番茄红素对镉中毒大鼠体内抗氧化酶活力影响

目的　观察番茄红素 (lycopene,LP)对镉 (Cd)中毒大鼠抗氧化酶系统的影响。 方法　大鼠饲喂CdCl2 和番茄红素 ,4周后处死 ,测定血清和肝匀浆的超氧化物歧化酶 (SOD)活性、过氧化氢酶 (CAT)活性、谷胱甘肽过氧化物酶 (GSH -Px)活力、丙二醛 (MDA)及还原型谷胱甘肽 (GSH)含量。结果　与模型组相比 ,番茄红素组的大鼠血清和肝组织的SOD活性、GSH -Px活力上升 ,MDA含量降低 ,有显著性差异 (P <0 0 5 )。结论　番茄红素可以拮抗镉的毒性 ,提高大鼠机体的抗氧化能力 ,抑制镉中毒所致的脂质过氧化。     

番茄红素对急性肝损伤大鼠抗氧化酶的影响

目的　观察四氯化碳急性中毒对大鼠机体抗氧化酶活力的影响及番茄红素 (lycopene ,LP)的保护作用。方法　大鼠灌胃番茄红素 ,4周后以四氯化碳腹腔注射 ,2 4h后处死 ,测定血清和肝匀浆的超氧化物岐化酶 (SOD)活性 ,谷胱甘肽过氧化物酶 (GSH Px)活力 ,丙二醛 (MDA)含量 ,还原型谷胱肝肽 (GSH)含量及总抗氧化能力 (T AOC)。结果　与模型组相比 ,各番茄红素组的大鼠血清和肝组织的SOD活性 ,GSH Px活力上升 ,MDA含量降低 ,GSH含量升高 ,T AOC升高 ,差异有统计学意义 (P <0 0 5 )。结论　番茄红素可以提高大鼠机体的抗氧化能力 ,减轻四氯化碳对机体造成的肝损伤。     

番茄红素对铅染毒小鼠脂质过氧化的保护作用

目的:观察染铅小鼠抗氧化系统的改变及番茄红素对抗氧化酶系统的影响。方法:小鼠经饮水铅染毒(醋酸铅)造成铅中毒模型后给予番茄红素,4周后处死,测定血清和肝匀浆的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH—Px)活力、丙二醛(MDA)含量。结果:给予番茄红素的小鼠血清和肝组织的SOD活性、GSH—Px活力上升,MDA含量降低,与中毒模型组相比,差异显著(P<0.05)。结论:铅中毒可引起小鼠过氧化损伤,番茄红素可以提高小鼠机体的抗氧化能力,减轻铅中毒引起的脂质过氧化。     

番茄红素对小鼠抗疲劳和抗氧化作用

目的 研究番茄红素的抗疲劳及抗氧化作用。方法 小鼠经口给予番茄红素30天后，采用负重游泳实验观察小鼠游泳死亡时间；检测血清尿素氮、肝糖原；测定血清和肝匀浆超氧化物歧化酶（SOD）活性、谷胱甘肽过氧化物酶（GSH—Px）活力、丙二醛（MDA）含量。结果 给予番茄红素后，小鼠负重游泳时间明显延长，肝糖原消耗量减少，降低运动后血清尿素氮水平；升高小鼠血清和肝匀浆SOD活性及血清GSH—Px活力，降低小鼠血清和肝匀浆MDA的含量。结论 番茄红素具有抗疲劳和抗氧化作用。     

番茄红素对大鼠体内抗氧化系统功能的影响

目的　观察番茄红素 (lycopene ,LP)对大鼠抗氧化酶系统的影响。方法　大鼠饲喂番茄红素 4周后处死 ,测定血清和肝匀浆的超氧化物歧化酶 (SOD)活性、过氧化氢酶 (CAT)活性、谷胱甘肽过氧化物酶(GSH -Px)活力、总抗氧化能力 (T -AOC)、丙二醛 (MDA)及还原型谷胱甘肽 (GSH)含量。结果　各番茄红素给药组的大鼠血清和肝组织的SOD活性、GSH -Px活力及T -AOC上升 ,MDA含量降低 ,与空白组相比 ,在统计学上差异有显著性 (P <0 0 5 )。结论　番茄红素可以提高大鼠机体的抗氧化能力 ,抑制脂质过氧化     

番茄红素对大鼠肺氧化损伤的影响

目的　观察臭氧对大鼠造成的氧化损伤和番茄红素 (LP)对损伤的影响。方法　利用臭氧吸入造成氧化损伤模型 ,以黄嘌呤氧化酶法测定血清和肺匀浆的SOD活性 ,硫代巴比妥显色法测定MDA含量 ,DTNB比色法测定GSH Px活力。结果　各番茄红素给药组的大鼠血清和肺组织的SOD活性、GSH Px活力上升 ,MDA含量降低 ,与模型组相比差异有显著性 (P <0 0 5 )。结论　番茄红素可以保护臭氧造成的大鼠氧化损伤     

番茄红素对CCl_4致大鼠肝肾抗氧化功能改变的保护作用

目的观察四氯化碳(CCl4)对大鼠肝肾抗氧化功能的影响及番茄红素的保护作用。方法大鼠灌胃番茄红素4周后,以CCl4腹腔注射24h后处死,测定血清和肝、肾匀浆的超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-Px)活力、丙二醛(MDA)含量、谷胱肝肽(GSH)含量及总抗氧化能力(T-AOC)。结果与CCl4组相比,番茄红素组大鼠血清和肝、肾组织的SOD活性、GSH-Px活力上升,MDA含量降低,GSH含量升高,T-AOC升高(P<0·05)。结论番茄红素可以提高大鼠肝和肾的抗氧化能力。     

α-硫辛酸和牛磺酸对急性镉氧化损伤影响的实验研究

目的探讨α-硫辛酸（LA）和牛磺酸（Tau）对急性镉氧化损伤的影响。方法实验用Wistar大鼠32只,分为4组,第一组为对照组,第二组为单纯染镉组,两组均先腹腔注射生理盐水,2h后分别皮下注射生理盐水和35μmol／kg CdCl2溶液。第三组和第四组为LA和Tau预处理组,先分别腹腔注射175μmol／kg的LA溶液和4mmol／kg的Tau溶液,2h后皮下注射35μmol／kg CdCl2溶液。染毒24h后腹主动脉取血并取肝肾,测定血清乳酸脱氢酶（LDH）、丙氨酸氨基转移酶（ALT）活性,肝、肾皮质中Cd、丙二醛（MDA）、谷胱甘肽（GSH）含量及谷胱甘肽过氧化物酶（GSH—Px）、超氧化物歧化酶（SOD）活性。结果与对照组比较,单纯染镉组的血清LDH、伽活性及肝、肾皮质镉含量显著升高,SOD活性显著下降。肝GSH、MDA含量显著升高,GSH—Px活性显著下降。与单纯染镉组比较,LA和Tau干预组的血清ALT和LDH活性及肝组织Cd含量显著降低,肝GSH—Px活性显著增高。LA干预组的肝MDA含量显著降低,肝、肾皮质SOD活性显著升高。Tau干预组肝GSH含量、肾皮质镉含量显著降低。结论LA和Tau预处理对镉所致急性肝脏氧化损伤有一定拮抗作用。     

亚硒酸钠对镉和汞肝肾氧化损伤影响的实验研究

目的:观察一次染镉和汞对大鼠肝、肾组织氧化损伤作用,探讨亚硒酸钠预处理对镉和汞氧化损伤的影响。方法:Wister大鼠48只,随机分成6组,每组8只,第1组为染镉实验对照组,第2组为单纯染镉组,第3组为亚硒酸钠预处理组,第4组为染汞实验对照组,第5组为单纯染汞组,第6组为亚硒酸钠预处理干预组。第1、4组大鼠先腹腔注射生理盐水,2 h后皮下注射生理盐水。第2组大鼠先腹腔注射生理盐水,2 h后皮下注射35μmol/kg氯化镉溶液。第3组大鼠先腹腔注射10μmol/kg亚硒酸钠溶液,2 h后皮下注射35μmol/kg氯化镉溶液。第5组大鼠先腹腔注射生理盐水,2 h后皮下注射2.5 mg/kg HgCl2溶液,第6组大鼠先腹腔注射20μmol/kg亚硒酸钠溶液,2 h后皮下注射2.5 mg/kg HgCl2溶液。染毒24 h后测定肝、肾皮质镉或汞、谷胱甘肽、丙二醛含量和谷胱甘肽过氧化物酶活性。结果:与对照组比较,单纯染镉组大鼠肝GSH、MDA含量显著升高,GSH—Px活性显著下降。Na2SeO3预处理组肝、肾皮质GSH和镉含量显著降低,肝脏GSH—Px活性及肾皮质MDA含量显著升高。单纯染汞组大鼠肝、肾皮质及尿汞含量均显著高于对照组。单纯染汞组肝MDA含量显著高于对照组,GSH含量和GSH—Px活性显著低于对照组。Na2SeO3预处理组的肝脏GSH含量和GSH—Px活性均较单纯染汞组升高,有显著性差异。单纯染汞组肾皮质MDA含量显著高于对照组,GSH含量和GSH—Px活性显著降低。Na2SeO3预处理组中肾皮质MDA含量低于单纯染汞组,GSH—Px含量高于单纯染汞组。结论:给大鼠一次染镉和汞,可以对肝和肾脏产生明显的氧化损伤作用。亚硒酸钠对急性染镉和汞所致肝肾损伤具有一定的拮抗作用,其机制可能与增加内源性GSH、使GSH—Px活性增强以及清除自由基能力提高有关。     

核酸对大鼠体内抗氧化酶活力的影响

目的　观察核酸对大鼠体内抗氧化酶系统的影响。方法　纯种雄性健康Wistar大鼠 ,随机分为 3组 :空白组、核酸低剂量组、核酸高剂量组。自由进食饮水 ,核酸组灌胃核酸 ,对照组灌蒸馏水 ,5周后断头处死动物 ,取血清、肝脏及肾脏 ,测定超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH -Px)活力、丙二醛 (MDA)及还原型谷胱甘肽(GSH)含量。结果　大鼠饲喂核酸后各抗氧化酶活力均有不同程度升高 ,MDA含量则降低。核酸组大鼠血清中SOD、GSH- Px活力明显升高 ,肝组织中GSH- Px活力明显升高 ,MDA含量明显降低 ,肾组织中MDA含量明显降低 ,与空白组相比 ,差异有统计学意义 (P <0 . 0 5 )。结论　饮食核酸可以提高大鼠机体的抗氧化能力 ,抑制脂质过氧化。     

Therapeutic effects of Teucrium polium extract on oxidative stress in pancreas of streptozotocin-induced diabetic rats

Increased oxidative stress is a widely accepted factor in the development and progression of diabetes and its complications. In this study, we evaluated the antioxidative potential of Teucrium polium (Family Lamiaceae) aqueous extract for protecting rat pancreatic tissue against streptozotocin (STZ)-induced oxidative stress. Diabetes was induced in rats by intraperitoneal injections of at a single dose of STZ at 40 mg/kg. The crude extract (equivalent to 0.5 g of plant powder/kg of body weight) was administered orally (intragastrically) to a group of STZ diabetic rats for 30 consecutive days. Changes in antioxidant status were evaluated by determining catalase (CAT) and superoxide dismutase (SOD) activities and the level of reduced glutathione (GSH) in pancreatic tissue. In addition, serum nitric oxide (NO) concentration, pancreatic tissue malondialdehyde (MDA) (an index of lipid peroxidation) level, and reliable markers of protein oxidation such as protein carbonyl content (PCO) and advanced oxidation protein products (AOPP) were also determined. Under diabetic conditions, blood glucose level, serum NO concentration, and pancreatic MDA, PCO, and AOPP levels were all increased. The diabetic rats also exhibited pancreatic GSH depletion along with significant reductions in activities of CAT and SOD. Rats treated with T. polium extract had significantly higher GSH levels along with enhanced CAT and SOD activities in pancreatic tissue. In addition to suppressed blood glucose levels, serum NO, pancreatic MDA, PCO, and AOPP levels were all lower than in the diabetic group. Our results strongly support the proposal that antioxidative activity of T. polium occurs by quenching the extent of lipid and protein oxidation. Based on these observations, it is concluded that T. polium may have protective effect(s) on pancreatic tissue in STZ-induced oxidative stress due to its high antioxidative potential.     

全饥饿对大鼠外周血抗氧化防御系统功能的影响

目的 探讨饥饿后外周血抗氧化防御系统功能的变化。方法 通过禁食大鼠造成饥饿,观察外周血红细胞还原性谷胱甘肽(GSH)含量、血清总抗氧化力、总超氧化物歧化酶(T—SOD)与谷胱甘肽过氧化物酶(GSHPx)．活性以及丙二醛(MDA)含量变化。结果 饥饿10d后,血清总抗氧化力及T—SOD与GSHPx活性显著下降,下降幅度分别为13．8％、8．5％、5．7％;血清MDA含量同时也显著下降,而红细胞GSH含量无显著变化。结论 全饥饿可使外周血抗氧化防御系统功能下降。     

The effects of physical training on antioxidative status under exercise-induced oxidative stress

This study investigated the effect of physical training and oxidative stress on the antioxidative activity and on plasma lipid profile. Forty eight rats were given either a physical training or no training for 4 weeks and were then subdivided into 3 groups: before-exercise (BE); during-exercise (DE); after-exercise (AE). The antioxidative activity was evaluated with the activities of catalase in plasma and superoxide dismutase (SOD), the ratio of reduced glutathione/oxidized glutathione (GSH/GSSG) and the level of malondialdehyde (MDA) in liver. The plasma concentrations of triglyceride (TG), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C)) were also compared. Compared to those of non-training group, catalase activities of training group were lower before exercise but higher during and after exercise. SOD activities were higher regardless of exercise. GSH/GSSG ratio was higher before exercise but was not significantly different during exercise and even lower after exercise. There were no differences between non-training group and training group in MDA levels regardless of exercise. Compared to those of non-training group, atherosclerotic index of training group was lower after exercise and there were no significant differences before and during exercise. There were no differences between non-training group and training group in HDL-C regardless of exercise. These results suggest that moderate physical training can activate antioxidant defenses and decrease the atherosclerotic index and this beneficial effect is evident under exercise-induced oxidative stress.     

补充硒和维生素E对大鼠心肌腺苷酸含量及抗氧化损伤的研究

研究低硒（Ｓｅ）低维生素Ｅ（ＶＥ）膳食及补充Ｓｅ和ＶＥ后对大鼠心肌腺苷酸含量和氧化损伤的关系。方法：采用高效液相和生化方法分别测定心肌腺苷酸和ＭＤＡ含量、ＳＯＤ、ＧＳＨ－Ｐｘ活性。结果：与补充Ｓｅ和／或ＶＥ饮食大鼠相比,低Ｓｅ低ＶＥ饮食大鼠心肌ＡＭＰ、ＡＤＰ含量无明显差异,而ＡＴＰ含量明显降低,ＭＤＡ含量增加,ＳＯＤ、ＧＳＨ－Ｐｘ活性降低,表明Ｓｅ和ＶＥ影响ＡＴＰ含量与其抗氧化作用有关,而其中以联合补充Ｓｅ和ＶＥ效果最佳。结论：Ｓｅ和ＶＥ缺乏可使心肌呈现明显的氧化损伤,补充Ｓｅ和ＶＥ有助于抗氧化损伤,使ＡＴＰ生成增加。     

β-胡萝卜素和核黄素对大鼠脂质过氧化的影响

目的：进一步探讨亚硝胺通过脂质过氧化而致癌的可能途径,以及研究β－胡萝卜素（β－Ｃ）和核黄素（ＶＢ２）通过抑制脂质过氧化反应而影响亚硝胺致癌的可能途径。方法：将５０只二级ＳＤ雄性大鼠随机分成５组。实验组在每日灌胃二甲基亚硝胺（ＮＤＭＮ）１．７５ｍｇ／ｋｇ的基础上,每日分别给予β－Ｃ２５ｍｇ／ｋｇ和／或ＶＢ２１８ｍｇ／ｋｇ补充,实验期为２８天。实验结束时,收集血液,摘取肝脏和肾脏,测红细胞和肝肾匀浆ＳＯＤ活性,全血ＧＳＨ－Ｐｘ活性,血清和肝肾匀浆ＭＤＡ含量,血清ＲＯＯＨ以及全血Ｈｂ含量。结果：１．ＮＤＭＮ可使ＳＯＤ和ＧＳＨ－Ｐｘ活性下降（Ｐ＜０．０５）,ＭＤＡ和ＲＯＯＨ产生增多（Ｐ＜０．０５）。２．添加β－Ｃ后,ＳＯＤ和ＧＳＨ－Ｐｘ活性有明显提高（Ｐ＜０．０５）,ＭＤＡ和ＲＯＯＨ的含量明显降低（Ｐ＜０．０５）。３．添加ＶＢ２后,肝ＳＯＤ和全血ＧＳＨ－Ｐｘ活性均有明显提高（Ｐ＜０．０５）,但ＭＤＡ和ＲＯＯＨ的含量没有差异（Ｐ＞０．０５）。４．同时补充β－Ｃ和ＶＢ２后,各项指标的变化与单纯β－Ｃ组基本一致。结论：脂质过氧化也是亚硝胺致癌的途径之一;一定剂量的β－Ｃ可对抗ＮＤＭＮ引发的脂质过氧化;核黄素对提高抗氧化?