运动对2,3,7,8-四氯二苯并二噁英持续暴露大鼠肝脏氧化应激的影响

为探索运动对2,3,7,8-四氯二苯并二噁英(2,3,7,8-TCDD)持续暴露大鼠肝脏氧化应激的影响,本研究将7周龄雄性SD大鼠适应性喂养1周后,随机分为对照(NC)、运动对照(EC)、染毒1(NT1)、运动染毒1(ET1)、染毒2(NT2)、运动染毒2(ET2)、染毒3(NT3)、运动染毒3(ET3)、染毒4(NT4)及运动染毒4(ET4)共10组。染毒组(NTs、ETs)腹腔注射TCDD(溶于玉米油),对照组及各染毒组首次剂量依次为0、0.4、1.6、6.4、25.6μg·kg~(-1)(以单位体重计),之后每周给予上述剂量的21%作为维持剂量,持续染毒8周;运动组尾部负重5%游泳,每周5 d,每次30 min。实验结束取材,测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、肝组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)、活性氧(ROS)含量。结果显示:1)染毒可升高各染毒组大鼠血清AST活性及NT4组大鼠血清ALT活性,增加NT2、NT3组肝脏MDA含量,而降低NT1、NT2组大鼠血清ALT活性;2)运动可升高大鼠血清AST及ALT活性,增加大鼠肝组织GSH-Px活性;3)运动可升高染毒大鼠血清AST活性(T1剂量),降低染毒大鼠血清ALT活性(T1剂量),降低染毒大鼠血清AST活性(T3剂量),升高染毒大鼠血清ALT活性(T3、T4剂量),增加染毒大鼠肝组织SOD活性(T2、T3剂量)、CAT活性(T1、T2、T3剂量)及GSH-Px活性(T2、T3、T4剂量),降低染毒大鼠肝组织MDA含量(T2、T3、T4剂量)及ROS含量(T1、T3剂量)。结果表明,2,3,7,8-TCDD持续暴露8周可引起大鼠肝细胞氧化应激损伤,并产生剂量依赖效应;而有氧运动可增加2,3,7,8-TCDD持续暴露(T2、T3剂量)大鼠肝组织抗氧化酶活性,有效降低氧化应激损伤而减轻肝毒性。     

Dichloroacetate- and trichloroacetate-induced modulation of superoxide dismutase,catalase, and glutathione peroxidase activities and glutathione level in the livers of mice after subacute and subchronic exposures

Dichloroacetate (DCA) and trichloroacetate (TCA) were previously found to induce various levels of oxidative stress in the hepatic tissues of mice after subacute and subchronic exposures. The cells are known to have several protective mechanisms against production of oxidative stress by different xenobiotics. To assess the roles of the antioxidant enzymes and glutathione (GSH) in DCA- and TCA-induced oxidative stress, groups of B6C3F1 mice were administered either DCA or TCA at doses of 7.7, 77, 154, and 410 mg kg^?1 day^?1, by gavage for 4 weeks (4-W) and 13 weeks (13-W), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as GSH were determined in the hepatic tissues. DCA at doses ranging between 7.7–410, and 7.7–77 mg kg^?1 day^?1, given for 4-W and 13-W, respectively, resulted in either suppression or no change in SOD, CAT, and GSH-Px activities, but doses of 154–410 mg DCA kg^?1 day^?1 administered for 13-W were found to result in a significant induction of the three enzyme activities. TCA administration on the other hand, resulted in increases in the SOD and CAT activities, but caused suppression of GSH-Px activity in both the periods. Except for the DCA doses of 77–154 mg kg^?1 day^?1 administered for 13-W that resulted in a significant reduction in the GSH levels, all other DCA as well as TCA treatments produced no changes in GSH. Since these enzymes are involved in the detoxification of the reactive oxygen species (ROS), superoxide anion (SA), and H₂O₂, it is concluded that SA is the main contributor to DCA-induced oxidative stress, while both ROS contribute to that of TCA. The increase in the enzyme activities associated with 154–410 mg DCA kg^1? day^?1 in the 13-W period suggest their role as protective mechanisms contributing to the survival of cells modified in response to those treatments.     

内质网应激在PFOS致大鼠肝损伤中的作用

通过全氟辛烷磺酸(PFOS)28 d大鼠经口染毒评价PFOS肝损伤效应,探讨内质网应激在PFOS毒效应中的作用。Wistar大鼠随机分组,分别以0 mg·kg~(-1)、5 mg·kg~(-1)和10 mg·kg~(-1)PFOS灌胃染毒28 d。HE染色观察大鼠肝脏形态改变。ELISA法测定各组丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)和淀粉酶(AMY)含量变化。紫外分光光度法测定肝组织匀浆中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性变化。RT-PCR检测肝脏内质网应激标志蛋白表达水平。结果表明,PFOS造成大鼠体重降低、肝重增高(P0.05),组织切片显示肝细胞出现脂质沉积。PFOS不同剂量组大鼠ALT随暴露浓度增加,分别为(50.96±10.02)U·L~(-1)、(71.73±11.55)U·L~(-1),显著高于对照组(P0.05),AST、ALP含量与对照组相比显著上升(P0.05),高剂量组AMY水平为(833.46±63.05)U·L~(-1),与对照组相比显著降低(P0.05)。GSH-Px和SOD水平随PFOS浓度增加出现了显著降低(P0.05),而MDA水平显著升高(P0.05)。内质网应激标志蛋白表达均较对照组显著上升(P0.05)。以上结果说明PFOS可导致大鼠肝细胞损伤,其机制可能与内质网应激调控有关。     

十溴二苯乙烷对草鱼幼鱼肝脏和肌肉组织氧化应激效应的影响

十溴二苯乙烷(DBDPE)是目前在全球范围内广泛使用的新型溴代阻燃剂,其环境风险已引起广泛关注,但目前仍缺乏针对水生生物的毒性研究数据。作者通过饲料中添加十溴二苯乙烷暴露的方式对草鱼幼鱼进行长期暴露实验,研究500、1 000和3 000 mg·kg~(-1)三个饲料添加剂量暴露组和1个对照组长期暴露对草鱼幼鱼肝脏和肌肉组织中氧化应激酶(SOD、CAT和GSH-PX)活性和抗氧化物质(GSH)含量的影响。结果显示:暴露8周后,随着DBDPE暴露水平的升高,草鱼幼鱼肝脏组织中氧化应激酶(SOD、CAT和GSH-PX)和抗氧化物质(GSH)均表现出低浓度诱导及高浓度抑制的效应。500和1 000 mg·kg~(-1)剂量组草鱼幼鱼肝脏组织中SOD、CAT和GSH-PX活性和GSH含量均显著高于对照组(P0.05),且均在500 mg·kg~(-1)剂量组达到最高。3 000 mg·kg~(-1)剂量组SOD、CAT和GSH-PX活性和GSH含量低于500和1 000 mg·kg~(-1)暴露组,但与对照组无显著性差异(P0.05)。草鱼幼鱼肌肉组织中氧化应激酶活性变化甚微,3个浓度剂量组肌肉组织中SOD、CAT活性和GSH含量以及500 mg·kg~(-1)剂量组GSH-PX活性与对照组均无显著性差异(P0.05)。研究成果表明DBDPE暴露影响草鱼幼鱼肝脏组织的抗氧化防御系统,可以诱导草鱼幼鱼产生氧化应激效应。     

水胺硫磷亚急性暴露对小鼠肝脏氧化应激的影响

为探讨水胺硫磷对小鼠肝脏损伤作用机制,设置0.11、1.08、2.16 mg·kg-13个低、中、高不同剂量组,以灌胃方式对昆明种小鼠进行染毒7 d后,测定小鼠肝脏组织超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)2种抗氧化酶的活性,以及抗氧化物质谷胱甘肽(GSH)和膜脂质过氧化物丙二醛(MDA)含量,同时观察肝脏的组织学变化。结果表明,除低剂量组外,中、高剂量组小鼠肝脏SOD和GSH-Px活性与对照组相比均受到显著抑制(P0.05),GSH的含量与对照组相比显著下降(P0.05),MDA含量与对照组相比却呈显著上升趋势(P0.01),同时各指标的变化均呈一定的剂量-效应关系。组织学观察显示中、高剂量组肝细胞出现明显水肿和坏死,肝窦狭窄甚至闭塞。结果表明氧化损伤可能是水胺硫磷致小鼠肝脏毒性损伤的作用机制之一。     

Effects of subchronic exposure to carbofuran on antioxidant defence system and malondialdehyde levels in common carp (Cyprinus carpio L.)

The present study focused on the assessment of oxidative stress induction by pesticides such as carbamates which are widely used as insecticides and nematicides and contaminate aquatic ecosystems on certain biomarkers in liver of common carp (Cyprinus carpio L.). Biomarkers selected for stress monitoring were malondialdehyde (MDA), an index of lipid peroxidation, and antioxidant defence system enzymes, mainly catalase (CAT), glutathione reductase (GR), and glutathione-S-transferase (GST) activities in liver of fish exposed to 0, 10, 50, or 100?µg?L^?1 of carbofuran for 4, 15, or 30 days. Oxidative stress was found in liver of common carp exposed to carbofuran which was manifested by a decrease in CAT and GR activities after 4 and 30 days of exposure. An adaptive response was probably produced since at day 15 no modifications in the CAT activity and increased GR activity were observed. In addition, a decrease in MDA content with the highest concentration of carbofuran used was found after 30 days of exposure. However, no significant changes were found in GST activity showing a varied response. The results concerning oxidative and antioxidant profiles indicate that subchronic exposure to the insecticide carbofuran is capable of inducing oxidative stress in fish.     

镧、铈、钕对小鼠肝细胞核的氧化损伤作用

轻稀土元素进入生物体后主要累积于肝脏,进入肝细胞,分布于细胞核上.为探讨轻稀土元素对小鼠肝细胞核的氧化损伤作用,选用5周龄雄性封闭群(ICR)小鼠灌喂10、20和40 mg·kg-1的稀土元素镧(La)、铈(Ce)和钕(Nd),6周后测定小鼠肝细胞核中超氧化物岐化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(...     

Subacute chlorpyrifos-induced alterations in serum lipids and some oxidative stress biomarkers in male Wistar rats: beneficial effect of acetyl-L-carnitine

The present study evaluated the beneficial effect of acetyl-L-carnitine (ALC) on subacute chlorpyrifos (CPF)-induced alterations in serum lipid profiles and some biomarkers of oxidative stress in Wistar rats. Twenty-eight adult male rats divided into four groups of seven animals each (group I–IV) were used: I (S/oil) received soya oil (2 ml kg^?1), II (ALC) received ALC (300 mg kg^?1); III (CPF) received CPF (8.5 mg kg^?1 ～ 1/10th LD₅₀); IV (ALC+CPF) was pretreated with ALC (300 mg kg^?1) and then exposed to CPF (8.5 mg kg^?1), 30 min later. The treatment was orally for 28 days duration. Sera obtained from blood samples were evaluated for the levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and catalase (CAT). The levels of low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), and atherogenic index (AI) were calculated. The result showed that elevated levels of TG, TC, LDL-c, VLDL-c, AI, and MDA, and the decreased levels of HDL-c, CAT, and SOD induced by CPF were modulated by ALC. It was concluded that ALC ameliorated the alterations in serum lipid and oxidative stress induced by CPF exposure in the rats, partly through its antioxidant properties.     

碲化镉量子点对小鼠睾丸组织的氧化损伤（Effects of CdTe Quantum Dots on the Antioxidant Enzymes Activity and Lipid Peroxidation in Testes of Mice）

为探讨碲化镉量子点(CdTeQDs)对小鼠睾丸的急性氧化损伤作用,将20只雄性ICR小鼠随机分成4组:对照组、1d、3d、7d(3个不同时间组),采用尾静脉注射进行一次性染毒2.5μmol·kg-1CdTeQDs,对照组注射等体积生理盐水.染毒后对睾丸的脏器系数以及组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性,丙二醛(MDA)含量分别进行测定,从而检测CdTeQDs对睾丸组织的急性氧化损伤作用.结果显示,与对照组相比,随染毒时间的延长,睾丸脏器系数无显著性变化(p>0.05);GSH-Px和SOD活性随染毒时间的延长呈逐渐升高趋势;而CAT活性呈逐渐降低趋势,且与对照组差异显著(p<0.01);MDA含量显著高于对照(p<0.01),且随时间变化不大.CdTeQDs染毒可导致小鼠睾丸组织氧化损伤,其损伤程度与染毒时间之间具有一定的时间-效应关系.     

Effects of Matricaria chamomilla L. on lipid peroxidation,antioxidant enzyme systems,and key liver enzymes in CCl4-treated rats

In this study, we investigated the effects of Matricaria chamomilla L. extract (MCE) on lipid peroxidation, antioxidant enzyme systems, and several liver enzymes in carbon tetrachloride (CCl₄)-treated rats. Rats were divided into five groups. The first group (control group) was fed on standard feed. The rats in the other groups (CCl₄, MCE50, MCE100, and MCE200) were injected intraperitoneally with 0.8?mL?kg^?1 CCl₄. Moreover, rats in the MCE50, MCE100, and MCE200 groups were gavaged with 50?mg?kg^?1, 100?mg?kg^?1, and 200?mg?kg^?1 MCE, respectively. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, whole blood malondialdehyde (MDA) and glutathione (GSH) levels, and erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity levels were measured after 14 days of exposure. ALT and AST in the CCl₄ group increased significantly in comparison to the control group (p?4, MCE50, MCE100, and MCE200 groups at different significance levels. In conclusion, the findings suggest that, depending on the dose administered, MCE decreases CCl₄-induced damage and consequent oxidative stress in rats; it affects the antioxidant system positively.     

Combined effects of 2,3,7,8-tetrachlorodibenzo- p -dioxin and polychlorinated biphenyl congeners in rats

The objective of this work was to evaluate potential interactions between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls congeners (PCBs) in rats. Groups of five adult female rats were given 0, 2.5, 25, 250, or 1000?ng TCDD/kg body weight/day or TCDD in combination with a mixture of PCB congeners at a concentration of 2 or 20?µg?kg^?1 body weight/day by gavage for 28 days. After the 28-day treatment period, the rats were killed for the analysis of biochemical, liver enzyme activities, and hematological and pathological end points. Growth suppression, increased absolute and relative liver weights, and decreased thymic weight were observed in the 1000?ng TCDD group alone, or the groups receiving a mixture of 1000?ng TCDD and 2 and 20?µg PCBs. TCDD-increased liver and thymic weights were not altered by PCBs; however, growth suppression was more pronounced in animals receiving 1000?ng TCDD and 2?µg PCBs. Increased hepatic microsomal methoxy resorufin-O-demethylase and ethoxy resorufin-O-deethylase activities occurred in 250 and 1000?ng?kg^?1 TCDD-treated animals, which were antagonized by PCBs. Effects of 250?ng TCDD on serum cholesterol and liver uridine diphosphate glucuronosyl transferase activity were reduced by 20?µg PCBs. Treatment with 1000?ng TCDD increased serum albumin, decreased liver vitamin A, increased kidney vitamin A, and liver microsomal glutathione-S-transferase activity, which were not affected by PCBs. Decreased hemoglobin, platelet, packet cell volume, and red cell indices were observed in TCDD-treated rats, but no interactive effects were seen. Histopathological evaluation revealed that liver, thyroid, and thymus were the target organs, but the effects of co-exposure to PCBs and TCDD were variable. These results indicate that the mixture effects of PCBs and TCDD may be additive, synergistic, or antagonistic depending on the dose level and end points measured.     

富勒烯对人胚肝细胞的氧化损伤

为初步探讨富勒烯(C60)对人体细胞的潜在危害,以人胚肝细胞(L-02)为研究对象,研究富勒烯暴露对人胚肝细胞的氧化损伤.人胚肝细胞暴露于0、1.25、2.50、5.00、10.00、20.00和40.00 μg·mL-1富勒烯悬液24h后,检测细胞内CAT活性和MDA与ROS含量.采用免疫组化法检测SOD蛋白在富勒烯...     

Effects of environmental hypercapnia on hemato-immunological parameters,carbonic anhydrase,and Na+, K+-ATPase enzyme activities in rainbow trout (Oncorhynchus mykiss) tissues

In this study, the effects of environmental hypercapnia on hemato-immunological parameters and the activities of respiratory enzymes such as carbonic anhydrase (CA) and Na⁺, K⁺-ATPase were investigated in rainbow trout (Oncorhynchus mykiss) tissues (gill, liver and kidney). Batches of 12 fish were exposed to 4.5 mg L^?1 (control) and 14 mg L^?1 CO₂. No mortalities occurred during the 14 days of the experimental period. Red blood cell (RBC), hemoglobin (Hb), and hematocrit (Ht) levels, and innate immune parameters such as nitro blue tetrazolium (NBT), lysozyme, and myeloperoxidase activities, and the melano-macrophage frequency were negatively affected by elevated CO₂ levels. Patterns of change in CA activity differed among the gill, liver, and kidney. Compared with the activities of CA in the control group, the CA enzyme was significantly stimulated at day 7 in the gill tissue, whereas it was stimulated at day 14 of the experiment in the liver tissue of fish exposed to 14 mg L^?1 CO₂ (P < 0.05). In contrast to the pattern of CA enzyme activities, the Na⁺, K⁺-ATPase enzymes were stimulated significantly in the liver after day 7 but inhibited in the kidney and gill (P < 0.05). These results suggest that a subchronic exposure to hypercapnia of rainbow trout tissues may lead to adaptive changes in the respiratory enzymes and negatively affects hemato-immunological parameters.     

长期饲喂钬对鲤鱼非特异性免疫酶活性的影响

以鲤鱼为研究对象,进行为期60 d的饲喂试验,研究了硝酸钬对其非特异性免疫的影响。结果表明:与对照组相比,在实验剂量范围内,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)在肝脏中呈先升高后降低的趋势,SOD、GSH-Px酶活性在20 mg·kg~(-1)时,升高显著(P0.05),三者在65 mg·kg~(-1)时都被显著抑制(P0.05);在肾中都被诱导,在65 mg·kg~(-1)升高显著(P0.05)。肝肾中丙二醛(MDA)含量都变化不显著(P0.05)。抗超氧阴离子自由基、抑制羟自由基能力和单胺氧化酶(MAO)活性都降低,且在65 mg·kg~(-1)时降低显著(P0.05或P0.01)。因此,在饲料中添加稀土元素钬20、42、65 mg·kg~(-1),能够影响非特异性免疫力,且鲤鱼肝组织比肾脏反应更敏感。     

Biomarkers of oxidative stress as indicators of water pollution in Nile tilapia (Oreochromis niloticus) from a water reservoir in Riyadh,Saudi Arabia

Antioxidant enzyme activities of fish (Oreochromis niloticus) were determined in order to assess the status of pollution in the Wadi Namar (WN), near Riyadh, Saudi Arabia. Activities of four antioxidant enzymes as superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and concentrations of glutathione (GSH) and oxidant malondialdehyde (MDA) were selected as bioindicators. Fish (n = 14) were sampled in the month of April 2013 from WN and a control site (CS). SOD activity was increased by 37.9%, 47%, and 29% in kidney, liver, and heart, respectively, while a significant decrease (36.4%) was observed in gills of O. niloticus from WN as compared to fish from CS. CAT activity was reduced by 51%, 55%, 47%, and 35% in kidney, liver, heart, and gills of O. niloticus from WN. The GST activities in kidney, liver, and heart of O. niloticus from WN were elevated by 34%, 48%, and 32%, respectively. However, significant fall (49%) in gills of fish was noted from WN compared to fish from CS. GSH levels were increased by 44%, 36%, and 38% in kidney, liver, and heart, respectively, but decreased by 30% in gills. MDA levels of O. niloticus were significantly increased in kidney, liver, and heart in fish from WN. Data indicated that WN is polluted mainly by industrial and urban discharge of liquid waste products.     

纳米硫硒化镉对小鼠肾脏和脑组织SOD活力和MDA含量的影响

为了探讨纳米硫硒化镉(CdSeS)对小鼠肾脏和脑组织的急性氧化损伤作用,将20只雄性昆明小鼠随机分成4组,采用尾部静脉注射进行一次性染毒,3个染毒组分别注入0.1、0.2、0.4mg·mL-1的纳米CdSeS粉末(20～30nm)悬液1mL,对照组注入等体积生理盐水.染毒3d后对肾脏和脑组织匀浆中超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量分别进行测定,从而检测纳米CdSeS对肾脏和脑组织的急性氧化损伤作用.结果显示,随着纳米CdSeS染毒浓度的升高,小鼠肾脏和脑组织中SOD活力呈逐渐降低趋势,而MDA含量呈逐渐升高趋势,均显示出一定的剂量-效应关系;较高浓度组(肾:ρCdSeS≥0.2mg·mL-1;脑:ρCdSeS≥0.4mg·mL-1)SOD活力、MDA含量与对照具有显著性差异(p<0.05,p<0.01),而较低浓度组则没有显著性差异(p>0.05).以上结果提示纳米CdSeS能够对小鼠肾脏和脑组织造成氧化损伤,并且能穿过血脑屏障作用于脑部。     

口服纳米银对大鼠的生物有效性及其体内分布的研究

由于独特的抗菌特性，纳米银(AgNP)在诸多领域得到广泛应用，但是其生物有效性、动物组织分布及排出尚不清楚。将聚乙烯吡咯烷酮包被的AgNP溶液按照10 mg kg^-1给雌性SD大鼠灌胃，采用ICP-MS检测SD大鼠组织、粪便及尿液中总银浓度。实验结果表明，AgNP通过小肠吸收后，可以通过血液循环快速分布在肝、肾、脾、肺、脑等靶器官。灌胃后1 h，大鼠各组织中总银浓度达到最大值(肝、肾、脾、肺、脑中银浓度分别为0.29 ± 0.13 mg kg^-1、0.23 ± 0.04 mg kg^-1、0.17 ± 0.05 mg kg^-1、0.11 ± 0.01 mg kg^-1、0.06 ±0.02 mg kg^-1)，之后银浓度随时间降低直至和对照组无显著性差异。在灌胃途径下，AgNP对SD大鼠的有效性为8.5%，且73%的AgNP是通过粪便的途径排出体外。     

十溴联苯醚(BDE-209)对紫红笛鲷鳃抗氧化酶活性的影响

十溴联苯醚(BDE-209)是目前唯一仍在全球范围内广泛使用的多溴联苯醚阻燃剂,其环境行为及生物效应逐渐成为环境污染领域研究的热点。选用2(LD组)、10(MLD组)、50(MHD组)及250μg.L-1(HD组)4个浓度的BDE-209作用于紫红笛鲷,探讨BDE-209对紫红笛鲷鳃抗氧化酶(SOD、CAT及POD)活性和MDA含量的影响。结果显示:BDE-209可以显著促进SOD和CAT活性,且随着暴露时间延长CAT活性呈现逐渐增加的趋势。暴露7d后,MLD组SOD活性达到最高68.31U.mg-1,是对照组(CK)的5.50倍,HD组CAT活性达到6.31U.mL-1,其次为MHD组的5.96U.mL-1。BDE-209对鳃POD活性呈现先促进后抑制的作用,暴露3d时各浓度POD活性均显著高于CK组(P<0.05);7d时各浓度POD活性则受到显著抑制(P<0.05),清水恢复15d后各浓度组与CK组没有显著差异(P>0.05)。暴露期间各浓度组MDA含量均显著高于CK组(P<,并且随暴露时间延长呈现先增加后减少的趋势,7d后HD组MDA含量达到最高,为6.99nmol.mg-1,清水恢复15d后,LD和MLD组MDA含量与CK组没有显著性差异(P>0.05)。以上结果表明:BDE-209可以诱导紫红笛鲷产生氧化应激效应,CAT和SOD则在氧自由基清除中发挥作用。     

The role of thymoquinone as antioxidant protection on oxidative stress induced by imidacloprid in male and female Swiss albino mice

The aim of the present study was to evaluate the possible protective effects of thymoquinone (TQ), an antioxidant agent, against imidacloprid (IMI)-induced oxidative stress in male and female mice. In total, 48 Swiss Albino male and female mice were fed a standard rodent diet and divided into 3 equal groups: the animals in the control group (vehicle treated) were given corn oil, the second group were orally administered 15 mg/kg/day IMI alone, and the third group were orally administered 15 mg/kg/day IMI and with TQ at 10 mg/kg/day for 21 days. During the experimental period, there were no significant changes between initial body weights and final body weights of IMI treated male and female mice. IMI produced significant increase in blood, liver, kidney, and heart malondialdehyde (MDA) levels and decrease in blood and liver glutathione (GSH) levels. In addition, IMI treatment decreased erythrocyte, liver, and kidney superoxide dismutase (SOD) activity in male mice and decreased erythrocyte and liver SOD activity in female mice. Erythrocyte catalase (CAT) activities were found to be low in male and female mice. However, treatment with TQ reversed IMI-induced oxidative stress, lipid peroxidation, and activities of antioxidant enzymes. Moreover, TQ exhibited protective action against the IMI-induced histopathological changes in tissues of male and female mice. In conclusion, TQ was found to be effective in protecting mice against IMI-induced oxidative stress by enhancing antioxidant defense mechanisms.