高(P<0.05)。与对照组和700 mg/kg组相比, 300 mg/kg组肝脏超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化酶活性和总抗氧化能力与血清超氧化物歧化酶、谷胱甘肽过氧化酶活性均显著高升高(P<0.05); 且300 mg/kg组血清丙二醛含量显著降低(P<0.05)。氨氮应激96h时, 与对照组相比, 300 mg/kg组肝脏和血清超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化酶活性力均显著升高(P<0.05), 且300 mg/kg组血清丙二醛含量显著降低(P<0.05)。由此可见, 饲料中添加谷胱甘肽能提高黄颡鱼幼鱼组织谷胱甘肽含量、免疫及抗氧化性能, 其中以300—500 mg/kg为宜。  相似文献   

11.
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.  相似文献   

12.
维生素C和酸应激对中华鳖幼鳖血清补体C3和C4含量的影响   总被引:12,自引:0,他引:12  
为研究维生素C对中华鳖(Pelodiscus sinensis)血清补体C3和C4的影响及其在酸应激条件下的变化,我们设置了6个实验组,饵料中维生素C的添加量依次为0、250、500、2500、5000和10000mg/kg,喂食4周后取其血清,用透射比浊法测定酸应激前后中华鳖血清补体C3和C4的含量。结果表明,维生素C添加量为250mg/kg时,血清补体C3的含量与对照组间没有明显不同;维生素C添加量为500、2500、5000和10000mg/kg的4组,血清补体C3的含量明显高于对照组和维生素C添加量为250mg/kg组;维生素C添加量为500mg/kg的一组,血清补体CA含量明显高于其它5组;维生素C添加量为250mg/kg组明显高于10000mg/kg组。酸应激后,补体C3的含量没有明显下降,将维生素C添加量为0、250和500mg/kg的三组并为一组处理,则应激后有明显下降。维生素C添加量为0、250和500mg/kg的3组,血清补体CA的含量在酸应激后明显下降,而维生素C添加量为2500、5000和10000mg/kg的3组,应激后血清补体C4没有明显变化。维生素C和酸应激对中华鳖血清补体C3和CA含量的影响没有交互作用。这说明,维生素C在一定剂量范围内,能提高中华鳖血清补体C3和CA的水平,酸应激能导致其含量降低,而高剂量的维生素C对其下降有颉颃作用[动物学报49(6):769~774,2003]。  相似文献   

13.
Abstract.  Objective : Oxidative stress is a likely molecular mechanism in long-term diazepam administration. The benefits of antioxidants (melatonin and vitamin C) against diazepam-induced cell proliferation, DNA synthesis and oxidative damage were investigated in this study. Materials & methods : Four equal-sized groups of male rats [control, diazepam (3 mg/kg), diazepam plus melatonin (5 mg/kg) and diazepam plus vitamin C (50 mg/kg)] were used. Levels of lipid peroxides (LPO), superoxide dismutase (SOD) activity and glutathione (GSH) concentration were measured in tissue homogenates. Cell proliferation and rate of DNA synthesis were detected by autoradiography. Results : Results documented increased labelling index, 3H-thymidine incorporation (DNA synthesis), LPO plus decrease in GSH levels and SOD activity in livers of diazepam-administered rats versus those of controls. When melatonin and vitamin C were given to diazepam-administered rats, they almost attenuated the increase of labelling index, DNA synthesis and LPO, and restored the levels of GSH and SOD activity. Conclusion : These results suggest long-term hazard in use of drugs such as diazepam; they may be toxic and damage terminates in complex liver damage. Furthermore, melatonin and vitamin C may be useful in combating free radical-induced liver injury resulting from hazard and/or repeated diazepam administration.  相似文献   

14.
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.  相似文献   

15.
人参皂苷抗衰老机制的研究进展   总被引:1,自引:0,他引:1  
人参皂苷的抗衰老作用被认为是人参皂苷的重要作用之一。人参皂苷主要通过四种途径实现其抗衰老功能:通过提高机体内SOD、CAT、GSH2Px活性,诱导SOD、CAT基因表达,减少LPO、MDA含量等实现其抗衰老作用;通过促进神经递质释放、增加神经递质传递者(Ach)含量、促进NBM神经元TrkB mRNA表达、阻止神经原产生过量硝酸盐等实现其抗衰老功能;通过免疫系统在细胞和分子水平上的适度调节延缓衰老;人参皂苷亦能通过影响细胞周期调控因子、衰老基因表达,延长端粒长度、增强端粒酶活性等来实现其抗衰老功能。人参皂苷抗衰老的更完善和更深入的分子作用机制研究将成为未来研究的重点之一。  相似文献   

16.
The metabolism of ethanol gives rise to the generation of excess amounts of reactive oxygen species and is also associated with immune dysfunction. We examined the efficacy of resveratrol and vitamin E on the immunomodulatory activity and vascular function in mice with liver abnormalities induced by chronic ethanol consumption by measuring the protein, liver-specific transaminase enzymes, antioxidant enzymes and non-enzymes such as reduced glutathione (GSH) content, thiobarbituric acid reactive substance (TBARS) level, nitrite level, and activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GPx) and glutathione-S-transferase (GST), and cytokines such as interleukin (IL)-2, IL-4, IL-10, tumor necrosis factor (TNF)-alpha, gamma interferon (IFN-gamma), vascular endothelial growth factor (VEGF)-A and transforming growth factor (TGF)-beta1 in mice blood. Ethanol (1.6 g/kg body wt/day) exposure for 12 wks significantly increased TBARS and nitrite levels and GST activity, and significantly decreased GSH content and the activities of SOD, CAT, GR and GPx in whole blood hemolyzate of 8-10 wks-old male BALB/c mice (weighing 20-30 g). Ethanol exposure also elevated the activities of transaminase enzymes (AST and ALT), IL-10, TNF-alpha, IFN-gamma, VEGF-A and TGF-beta1, while decreasing the albumin concentration and IL-4 activity in the serum. Both resveratrol (5 mg kg(-1) day(-1)) and vitamin E (80 mg kg(-1) day(-1)) treatment significantly reduced AST, ALT, GST, IL-10, TNF-alpha, IFN-gamma, VEGF-A and TGF-beta1 activities and levels of TBARS and nitrite, and elevated albumin content, GSH level and activities of SOD, CAT, GR and GPx, compared to ethanol-treated group. Thus, results from the study demonstrated that both resveratrol (5 mg kg(-1) day(-1)) and vitamin E (80 mg kg(-1) day(-1)) can effectively ameliorate ethanol (1.6 g kg(-1) day(-1))-induced oxidative challenges, immunomodulatory activity and angiogenesis processes.  相似文献   

17.
The antiulcerogenic effect of diffractaic acid (DA) isolated from Usnea longissima, a lichen species, on indomethacin (IND)-induced gastric lesions was investigated in rats. Administration of 25, 50, 100 and 200 mg/kg doses of DA and ranitidine (RAN) (50 mg/kg dose) reduced the gastric lesions by 43.5%, 52.9%, 91.4%, 96.7% and 72.7%, respectively. It is known that oxidative stress leads to tissue injury in organisms. Thus, in all treated groups of rats, the in vivo activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and the levels of reduced glutathione (GSH) and lipid peroxidation (LPO) were evaluated. IND caused oxidative stress, which resulted in LPO in tissues, by decreasing the levels of GPx, SOD and GSH as compared to healthy rats. In contrast to IND, the administration of DA and RAN showed a significant decrease in LPO level and an increase in tissue SOD, GPx and GSH levels. However, while CAT activity was significantly increased by the administration of IND, the administration of DA and RAN decreased CAT activity. The administration of IND also increased the myeloperoxidase (MPx) activity, which shows neutrophil infiltration into the gastric mucosal tissues. In contrast to IND, the administration of DA and RAN decreased MPx activity. The changes in activities of gastric mucosal nitric oxide synthases (NOS) throughout the development of gastric mucosal damage induced by IND were also studied. A decrease in constitutive NOS (cNOS) activity and an increase in inducible NOS (iNOS) activity were determined in gastric damaged tissues induced by IND. The administration of DA (100 mg/kg dose) and RAN reversed the activities of iNOS and cNOS. These results suggest that the gastroprotective effect of DA can be attributed to its enhancing effects on antioxidant defense systems as well as reducing effects of neutrophil infiltration.  相似文献   

18.
The aims of this study were to clarify the effects of high dietary supplementation with boric acid and borax, called boron (B) compounds, on lipid peroxidation (LPO), antioxidant activity, some vitamin levels, and DNA damage in rats. Thirty Sprague Dawley male rats were divided into three equal groups: the animals in the first group (control) were fed with a standard rodent diet containing 6.4 mg B/kg, and the animals in the experimental group were fed with a standard rodent diet added with a supra-nutritional amount of boric acid and borax (100 mg B/kg) throughout the experimental period of 28 days. The B compounds decreased malondialdehyde (MDA), DNA damage, the protein carbonyl content (PCO) level in blood, and glutathione (GSH) concentration in the liver, Cu–Zn superoxide dismutase (SOD), and catalase (CAT) activity in the kidney. The B compounds increased GSH concentration in blood and the vitamin C level in plasma. Consequently, our results demonstrate that B supplementation (100 mg/kg) in diet decreases LPO, and enhances the antioxidant defense mechanism and vitamin status. There are no differences in oxidant/antioxidant balance and biochemical parameters except for serum vitamin A and liver GSH concentration, between the boron compounds used in this study.  相似文献   

19.
The purpose of this study was to investigate the effects of dietary zinc on free radical generation, lipid peroxidation, and superoxide dismutase (SOD) in exercised mice. In the first part of the study, 48 male weanling mice were randomly divided into three groups. They were fed a zinc-deficient diet containing 1.6 mg/kg zinc or were pair-fed or fed ad libitum a zinc-adequate diet supplemented with 50 mg/kg zinc. Half of each group received an exercise training program that consisted of swimming for 60 min per day in deionized water. The diets and exercise program persisted for 6 weeks. In the second part of the study, 64 mice were fed zinc-deficient diets for 6 weeks, and then one group was fed the zinc-deficient diet for an additional 3 weeks, and the other three groups were fed diets supplemented with 5, 50, and 500 mg/kg zinc, respectively. Half of each group also received the exercise program. Both blood and liver samples were examined. Free radicals in liver were directly detected by electron spin resonance techniques and the extent of lipid peroxidation was indicated by malonic dialdehyde (MDA). Both CuZn-SOD and Mn-SOD were measured. The results showed that exercise training increased the metabolism of zinc, and zinc deficiency induced an increased free radical generation and lipid peroxidation and a decreased hepatic CuZn-SOD activity in exercised mice. Furthermore, although exercise training had no effect on the level of free radicals in zinc-adequate mice, it could increase the hepatic mitochondrial MDA formation further in zinc-deficient animals and zinc deficiency would eliminate the exercise-induced increase in SOD activities which existed in zinc-adequate mice. A total of 50 mg/kg zinc supplemented in the diet was adequate to correct the zinc-deficient status in exercised mice while 5 mg/kg zinc had a satisfactory effect on the recovery of only sedentary zinc-deficient mice. However, 500 mg/kg zinc had a harmful effect on both sedentary and exercised zinc-deficient animals.  相似文献   

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