内毒素致大鼠肝组织氧化应激作用

[目的]探讨内毒素腹腔注射染毒对大鼠肝组织抗氧化酶的影响。[方法]采用腹腔注射技术,以脂多糖（LPS）对Wister大鼠进行染毒,染毒浓度分别为0.01、0.05、0.10、1.00mg/kg,对肝组织匀浆上清液中的超氧化物歧化酶（SOD）、Cu,Zn-SOD酶、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-PX）活性以及谷胱甘肽（GSH）和丙二醛（MDA）含量进行测定。[结果]与对照组相比,染毒浓度分别为0.01、0.05和0.10mg/kg时,SOD酶活性变化无统计学差异（P〉0.05）;染毒浓度为1.00mg/kg时,有明显降低（P〈0.01）。与对照组相比,Cu,Zn-SOD酶活性随着染毒浓度的增大,呈现先升后降的趋势,浓度达0.05mg/kg时,升高具有统计学意义（P〈0.01）。与对照组相比,CAT酶活性和MDA含量的变化呈现先降后升的趋势,二者下降的最低点分别为0.05mg/kg和0.01mg/kg;GSH含量和GSH-PX活性均呈现先增后减的趋势,染毒浓度为0.05mg/kg时,二者的增高具有统计学意义（P〈0.01）。[结论]低浓度的LPS可致大鼠肝组织产生适应性反应;高浓度的LPS可引起大鼠肝组织抗氧化能力降低,提示高浓度LPS对大鼠肝的毒作用可能与诱发体内产生过量自由基有关。     

Effect of Vitamin E Supplementation on Arsenic Induced Oxidative Stress in Goats

The present study was designed to assess whether supplementation of different levels of vitamin E to long-term arsenic exposed goats affords protection against the oxidative stress caused by the metalloid. Twenty-four crossbred lactating goats were distributed randomly into four groups (control, T₁, T₂ and T₃) of six in each. The animals in T₁, T₂ and T₃ were given 50 mg/kg DM arsenic daily, while in T₂ and T₃, vitamin E @100 IU and 150 IU/kg DM, respectively, was also supplemented additionally for the period of 12 months. Compared to control, significant (p < 0.05) decline in SOD (45 %), CAT activities of erythrocytes (63 %), plasma total Ig (22 %) and total antioxidant activity (24 %) was observed in only arsenic treated groups and vitamin E supplementation in both doses produced partial mitigation effect against SOD (23 %, 20 %) and CAT (39 %, 48 %) while complete mitigation against total Ig (16 %, 7 %) and antioxidant activity (10 %, 8 %) was found. Average lymphocyte stimulation index at the end of experiment was (p < 0.05) lower in arsenic exposed groups (1.003 ± 0.01) and significant (p < 0.05) recovery was observed in response of vitamin E supplementation at higher doses (1.138 ± 0.03). So, vitamin E is helpful in reducing the burden of arsenic induced oxidative stress and activities of antioxidant enzymes in goats.     

Vitamin E and Neurodegenerative Disorders Associated with Oxidative Stress

Abstract

Several neurodegenerative disorders are associated with oxidative stress that is manifested by lipid peroxidation, protein oxidation and other markers. Included in these disorders in which oxidative stress is thought to play an important role in their pathogenesis are Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), tardive dyskinesia, Huntington's disease (HD), and multiple sclerosis. This review presents some of the chemistry of vitamin E as an antioxidant and summarizes studies in which vitamin E has been employed in these disorders and models thereof.     

Protection of Vitamin C on Oxidative Damage Caused by Long-Term Excess Iodine Exposure in Wistar Rats

Vitamin C was reported to be able to protect against oxidative damage due to its reducibility. 120 Wistar rats were randomly divided into 4 × 2 groups, including normal iodine (NI), high iodine (HI), low vitamin C (HI + LC), and high vitamin C (HI + HC); potassium iodide (KI) and potassium iodate (KIO₃) were commonly used as additives for iodized salt, so every group was also divided into KI and KIO₃ groups. After 6 months’ feed, the activities of antioxidant enzymes and Lipid Peroxide (MDA) content in serum, liver, kidney, brain, thyroid and lens were determined. In serum, for males, long-term excess iodine intake caused oxidative damage; in the liver, male rats in the HI + LC group had the highest MDA content, which showed that low-dose vitamin C might promote oxidative damage; in kidneys, the MDA content in the HI and HI + LC groups of females was higher; in the brain, high-dose vitamin C could increase the activity of superoxide dismutase (SOD), which was decreased by high iodine intake, and it also decreased MDA content; in the thyroid, for KIO₃, the activity of SOD in the HI group was lower than NI and HI + LC; in the lens, the MDA content in females was lower than males. Long-term excess iodine exposure caused oxidative damage and showed sex difference, and vitamin C had a protective effect on it, especially for high-dose vitamin C.     

汞矿地区大米对大鼠生长发育及氧化损伤的影响

目的探讨汞矿地区大米暴露对大鼠生长发育的影响及氧化损伤机制。方法利用汞矿地区大米及对照组大米分别对SD大鼠进行90d暴露实验,观察大鼠的体重变化情况,90d后处死,测定大鼠脑、肝、肾组织谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活力及还原型谷胱甘肽(GSH)、丙二醛(MDA)含量。结果与对照组相比,实验组大鼠的体重增幅较大,脑、肝、肾组织中GSH-Px、SOD活力和GSH含量降低(P<0.05),MDA含量升高,差异均有统计学意义(P<0.01)。结论大鼠暴露于汞污染大米90d后脑、肝、肾均产生了明显的脂质过氧化。     

茶多酚、维生素C对染石英尘大鼠氧化损伤的缓解作用

目的 探讨抗氧化剂茶多酚、维生素C对染尘大鼠血液中一氧化氮及抗氧化酶活性的影响。方法 Wistar大鼠随机分成对照组、石英粉尘组及预防组（茶多酚组,茶多酚＋Vit C组）。检测实验大鼠血液中NO和NOS、SOD、GSH－Px的活性。结果 与石英粉尘组比较,预防组大鼠血液中NO的含量及NOS活性下降,SOD、GSH－Px活性上升。结论 抗氧化剂茶多酚、维生素C对石英粉尘引起的氧化损伤有一定的缓解作用。     

氯氰菊酯对小鼠睾丸组织的氧化损伤和维生素E的抗氧化作用

[目的]研究氯氰菊酯(CP)对小鼠睾丸组织的氧化损伤和维生素E的抗氧化作用. [方法]以36只昆明小鼠为受试动物,随机分为6组,包括1个阴性对照组、3个氯氰菊酯染毒组、1个维生素E组和1个高剂量氯氰菊酯(40mg/kg)加维生素E组(100 mg/kg),染毒组按10、20和40 mg/kg 3个剂量水平,维生素E的剂量为100mg/kg,小鼠灌胃染毒7d.取睾丸称重测定脏器系数;以睾丸组织匀浆测定活性氧(ROS)、还原型谷胱甘肽(GSH)和丙二醛(MDA)的含量;以睾丸细胞测定DNA-蛋白质交联(DPC)系数;并制作睾丸组织切片,观察其病理损伤. [结果]随着氯氰菊酯染毒剂量的升高,睾丸的脏器系数、ROS、MDA含量和DPC系数逐渐上升,GSH含量逐渐降低,各指标呈一定的剂量-效应关系.与对照组比较,染毒剂量为20mg/kg时,睾丸脏器系数(0.568±0.027)、ROS含量(586.2±43.94)、GSH含量(18.15±2.351)、DPC系数(0.186±0.017)和MDA含量(2.051±0.137)差异有统计学意义(P＜0.05,P＜0.01),睾丸部分生精小管生精细胞减少,生精细胞脱落管腔;染毒剂量为40 mg/kg时,GSH含量(17.13±1.203)、脏器系数(0.643±0.028)、ROS含量(898.8±100.23)、MDA含量(2.299±0.157)和DPC系数(0.229±0.020)差异有统计学意义(P＜0.05,P＜0.01),睾丸生精细胞明显减少,部分生精细胞脱落坏死,阻塞管腔.高剂量染毒加维生素E组与高剂量染毒组相比较,睾丸的脏器系数、ROS、MDA含量和DPC系数均有下降,GSH含量上升.ROS含量(550.4±102.3)、GSH含量(24.65±2.892)和MDA含量(1.291±0.289)差异有统计学意义(P＜0.05);睾丸的脏器系数(0.507±0.026)和DPC系数(0.139±0.017)差异有统计学意义(P＜0.01). [结论]较高剂量(20、40 mg/kg)的氯氰菊酯能造成小鼠睾丸的氧化损伤和病理损伤,且可以被维生素E的抗氧化作用所拮抗.     

高果糖饲料诱导SD大鼠氧化应激及对其脂质代谢的影响

目的探讨高果糖饲料诱导SD大鼠氧化应激和对其脂质代谢的影响。方法实验大鼠分为2组熏分别用普通饲料和高果糖饲料喂养8周,检测大鼠空腹血糖(FBG)、血胰岛素(FSI)、血脂、总抗氧化力(T鄄AOC)、丙二醛(MDA)及超氧化物岐化酶(SOD)等。结果高果糖饲料组胰岛素敏感指数(ISI)低于普通饲料组(P<0.01),甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL鄄C)升高(分别为P<0.01,P<0.05和P<0.01),高密度脂蛋白胆固醇(HDL鄄C)降低(P<0.05),T鄄AOC、SOD活性降低(P<0.01),MDA水平升高(P<0.01)。结论高果糖饲料可诱导SD大鼠产生氧化应激,引起脂质代谢紊乱。     

Sub-acute Deltamethrin and Fluoride Toxicity Induced Hepatic Oxidative Stress and Biochemical Alterations in Rats

The current study investigated the effects of deltamethrin, fluoride (F^?) and their combination on the hepatic oxidative stress and consequent alterations in blood biochemical markers of hepatic damage in rats. Significant hepatic oxidative stress and hepatic damage were observed in the toxicant exposed groups. These changes were higher in the deltamethrin-F^? co-exposure treatment group, depicting a positive interaction between the two chemicals.     

Dual Role of Vitamin C Utilization in NO2-Induced Oxidative Stress in Lung Tissues of Mice

Earlier studies with in vitro models have revealed that application of vitamin C can act as a primary NO₂ absorption substrate to contribute to NO₂-induced cellular injury. In the present study, we showed that the pharmacological application of vitamin C had dual role in lungs of mice exposed to NO₂, with an exacerbated oxidative stress occurring at low concentrations, as indicated by excessive reactive oxygen species production and lipid peroxidation. However, at high concentrations, vitamin C functioned as an antioxidant removing reactive oxygen species and maintaining a reducing status in cells, alleviating NO₂-induced oxidative toxicity.     

Oxidative Stress Response Induced by Butachlor in Zebrafish Embryo/Larvae: The Protective Effect of Vitamin C

The widespread contamination and persistence of the herbicide butachlor in the environment resulted in the exposure of non-target organisms. The present study investigated the toxicity effect of butachlor (1–15 µmol/L) and the protective effect of vitamin C (VC) against butachlor-induced toxicity in zebrafish. It was found that butachlor significantly increased the mortality and malformation rates in a dose-dependent manner, which caused elevation in reactive oxygen species (ROS) and malondialdehyde (MDA) after 72 h exposure. Compared with butachlor treatment group, the protective effect of VC against butachlor-induced toxicity were observed after adding 40, 80 mg/L VC respectively. VC significantly decreased the mortality, malformation rates, ROS, MDA, and normalized antioxidant enzymes activities of zebrafish after 72 h exposure. The result shows VC has mitigative effect on butachlor-induced toxicity and it can be used as an effective antioxidant in aquaculture.     

2-氨基-1-甲基-6-苯基-咪唑并[4,5-b]吡啶对大鼠不同组织的蛋白质氧化损伤作用

目的 观察杂环胺代表物2-氨基-1-甲基-6-苯基-咪唑并[4,5-b]吡啶(PhIP)对雄性Wistar大鼠不同组织蛋白质氧化损伤.方法 将20只健康成年清洁级Wistar雄性大鼠随机分为4组,分别为对照(pH=4.5的55％乙醇-生理盐水)组和低(5 mg/kg)、中(10mg/kg)、高(15 mg/kg)剂量P...     

硫辛酸对高脂诱导肥胖大鼠氧化应激影响的实验研究

目的探讨硫辛酸（LA）对高脂诱导肥胖大鼠氧化应激水平的影响。方法 29只5~6周龄Wistar雄性大鼠,按体重随机分为2组：基础组（n=8）和高脂组（n=21）。高脂组大鼠饲养6周末尾尖采血,测定空腹血糖,按血糖水平随机分为2组：高脂组,高脂＋硫辛酸干预组（硫辛酸组）,分别用生理盐水和LA进行腹腔注射,4周后测定大鼠体重、内脏脂肪含量以及血清丙二醛（MDA）、超氧化物歧化酶（SOD）、总抗氧化能力（T-AOC）和全血谷胱甘肽过氧化物酶（GSH-Px）。结果与基础组比较,高脂组大鼠的血清MDA水平和SOD活性明显增高,T-AOC下降,差异均有统计学意义（P〈0.05）;与高脂组比较,LA组大鼠体重和内脏脂肪含量明显降低,血清T-AOC明显升高,差异有统计学意义（P〈0.05）;三组大鼠GSH-Px差异无统计学意义（P〉0.05）。结论 LA能显著降低高脂诱导肥胖大鼠的体重和内脏脂肪含量,提高肥胖大鼠的抗氧化能力。     

纳米铜对大鼠肝脏和肾脏的氧化损伤作用

目的 比较纳米铜与微米铜对大鼠肝脏和肾脏的氧化损伤,探讨氧化损伤在纳米铜致大鼠肝毒性和肾毒性中的作用.方法 SPF级雄性Wistar大鼠30只,随机分为溶剂对照组(1%羟丙甲基纤维素),微米铜组(200 mg/kg),纳米铜3个不同剂量组(50、100和200mg/kg),每组6只,10 ml/kg经口灌胃染毒,每日一次,连续5 d.染毒结束后,留取大鼠肝脏和肾脏用硫代巴比妥酸法(TBA)测定丙二醛(MDA)含量,二硫代双硝基苯甲酸法(DTNB)测定总巯基(TSH)和非蛋白巯基(NPSH)含量.结果 纳米铜染毒组大鼠肝脏和肾脏组织中NPSH的含量随染毒剂量增加先增后降,而MDA含量呈剂量依赖性增加,尤其是在纳米铜高剂量组(200 mg/kg),与对照组比较,差异有统计学意义(P＜0.05,P＜0.01),而在微米铜组却未发现相应改变.结论 在相同剂量和暴露时间条件下,纳米铜对大鼠的毒性明显强于微米铜,纳米铜导致大鼠肝脏和肾脏损伤的机制可能与肝、肾组织中NPSH的耗竭及脂质过氧化有关.     

亚砷酸钠致Chang liver细胞氧化应激作用的研究

目的 研究不同浓度亚砷酸钠(NaAsO2)对人肝细胞株Chang liver的氧化应激作用.方法 采用四甲基偶氮唑(MTF)比色法检测NaAsO2(0、0.1、1、5、10、20、30、50、80、100、200 μmol/L)对Chang liver细胞活力的影响,利用2',7'-二乙酰二氯荧光素(DCFH-DA)检测细胞内活性氧(ROS)水平,利用黄嘌呤氧化法和硫代巴比妥酸比色法测定细胞内超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量.结果 与对照组比较,0.1 μmol/LNaAsO2组细胞活力显著增强(P<05);10～200μmol/L NaAsO2浓度范围内,细胞活力随NaAsO2浓度升高而下降(P<0.05).在0～30 μmol/LNaAsO2浓度范围内,随着NaAsO2浓度的增高,细胞内ROS水平升高(P<0.05),SOD活力降低(P<0.001),MDA含量升高(P<0.001).结论 氧化应激可能是NaAsO2对Chang liver细胞毒性作用的机制之一.     

亚砷酸钠致SV-HUC-1细胞氧化应激作用的研究

目的 探讨亚砷酸钠(NaAsO_2)对人膀胱上皮永生化细胞SV-HUC-1的氧化应激作用.方法 以不同浓度NaAsO_2(0、0.1、0.2、0.5、1、2、4、6、8、10、20 μmol/L)对SV-HUC-1细胞进行染毒,采用四甲基偶氮唑(MTT)比色法检测细胞活力,利用2',7'-二乙酰二氯荧光素(DCFH-DA)检测细胞内活性氧(ROS)水平,分别应用DTNB比色法、硫代巴比妥酸比色法和黄嘌呤氧化法检测细胞内谷胱甘肽(GSH)含量、丙二醛(MDA)含量以及超氧化物歧化酶(SOD)活力.结果 与空白对照组比较,全部染毒组细胞活力均下降(P<0.05);染毒24 h后,全部染毒组ROS水平均显著升高(P<0.05);2、4 μmol/LNaAsO_2组细胞GSH含量显著升高(P<0.05);全部染毒组细胞MDA含量均无变化(P>0.05);全部染毒组细胞SOD活力均显著降低(P<0.05).结论 氧化应激可能是NaAsO_2致SV-HUC-1细胞毒性作用的机制之一.     

Wheat Germ Supplementation of a Low Vitamin E Diet in Rats Affords Effective Antioxidant Protection in Tissues

Background: Oxidative stress is implicated in the etiology of many diseases, but most of clinical trials failed to demonstrate beneficial effects of antioxidant supplementation.

Methods: In the present experiment, we assessed the mean-term effect of wheat germ supplementation, as a dietary source of vitamin E, on antioxidant protection in rat.

Results: Feeding rats a 20% wheat germ diet significantly increased plasma and liver vitamin E levels, compared to the low vitamin E basal diet. Concurrently, wheat germ diet consumption strongly decreased the susceptibility of heart and liver lipids to oxidation, as well as the plasma. Wheat germ feeding did not change triglycerides (TG) nor total cholesterol concentrations in plasma or liver, resulting in higher vitamin E/ TG ratio compared to controls. Similar results were found with a diet in which wheat germ oil provided the same amount of vitamin E.

Conclusions: Wheat germ appears thus very effective to improve antioxidant defense status, especially in tissues, irrespective of modifications of lipids status.     

Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

Non-alcoholic fatty liver disease (NAFLD) is currently estimated as the most prevalent chronic liver disease in all age groups. An increasing body of evidence obtained in experimental and clinical data indicates that oxidative stress is the most important pathogenic factor in the development of NAFLD. The study aimed to investigate the impact of α-lipoic acid (LA), widely used as an antioxidant, on the effects of a hypercaloric choline-deficient diet. Male Wistar rats were divided into three groups: control diet (C); hypercaloric choline-deficient diet (HCCD), and hypercaloric choline-deficient diet with α-lipoic acid (HCCD+LA). Supplementation of HCCD with LA for eight weeks led to a decrease in visceral adipose tissue/body weight ratio, the activity of liver glutathione peroxidase and paraoxonase-1, plasma, and liver total antioxidant activity, as well as an increase in liver/body weight ratio, liver total lipid and triglyceride content, and liver transaminase activities compared to the HCCD group without LA. In conclusion, our study shows that α-lipoic acid detains obesity development but exacerbates the severity of diet-induced oxidative stress and lipid accumulation in the liver of male Wistar rats fed a hypercaloric choline-deficient diet.     

番茄红素抗氧化损伤的实验研究

目的观察番茄红素对臭氧所致大鼠氧化损伤的保护作用。方法利用大鼠吸入臭氧制造损伤模型,同时灌胃番茄红素,6周后检测大鼠血清及肝脏中的超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量。结果高、低剂量组与损伤模型组相比,SOD和GSH-Px活力升高,MDA含量下降,差异显著(P<0.05)。结论番茄红素对臭氧所致大鼠氧化损伤具有一定的保护作用。     

煤烟颗粒提取物对大鼠肺细胞的氧化 性损伤作用

目的：通过加入抗氧化剂N－乙酰半胱氨酸,作为实验干预手段。方法：观察煤烟对大鼠肺Ⅱ型细胞生长和DNA交联形成作用的影响。结果：与对照组相比,分别加入10、30mmol/L N－N乙酰半胱氨酸后的实验组细胞毒性有所下降, 从而间接地证实了氧化性损伤的存在;同时,N－乙酰半胱氨酸还可以降低煤烟经细胞染毒所致的DNA交联作用 。结论：煤烟可能是经过细胞代谢活化后产生的某些代谢产物而导致细胞的氧化性损伤。