糖脉康治疗早期糖尿病肾病疗效观察及对患者血清超氧化物岐化酶、过氧化氢酶、丙二醛水平的影响

目的 观察糖脉康治疗早期糖尿病肾病的临床疗效,并探讨其对患者血清超氧化物岐化酶(SOD)、过氧化氢酶(CAT)、丙二醛(MDA)水平的影响.方法 选择94例早期糖尿病肾病患者,按数字表法随机平均分为两组,对照组(47例)给予常规治疗,观察组(47例)在常规治疗的基础上加用糖脉康治疗,两组均治疗8周.观察两组临床治疗疗效,同时观察氧化应激指标SOD、CAT、MDA水平变化.结果 观察组治疗总有效率为91.5％,显著高于对照组的68.1％(x2=57.31,P＜0.05);观察组SOD显著升高至(81.2±8.9)μU/L,CAT显著升高至(27.3±2.5)μU/L,MDA显著降低至(4.9±0.5)μmol/L,与对照组差异均有统计学意义(t=3.01、2.75、2.14,均P＜0.05).结论 糖脉康治疗早期糖尿病肾病临床疗效确切,可能通过抑制氧化应激机制来发挥肾脏保护作用.     

Spirulina fusiformis provides protection against mercuric chloride induced oxidative stress in Swiss albino mice

Oxidative stress induced by mercuric chloride (5 mg/kg body weight i.p.) in mice substantially increases the lipid peroxidation level along with corresponding decrease in the reduced glutathione and various antioxidant enzymes in liver and increase in serum transaminases activity. Supplementation of Spirulina (800 mg/kg body weight orally, in olive oil, along with mercuric chloride) for 40 days resulted in decreased LPO level, serum glutamate oxaloacetate and serum glutamate pyruvate transaminase activity along with increase in liver GSH level. The activities of antioxidants enzymes superoxide dismutase, catalase and glutathione-S-transferase were also concomitantly restored to near normal level by Spirulina supplementation to mercuric chloride intoxicated mice. The results clearly demonstrate that Spirulina treatment augments the antioxidants defense mechanism in mercuric chloride induced toxicity and provides evidence that it may have a therapeutic role in free radical mediated diseases.     

The influence of extraction methods on rutin yield of cassava leaves (Manihot esculenta Crantz)

Rutin, a well-known bioflavonoid, was found abundantly in cassava leaves. In the present study, extraction techniques including maceration, boiling, reflux, ultrasound-assisted extraction (UAE), and microwave-assisted extraction (MAE) were optimised to increase the yield of rutin. Extraction parameters such as solvents, solid-liquid ratio, temperature, and time were optimised to give better extraction yields for each method. HPLC analysis showed a high content of rutin which is up to 2.4% per dry weight of cassava leaves. The extraction yields under optimised condition were found to be 16.00 ± 0.21, 20.38 ± 0.66, 22.33 ± 2.3, 24.49 ± 0.41, and 23.37 ± 1.00 g rutin per kg dry weight for maceration, boiling, reflux, UAE and MAE methods, respectively. Specifically, UAE reduced the extraction time to 90 min, using only 40–60% of aqueous ethanol. Meanwhile, MAE completed the extraction under 5 min and no significant differences in output was observed between the use of water and aqueous ethanol. Accordingly, with the extraction efficiency of up to 99 and 94%, respectively, both processes provided better results. The subsequent green purification using chilling method produced a typical cassava bioflavonoid containing 82% of rutin and 17% of nicotiflorin. This study informs a new abundant source of rutin and provides the optimum condition of extraction methods for high yield of rutin from cassava leaves.     

急性运动所致氧化应激及谷氨酰胺的保护作用

目的探讨补充外源性谷氨酰胺(Gln)对急性运动应激大鼠的抗氧化保护作用。方法采用大鼠力竭性游泳方式,通过补充Gln对比实验,于力竭游泳后2小时,观察大鼠血清、股四头肌和心肌组织中谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量的变化。结果力竭性游泳大鼠骨骼肌MDA显著升高;血清、骨骼肌SOD显著升高,心肌SOD显著下降;血清GSH显著下降。补充Gln能抑制力竭游泳后大鼠骨骼肌MDA升高;抑制血清、骨骼肌SOD升高和心肌SOD下降。结论Gln对急性运动所致的氧化应激有一定的保护作用。     

Effect of co-administration of cassava (Manihot esculenta Crantz) rich diet and alcohol in rats

The effects of co-administration of a cassava rich diet and alcohol in rats were investigated. The animals were divided into four groups (1) Control, (2) Alcohol, (3) Cassava and (4) Alcohol + Cassava. Consumption of alcohol along with cassava reduced the alcohol induced toxicity which was evidenced by the lower activities of GOT, GPT, GGT, acid phosphatase and alkaline phosphatase in the liver and serum of co-administered group. The pyruvate content in the blood increased while the lactate content, lactate/pyruvate ratio and the activity of LDH decreased in the blood due to co-administration. The blood cyanide content, serum thiocyanate content and the activities of rhodanase and beta-glucuronidase increased on co-administration. The histopathological studies also revealed that co-administration reduced the alcohol induced toxicity.     

黄芪对应激性大鼠胃黏膜抗氧化作用研究

目的 测定黄芪注射液对应激状态下大鼠胃黏膜中超氧化物歧化酶(SOD)活性和丙二醛含量的影响,为临床应用黄芪治疗应激性溃疡提供理论依据.方法 采用水浸束缚应激方法复制大鼠应激性溃疡模型.健康雄性SD大鼠40只完全随机分为5组,每组8只,即对照组、模型组、黄芪低剂量组(低剂量组)、黄芪高剂量组(高剂量组)及硫糖铝组.对照组、模型组采用生理盐水,低剂量组采用10 g/kg黄芪注射液,高剂量组采用20 g/kg黄芪注射液,硫糖铝组采用硫糖铝500 mg/kg连续灌胃5 d,水浸束缚应激12 h后,采用黄嘌呤氧化酶法和硫代巴比妥酸法(TBA法)测定胃黏膜中SOD活性和丙二醛含量.结果 应激12 h后,对照组、模型组、硫糖铝组及低、高剂量组的丙二醛含量分别为(5.24±1.70)、(13.31±1.69)、(7.76±1.11)、(7.13±0.83)、(6.53±0.73)nmol/mg prot;上述5组的SOD活性水平分别为(191.87±24.38)、(112.00±16.74)、(203.00±16.24)、(174.00±19.74)、(197.75±18.43)U/mg prot.与对照组相比,其他4组大鼠胃黏膜丙二醛含量明显增高(P＜0.01).与模型组相比较,硫糖铝组和低、高剂量组大鼠胃黏膜丙二醛含量明显降低,差异具有统计学意义(P＜0.01).同时,与对照组相比较,模型组、低剂量组大鼠胃黏膜SOD活性明显降低,差异有统计学意义(P＜0.01或P＜0.05).与模型组相比较,硫糖铝组和低、高剂量组大鼠胃黏膜SOD活性明显增高,差异具有统计学意义(P＜0.01).高剂量组的胃黏膜SOD活性高于低剂量组,差异有统计学意义(P＜0.01).结论 黄芪对应激性溃疡大鼠具有显著的胃黏膜保护作用.其机制可能是增强大鼠血清和胃黏膜局部抗氧化能力.

Abstract：

Objective To investigate the antioxidation on gastric mucosa of radix injection in rats on stress ulcer, and to explore the possible mechanism. Methods Water immersion and restraint stress(WRS) induced acute gastric injury was used as the experimental model of stress ulcer of rats. All the animals were randomly divided into 5 groups, the control group, the model group, Radix injection 10, 20 g/kg and sucralfate 500 mg/kg group.Rats were orally administrated with Radix injection or sucralfate for 5 days before stressed. 12 h after WRS, The activity of total superoxide dismutase (SOD) and malondialdehyde (MDA) level in gastric mucosa were measured by xanthine oxidase method and thibabituric acid(TBA) method respectively. Results In radix 20 g/kg group, radix exhibited the strong ability to rise the activity of SOD in gastric mucosa( P ＜0.01 ) and lower the mucosal MDA concentration(P＜0. 01). Conclusions Radix exhibits remarkable protective effects on WRS induced stress ulcer in rats. The protective effects might be related to trigger the intrinsic protective mechanism by enhancing the antioxidatire effect. It provides theoretical principle for clinical application of radix on stress ulcer.     

间歇低氧小鼠血清氧化应激指标的变化及N-乙酰半胱氨酸的治疗作用

目的观察间歇低氧(I H)小鼠血清氧化应激指标的变化情况,并探讨N-乙酰半胱氨酸(NAC)的治疗作用。方法随机将50只小鼠分为对照组(A组,20只),IH组(B组,30只),分别造模3d、1周、2周、3周、4周;另设IH4周+NAC组(C组,6只)。检测各组小鼠血清超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-PX)表达水平。结果与A组同期比较,B组MDA表达均升高(P<0.05);造模1周后,SOD、GSH-PX表达均降低(P<0.05)。随低氧时间的延长,B组MDA逐渐升高,SOD、GSH-PX逐渐降低(P<0.05)。与B组比较,C组MDA降低,SOD、GSH-PX升高(P<0.05)。结论 IH可导致机体氧化应激水平增加,而NAC治疗能够改善IH导致的氧化应激反应。     

Acute and chronic vitamin A supplementation at therapeutic doses induces oxidative stress in submitochondrial particles isolated from cerebral cortex and cerebellum of adult rats

Vitamin A is an essential micronutrient to the normal brain function. However, there is an increasing concern regarding the use of vitamin A at high doses even therapeutically. Here, we show that acute and chronic vitamin A supplementation induces oxidative stress to submitochondrial particles (SMP) isolated from rat cerebral cortex and cerebellum. Both chronic and acute vitamin A supplementation at therapeutic (1000 IU/kg or 2500 IU/kg) or excessive (4500 IU/kg or 9000 IU/kg) doses induced lipid peroxidation, protein carbonylation, and oxidation of protein thiol groups in cerebral cortex and cerebellum SMP. Furthermore, vitamin A supplementation induced an increase in the superoxide (O(2)(-)) anion production, indicating an uncoupling in the electron transfer chain (ETC). Locomotory and exploratory activity, which are associated to cerebral cortex and cerebellum, also were affected by both acute and chronic vitamin A supplementation. Vitamin A induced a decrease in both locomotory and exploratory behavior. Together, these results show that vitamin A could be toxic at the sub cellular level, inducing mitochondrial dysfunction and altering cerebral cortex and/or cerebellum-dependent behavior.     

Neurotoxic effect of linamarin in rats associated with cassava (Manihot esculenta Crantz) consumption

Cassava (Manihot esculenta Crantz) is a plant widely used for food consumption in different processed products in rural areas of Africa, Asia, and Latin America. Cassava is a good source of carbohydrates and micronutrients. However, if it is not adequately processed or the consumer has nutritional deficiencies, then its cyanogenic glycoside (i.e., linamarin and lotaustralin) content makes it potentially neurotoxic. In the present study, the neurotoxic effects of different concentrations of linamarin (0.075, 0.15, 0.22, and 0.30 mg/kg) contained in cassava juice were evaluated in the open field and swim tests to identify locomotor alterations in adult male Wistar rats. The linamarin concentration in cassava juice was determined by high-performance liquid chromatography, and the juice was administered intraesophageally for 28 days. The results suggested that the consumption of linamarin in cassava juice increased the number of crossings and rearings in the open field test and caused behavioral deficiency, reflected by lateral swimming, in the swim test on days 21 and 28 of treatment. These alterations are possibly related to neuronal damage caused by linamarin in cassava juice in structures of the central nervous system involved in motor processing.     

葛根素对异丙肾上腺素诱导小鼠心肌纤维化的保护作用

目的探讨葛根素对异丙肾上腺素诱导的小鼠心肌纤维化的保护作用及其可能机制。方法将昆明种小鼠分为溶媒对照组、心肌纤维化模型组、葛根素低、高剂量(0.6、1.2 g.kg-1)组、卡托普利(25 mg.kg-1)组。预先ig给药3 d后,同时皮下注射5 mg.kg-1异丙肾上腺素1 d后,以2.5 mg.kg-1.d-1连续注射30 d。停止注射异丙肾上腺素后,再继续ig给药7 d。称重小鼠,取心脏称重,计算心重指数(CWI);消化法测定心肌羟脯氨酸(Hydro)的含量;Masson染色观察心肌纤维化的程度并计算心肌胶原容积分数(CVF);测定小鼠心肌匀浆中超氧化物歧化酶(SOD)、丙二醛(MDA)的含量。结果葛根素给药组与模型组比较均能降低CWI和Hydro的含量;Masson染色结果显示:葛根素给药组心肌细胞间的胶原含量明显减少,CVF明显下降;与模型组比较,葛根素给药组心肌匀浆中SOD水平增高,MDA含量下降。结论葛根素对异丙肾上腺素诱导的小鼠心肌纤维化有一定的预防作用,该作用与抑制胶原的形成、抗脂质过氧化及清除氧自由基有关。     

Enzymatic studies of cisplatin induced oxidative stress in hepatic tissue of rats

Cisplatin is an active cytotoxic agent that has proved to be successful in the treatment of various types of solid tumors. The drug-induced nephrotoxicity has been very well documented in clinical oncology. However, hepatotoxicity has been rarely characterized and paid attention to, and is the least studied. We have used rat as the model to evaluate the effect of cisplatin on liver antioxidant enzymes and to determine whether these modulations in enzymatic activities are involved in hepatotoxicity. Reports obtained from our study indicate that cisplatin increases lipid peroxidation in the treated tissue of rat. The drug is also involved in altering the thiol status of the tissue with concomitant alterations in the enzymatic antioxidants. Glutathione and glutathione reductase levels were significantly decreased after cisplatin therapy, whereas glutathione peroxidase, gamma-glutamyl transpeptidase and catalase showed a significant increase. No statistically significant change was observed in glutathione-S-transferase activity. After cisplatin treatment, cytochrome P 450 showed a significant increase, whereas cytochrome b5 was decreased. Thus, an alteration in enzymatic antioxidant status with increase in lipid peroxidation indicates that the enzymes play an important role in combating free radical induced oxidative stress on the tissue.     

Evaluation of oxidative stress induction in rats following exposure to silver nanorods

The study investigated the oxidative stress induction by the 10 and 25?nm silver nanorods (SNRs) following intra-tracheal instillation in rats after 1?day, 1 week, 1 month and 3 months post instillation periods at 1 and 5?mg/kg b.w. doses. The blood was withdrawn by retro orbital plexus method after exposure periods and different oxidative stress markers were estimated. The results showed that the both sizes of SNRs induced increased levels of malondialdehyde (MDA) and depleted glutathione (GSH) levels after 1?day and 1 week post exposure periods. The 10 and 25?nm SNRs at both doses displayed that significantly reduced levels of superoxide dismutase (SOD) and catalase following 1?day and 1 week post exposure periods. Also, the results have shown that decrease in total antioxidant capacity (TAC) of both sizes of SNRs significantly following 1?day and 1 week post exposure periods, indicating the oxidative stress induction by SNRs. In spite, there were no significant changes in oxidative stress markers following 1 month and 3 months post exposure periods may be due to recovery. The increased levels of MDA and decreased levels of GSH, SOD, catalase and TAC activity are strongly associated to ROS production and lipid peroxidation, suggesting the induction of oxidative stress in rats. The 10?nm SNRs at 5?mg/kg b.w. dose exposures in rats have shown greater changes in all oxidative stress parameters, indicating the greater induction of oxidative stress when compared with the 25?nm SNRs, representing the size–dose-dependent induction of oxidative stress of SNRs.     

Influence of polyphenolic extracts from Enydra fluctuans on oxidative stress induced by acephate in rats

Acephate, an organophosphorus pesticide, has been proved to play an important role in tissue damage by inducing oxidative stress through the release of free radicals. The aim of this study was to evaluate the protective effect of the plant phenolic compounds present in Enydra fluctuans against acephate toxicity based on lipid peroxidation and antioxidant enzymes profile in rats. An oral dose of acephate at 30 mg/kg of body weight has been given against the extracts containing 20 mg of polyphenolic compounds (expressed as gallic acid equivalents)/kg body weight for 14 days. The results showed that under the influence of the pesticides, there was significant decrease in the activities of the antioxidant enzymes SOD, Catalase and Glutathione peroxidase (GPx) and an increase in the non-enzymatic Glutathione, with respect to the normal and the plant extract gavaged groups. Also that there was an increase in the plasma and erythrocyte membrane lipid peroxidation levels in the pesticide treated group compared to the normal or the group treated with the plant extract. The present study thus gives an insight into the ill-effects of this organophosphate and the protective role of plant polyphenols in minimizing those effects.     

阿托伐他汀对慢性心衰患者NT-proBNP水平及氧化应激状态的影响

目的 探讨阿托伐他汀对慢性心衰患者NT-proBNP水平及氧化应激状态的影响。方法 选择2015年9月—2017年2月非缺血性心脏病慢性心衰患者102例,将所有患者随机分为对照组（n=51）和阿托伐他汀组（n=51）。对照组实施常规抗心衰药物治疗,阿托伐他汀组在常规抗心衰治疗基础上加用阿托伐他汀治疗,20 mg/d。两组疗程均为24周。观察并比较两组治疗前后三酰甘油（TG）、总胆固醇（TC）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）、NYHA分级、左室射血分数（LVEF）、NT-proBNP、6 min步行距离（6MWT）、超氧化物歧化酶（SOD）、髓过氧化物酶（MPO）、丙二醛（MDA）等指标。结果 阿托伐他汀组治疗后TG、TC、LDL-C水平明显下降,与治疗前及对照组比较,差异均有统计学意义（P<0.05）。两组患者治疗后NT-proBNP水平均有明显下降,与治疗前比较,差异有统计学意义（P<0.05）,但阿托伐他汀组下降幅度优于对照组,组间比较差异有统计学意义（P<0.05）。与同组治疗前及对照组比较,阿托伐他汀组治疗后SOD明显增高,MDA、MPO明显下降,差异均有统计学意义（P<0.05）;而对照组治疗前后无明显变化。结论 在常规抗心衰治疗的基础上加用阿托伐他汀,能有效降低CHF患者的NT-proBNP水平和抑制患者的氧化应激状态。     

Chromium(VI) induces oxidative stress in the mouse brain

Potassium dichromate was given to female Swiss mice (25 mg/kg per day) orally in water for 1–3 days. Brain homogenates were prepared to evaluate the occurrence of oxidative stress in this organ through the measurement of the antioxidant defense levels, and the extent of lipid peroxidation. In addition, mitochondrial fractions were isolated from brain homogenates to determine the production of reactive oxygen species in this subcellular fraction. The administration of potassium dichromate for 3 days caused increases of 72 and 74% in superoxide dismutase and catalase activities, respectively, in the homogenates. The treatment with this metal for 3 days increased brain homogenate chemiluminescence and thiobarbituric acid-reactive substances by 34 and 29%, respectively. The brain contents of the non-enzymatic antioxidants -tocopherol and sulfhydryl groups decreased by 35 and 32%, respectively. Ascorbic acid levels were not modified by the administration of potassium dichromate. Finally, there was a significant increment in the mitochondrial production of oxidants in the brain of treated mice as compared with controls. These results suggest that chromium(VI) produces an increased formation of reactive oxygen species and brain lipid peroxidation. The increase in the antioxidant enzyme activities reflects an adaptive response against oxidative stress, while the reduction in the levels of non-enzymatic antioxidants might be due to their reaction with reactive oxygen species generated during the metabolism of chromium(VI).     

普罗布考对过氧化氢诱导心肌细胞凋亡的影响

目的探讨普罗布考对过氧化氢(H2O2)诱导的心肌细胞凋亡的影响,探讨其可能的机制。方法培养的新生鼠心肌细胞随机分组并给予0.2mmol.L-1H2O2或0.2mmol.L-1 H2O2及不同浓度的普罗布考(100μmol.L-1、10μmol.L-1和1μmol.L-1)。采用琼脂糖凝聚电泳检测细胞凋亡;逆转录聚合酶链式反应(RT-PCR)法检测细胞Bcl-2 mRNA及Bax mRNA表达;黄嘌呤氧化酶法测定细胞内超氧化物歧化酶(SOD)活性,硫代巴比妥酸法检测细胞内丙二醛(MDA)含量。结果普罗布考明显抑制H2O2诱导的心肌细胞凋亡,降低心肌细胞BaxmRNA表达,升高Bcl-2mRNA表达。经不同浓度普罗布考干预后,心肌细胞SOD活性显著升高,MDA含量显著降低。以上这些效应均呈剂量依赖性。结论普罗布考抑制H2O2诱导的心肌细胞凋亡,其作用机制与改善心肌细胞氧化应激水平有关。     

不同价态锰对不同月龄大鼠脂质过氧化的影响

目的　研究不同价态锰染毒后对大鼠脑、肝和心肌内脂质过氧化(MDA)和超氧化物歧化酶(SOD)活力的影响。方法　大鼠经腹腔分别注射氯化锰(MnCl2 ·4H2 O ,Mn2 )和醋酸锰(C6 H9O6 Mn·2H2 O ,Mn3 ) ,按6mg kg剂量连续染毒1个月后,测定脑、肝和心肌组织中MDA含量和SOD活力。结果　(1)经Mn2 染毒后大鼠脑组织MDA含量与对照组相比,差异有显著性(P <0 0 5 ) ,而Mn3 染毒后只有18月龄大鼠脑组织MDA含量显著高于对照组(P <0 0 5 ) ;在肝组织MDA含量,Mn2 组与对照组相比,差异有显著性(P <0 0 5 )。(2 )经Mn2 、Mn3 染毒后18月龄和4月龄大鼠脑组织SOD活力显著低于对照组(P <0 0 5 ) ;经Mn2 染毒后,18月龄和4月龄大鼠肝SOD活力明显低于对照组(P <0 0 5 ) ;经Mn3 染毒后,18月龄大鼠肝SOD活力显著低于对照组(P <0 0 5 )。(3 )心肌组织MDA含量,SOD活力与对照组相比,差异均无显著性。结论　不同价态、不同剂量锰染毒不同月龄大鼠对其不同组织MDA含量和SOD活力的影响是不同的。     

SOD脂质体在小鼠体内的分布及其对脂质过氧化物的影响

目的 优化超氧化物岐化酶(SOD)脂质体的制备工艺,并考察SOD脂质体和SOD溶液在小鼠体内组织的分布.方法 采用逆相蒸发法和正交试验优化工艺制备SOD脂质体;以邻苯三酚自氧化法和脂质过氧化物法确定药物在小鼠体内组织的分布.结果 SOD脂质体的各质量评价结果良好.与SOD溶液相比,前者可提高各组织中SOD的含量,并降低脂质过氧化物水平,以血、脑、肾等最为显著.注射SOD脂质体小鼠的各组织中SOD增量最高可达102.9%,脂质过氧化物含量最低降至25.0%.结论 所得SOD脂质体有较高的包封率和稳定性,在小鼠体内具有明显的缓释和降低脂质过氧化物含量的效果.     

Effect of Quercetin-loaded liposomes on induced oxidative stress in human spermatozoa

A strategy to circumvent the poor polyphenols bioavailability is to load these compounds into liposomes. We evaluated the in vitro effects of quercetin (Q) and Q-loaded liposomes (QLL, 30, 50, 100 μM) on motility, viability and chromatin integrity of swim-up selected human sperm. Antioxidant power was assayed against tert-butylhydroperoxide induced lipid peroxidation (LPO) using C11-BODIPY581/591 fluorescent probe and transmission electron microscopy. QLL showed decreased toxicity for sperm motility and viability and increased DNA damage compared to Q. The percentage of sperm with fluorescence, marker of LPO, was decreased in samples incubated with Q vs QLL (P < 0.001). The ultrastructure of acrosomes and membranes was preserved with Q 30/100 μM, whereas QLL did not prevent membrane injury.Q alone appeared more effective than Q incorporated into liposomes; however liposomes could be considered as carriers that may convey different compounds inside sperm; they may therefore represent a field of research rich of many applications.     

The role of vitamin C as antioxidant in protection of oxidative stress induced by imidacloprid

Pesticides may induce oxidative stress leading to generate free radicals and alternate antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the acute toxicity of imidacloprid toward male mice and the oxidative stress of the sublethal dose (1/10 LD₅₀) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and activities of the antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-s-transferase (GST). Also, the protective effect of vitamin C (200 mg/kg bw) 30 min before or after administration of imidacloprid were investigated. The results demonstrated that the median lethal dose (LD₅₀) of imidacloprid after 24 h was 149.76 mg/kg bw. The oral administration of 14.976 mg/kg imidacloprid significantly caused elevation in LPO level and the activities of antioxidant enzymes including CAT, SOD, GPx and GST. However, G6PD activity remained unchanged, while the level of GSH content was decreased. In addition, the results showed that vitamin C might ameliorate imidacloprid-induced oxidative damage by decreasing LPO and altering antioxidant defense system in liver. The protective effect of the pre-treatment with vitamin C against imidacloprid-induced oxidative stress in liver mice is better than the post-treatment.