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1.
研究增塑剂邻苯二甲酸二异癸酯(didecyl phthalate, DIDP)致雄性小鼠肝损伤作用及其机理。以雄性BALB/c小鼠为受试动物,随机分为7组,包括溶剂对照组(生理盐水)、4个DIDP染毒组(0.15、1.5、15和150 mg·kg~(-1))、维生素E(vitamin E, VitE)(100 mg·kg~(-1))处理组和DIDP+维生素E处理组(150 mg·kg~(-1)DIDP+100 mg·kg~(-1)VitE),连续灌胃14 d。以肝组织匀浆测定活性氧(reactive oxygen species, ROS)、还原型谷胱甘肽(glutathione, GSH)、丙二醛(malondialdehyde, MDA)和细胞凋亡因子半胱氨酸天冬氨酸蛋白酶3(cysteine aspartic proteinase 3, Caspase-3)水平。采用动物自动生化分析仪检测肝功能指标血清中丙氨酸氨基转移酶(alanine aminotransferase, ALT)、天门冬氨酸氨基转移酶(aspartate aminotransferase, AST)、白蛋白(albumin, ALB)水平,并同时观察肝组织的病理变化与荧光染色结果。随着DIDP染毒剂量的增加,小鼠肝组织ROS、MDA和Caspase-3含量逐渐上升,血清ALT和AST水平也逐渐上升,GSH含量逐渐降低,血清ALB水平也逐渐降低,差异具有统计学意义(P 0.05,P 0.01); VitE处理组ROS、MDA和Caspase-3含量相应降低,血清ALT和AST水平也相应降低,GSH含量逐渐上升,血清ALB水平也相应上升。小鼠肝组织形态观察结果表明,随着DIDP染毒剂量的增加,小鼠肝组织的病理损伤程度呈上升趋势。研究表明,较高剂量(≥15 mg·kg~(-1))的DIDP能造成小鼠的肝脏损伤与细胞凋亡,抗氧化剂VitE可使肝脏损伤与细胞凋亡减轻,对小鼠肝组织起保护作用,说明氧化应激介导了DIDP对机体的损伤。  相似文献   

2.
为探讨ROS介导的氧化应激在异烟肼(INH)诱导L-02细胞毒性中的作用及槲皮素的干预作用,建立体外培养INH诱导L-02细胞氧化损伤模型,实验分为对照组(A)、INH组(B)、槲皮素低剂量组(C)及槲皮素高剂量组(D)。采用生化分析法检测L-02细胞培养液中天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)的活性;利用荧光探针检测L-02细胞线粒体内活性氧(ROS)水平;应用比色法检测L-02细胞内丙二醛(MDA)、谷胱甘肽(GSH)的含量以及主要抗氧化物酶的活性。结果表明,与对照组相比,INH能显著增加L-02细胞培养液中AST和ALT的活性、细胞线粒体内ROS水平及细胞内MDA的含量(P0.01),并显著减少L-02细胞内GSH的含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性(P0.01)。与INH组比较,槲皮素低剂量组L-02细胞培养液中AST的活性、线粒体内ROS水平及细胞内MDA的含量明显降低(P0.05),而细胞内SOD的活性明显增加(P0.05);高剂量槲皮素能显著降低L-02细胞培养液中AST和ALT的活性、细胞线粒体内ROS水平及细胞内MDA的含量(P0.01),并能显著增高L-02细胞内GSH的含量和主要抗氧化物酶的活性(P0.01)。与槲皮素低剂量组相比,槲皮素高剂量组的保护效应更明显(P0.05)。可见,ROS介导的氧化应激在INH诱导的L-02细胞毒性中发挥了重要作用,且槲皮素对INH诱导的L-02细胞氧化损伤具有保护作用。  相似文献   

3.
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。  相似文献   

4.
观察8周中等强度游泳运动对2,3,7,8-四氯二苯并二恶英(2,3,7,8-tetrachlorodibenzo-p-dioxin,2,3,7,8-TCDD)急性暴露大鼠肝脏氧化应激的影响。以8周龄雄性Sprague Dawley大鼠为研究对象,将大鼠随机分为玉米油静养组(NC组)、玉米油运动组(EC组)、TCDD静养组(NT)和TCDD运动组(ET组)。将TCDD溶于玉米油中,NT和ET组大鼠按照10μg·kg-1(以单位体重计)腹腔注射TCDD,NC和EC组大鼠注射等量玉米油。正式实验开始后,EC和ET组大鼠进行运动(尾部负重5%游泳30min),每周运动5 d,共8周,NC和NT组大鼠不进行任何运动干预。8周后,称重并宰杀大鼠,收集血清和肝组织样本,待测血清天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)的活性;肝组织丙二醛(MDA)含量,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)以及谷胱甘肽过氧化物酶(GSH-Px)的活性。将数据进行多因素方差分析,结果表明,染毒可升高大鼠血清AST的活性,增加肝脏MDA的含量,降低肝脏SOD、CAT和GSH-Px的活性;运动可降低大鼠肝脏GSH-Px的活性;染毒后运动可减少肝脏MDA的含量,升高肝脏SOD、CAT和GSH-Px的活性。研究表明,TCDD急性暴露可导致大鼠肝细胞功能受损,导致大鼠肝脏发生氧化应激。8周有氧运动改善TCDD急性暴露诱导的肝细胞损伤,改善肝脏氧化应激,这可能是运动改善TCDD肝毒性的机制之一。  相似文献   

5.
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。  相似文献   

6.
PFOS是典型的持久性有机污染物,迁移能力强,具有较高的生物可利用性和蓄积能力,且具有广泛的生物毒性。为探究PFOS对淡水底栖生物的毒性作用机制,以三角帆蚌为研究对象,进行了不同剂量(0.1、1.0、5.0 mg·L-1)的PFOS胁迫和净水恢复实验,期间对受试生物肝胰腺中的谷胱甘肽(GSH)含量、谷胱甘肽-S转移酶(GST)活性、超氧化物歧化酶(SOD)活性,以及谷丙转氨酶(ALT)和谷草转氨酶(AST)的活性进行了连续测定。结果发现,低浓度胁迫(0.1 mg·L-1)对各项指标均有不同程度的诱导作用,且持续时间较长;而在中高浓度PFOS胁迫下,则呈现出明显的诱导向抑制过渡的时间效应。GSH含量和GST活性具有较高的相关性(P0.05)。恢复实验中,所测指标普遍未恢复到对照组水平,说明P FOS胁迫损伤的恢复需要更长的时间。研究表明,PFOS对三角帆蚌肝胰腺的氧化胁迫显著,并能快速地激活肝胰腺细胞的解毒代谢;但长期的PFOS胁迫则会造成肝胰腺细胞的实质性损伤。  相似文献   

7.
沉水植物对阿特拉津胁迫的毒理响应   总被引:1,自引:0,他引:1  
为揭示在阿特拉津胁迫下沉水植物生长及其与谷胱甘肽代谢途径的关系,通过培养实验研究了沉水植物菹草(Potamogeton crispus)和穗花狐尾藻(Myriophyllum spicatum)对0、0.5、1.0和2.0 mg·kg~(-1)阿特拉津的吸收特性,并对不同培养时期沉水植物的鲜重、总谷胱甘肽含量(T-GSH,即还原型谷胱甘肽GSH和氧化型谷胱甘肽GSSG之和)、GSH/GSSG比值及其形态变化、谷胱甘肽还原酶(GR)活性和谷胱甘肽-S-转移酶(GST)活性进行了测定。结果表明:沉积物阿特拉津初始浓度越高,植物体内阿特拉津浓度也越高。在培养60 d内,添加的阿特拉津对2种沉水植物的生长均产生显著抑制作用(P0.05)。在阿特拉津胁迫60 d后,各处理植物体内GSH/GSSG比值有所回升,其GR和GST活性均高于空白对照组。处理组植物体内GR和GST活性在30 d时达到最高值。与此同时,GSH脱去谷氨酸后能与阿特拉津形成共轭物。以上结果提示,≤2 mg·kg~(-1)阿特拉津在培养前60 d内会对植物生长产生抑制,但在90 d时植物会从伤害中恢复过来。沉水植物体内的谷胱甘肽在GR和GST作用下,对阿特拉津及其产生的活性氧具有一定去除作用,并通过控制酶活使植物体保持一定的GSH含量;另一方面,GSH可以与阿特拉津结合形成新的共轭物,以此缓解阿特拉津对沉水植物的毒害。  相似文献   

8.
三氯生(triclosan,TCS)在环境中被广泛检出,已成为重要的环境污染物,且TCS暴露能够影响机体的肠道菌群组成和脂类物质代谢过程.为了探讨TCS暴露对高脂饮食(high fat diet,HFD)诱导的肝脏功能损伤的影响及其机制,C57BL/6J小鼠随机分为正常饮食对照组、TCS组、HFD组和HFD+TCS组;首先对TCS组和HFD+TCS组小鼠进行提前一周TCS(10μg·g-1饲料)暴露,然后再同时进行6周的TCS暴露和HFD喂养.实验结束后,利用细菌特征序列对肠道菌群进行绝对定量分析,利用苏木精-伊红染色、实时荧光定量PCR、酶联免疫吸附测定、蛋白免疫印迹和流式细胞术等试验技术检测小鼠肠道和肝脏等生理变化状况.与对照组相比,TCS暴露和高脂饮食均能明显引起肠道菌群中厚壁菌门和拟杆菌门含量降低,同时引起小鼠脾脏中CD8+和CD4+T细胞比例失调,但未导致显著的肠道屏障损伤和脂多糖(lipopolysaccharide,LPS)异位;高脂饮食能够显著提高小鼠血清中丙氨酸氨基转移酶(alanine aminotransferase,ALT)、天门冬氨酸氨基转移酶(aspartate aminotransferase,AST)和甘油三酯(triglyceride,TG)的水平,而单独TCS暴露并没有引起明显的肝脏功能紊乱.与HFD组相比,HFD和TCS协同作用激活了小鼠肝脏中Toll样受体4(toll-like receptor 4,TLR4)炎症通路,造成小鼠肝脏炎症反应,并显著提高了小鼠ALT和AST水平,加剧了高脂饮食对小鼠肝脏功能的损伤.由此可知,TCS暴露通过引起小鼠肠道菌群紊乱和机体免疫响应,加剧高脂饮食诱导的小鼠肠道损伤和肝脏功能紊乱.  相似文献   

9.
低剂量中长期暴露下的氧化胁迫是砷对水生生物致毒的重要机制之一。本文通过对罗非鱼进行32 d的食物相砷暴露,测定不同时间点罗非鱼肝脏中谷胱甘肽(glutathione,GSH)含量和谷胱甘肽巯基转移酶(glutathione S-transferase,GST)活性,揭示不同价态无机砷对罗非鱼肝脏中GSH/GST的影响机制。经三价砷(As(III))暴露后,砷含量在2 d内显著增加而在随后的30 d内无显著性差异; 0~2 d内GSH含量显著增加,后降低,13 d后GSH含量均低于空白组; 0~6 d GST活性均大于空白组,6~8 d GST活性降低,8 d后活性高于空白组,且32 d达到最大值。经五价砷(As(V))暴露后,罗非鱼肝脏中砷含量逐渐增加,在20 d时达到最大值而后无显著性差异; 0~2 d时GSH含量降低,随后逐渐增加,在16 d达到最大值,16 d后GSH含量均低于空白组; 0~8 d时GST被大量诱导合成,8~20 d时GST合成被抑制,20 d后活性增加,在32 d达到最大值。As(III)和As(V)对罗非鱼GSH/GST的不同影响与其在罗非鱼体内的积累量有关。As(III)暴露后各时间点罗非鱼肝脏中的砷含量与GSH含量呈统计学正相关,而As(V)暴露无明显相关性。这是因为As(V)进入罗非鱼肝脏后会还原为As(III),进而GSH作为可提供巯基的还原剂而被大量消耗。另外,As(III)暴露后各时间点罗非鱼肝脏中的砷含量与GST活性呈显著负相关,而As(V)暴露却呈现出很强的滞后性,这是由于进入生物体内的As(V)需转化为As(III)后,才可直接作用于酶系统。可见,不同形态砷对水生生物的致毒机制需进一步深入研究。  相似文献   

10.
SO2吸入对小鼠组织谷胱甘肽氧化还原系统的影响   总被引:1,自引:2,他引:1  
从SO2吸入对雄性小鼠组织谷胱甘肽氧化还原系统中的抗氧化酶谷胱甘肽硫转移酶(GST)和葡萄糖6-磷酸脱氢酶(G6PD)以及还原型谷胱甘肽(GSH)和脂质过氧化物(TBARS)的影响探讨SO2的毒性作用机理.将昆明种纯系雄性小鼠60只随机分成3大组,每组20只,每一大组再随机分成SO2吸入组和对照组(SO2吸入组10只,对照组10只).吸入组吸入SO2浓度分别为(22±2)mg/m3,(64±3)mg/m3和(148±23)mg/m3.分别检测其脑、肺、心、肝、肾组织中GST、G6PD的活性以及GSH、TBARS的含量变化.当SO2浓度为(148±23)mg/m3时,脑、肺、心、肝、肾组织中GST和G6PD活性以及GSH含量均比对照组达到极显著(P<0.01)或显著降低(P<0.05),而脑和肺、心、肝、肾组织中TBARS水平则是显著(P<0.05)或极显著升高(P<0.01),且各指标与SO2浓度间有显著的剂量依赖关系.SO2吸入可使谷胱甘肽氧化还原系统中的关键性酶GST和G6PD活性发生显著降低,可使抗氧化物质GSH含量显著下降,而脂质过氧化物TBARS则显著升高,最终使谷胱甘肽氧化还原系统发生大的变化,导致氧化损伤.图2表2参16  相似文献   

11.
The present study was carried out to observe the possible beneficial effects of Vitamin E, a natural antioxidant on methomyl-induced biochemical and histological alterations in rat liver. To carry out the investigations, animals were segregated in four different groups. Animals in Group I served as normal controls. Animals in Group II were given single methomyl dose orally in water (9 mg kg?1 b.wt). Animals in Group III were injected intraperitoneally with Vitamin E (50 mg kg?1 b.wt) for 1 week on alternate days. Animals in Group IV were administered Vitamin E 1 week before subjecting them to methomyl treatment. Animals in all the groups were sacrificed 24 h after the end of treatments. Different biochemical estimations were carried out, which included estimation of aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), alkaline phosphatase (ALP) and acetylcholinesterase (AChE). Further, to examine the oxidative damage lipid peroxidation (LPO) and glutathione (GSH) levels as well as antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GSHPx), and glutathione-6-phosphate dehydrogenase were estimated in liver samples. AchE activity was inhibited significantly both in serum and liver following methomyl treatment. Administration of methomyl caused a significant increase in serum AST, ALT and ALP which indicated hepatic damage. LPO was found to be significantly increased, whereas GSH levels were decreased in the liver of methomyl-treated animals. The activities of SOD and catalase were significantly decreased whereas GST and GSHPx activities were found to be elevated significantly following methomyl treatment. No significant change in the enzyme activity of GR and glutathione-6-phosphatase dehydrogenase was observed after methomyl treatment. Vitamin E supplementation was able to attenuate appreciably the methomyl-induced changes in LPO levels along with SOD and GST activities. Histopathological studies following methomyl treatment revealed that hepatocytes, were not very well delineated and nuclei showed degenerative changes. Whereas, following Vitamin E supplementation in combined treatment group nuclei showing degenerative changes become less in number. The study, therefore, concludes that Vitamin E has a potential in mitigating most of the adverse effects induced by methomyl acute toxicity.  相似文献   

12.
为了考察偏钒酸铵对小鼠血清和肝脏转氨酶活力的影响,50只小鼠随机分为5组,对照组饮用三重蒸馏水,4个暴露组分别饮用剂量为5、10、15和20 mg·kg-1·d-1的偏钒酸铵,15 d后取血和肝脏样品,测定血清和肝脏中谷丙转氨酶(alanine transaminase,ALT)和谷草转氨酶(aspartate ami...  相似文献   

13.
An attempt has been made to study the influence of taurine on mercury intoxicated rats. The animals were treated with sublethal dose of mercuric chloride (2 mg/kg body wt.) for 30 days. During the mercury treatment, the level ofAspartate transaminase(AST), Alanine transaminase (ALT) and Alkaline phosphatase(ALP) in serum and lipid peroxidation (LPO) in liver tissue significantly increased whereas Glutathione (GSH), Glutathione peroxidase(GPx), Catalase (CAT) and Superoxide dismutase (SOD) were simultaneously decreased in the liver tissue. Present results indicate that the liver tissue was completely damaged, after mercury treatment. In another group of animals, taurine (5 mg/kg body wt.) was administrated for another 15 days. Taurine administration was observed to improve the liver function in mercury intoxicated animal as indicated by the decline in increased levels of AST, ALT and ALP in serum and LPO content in liver tissue. The decreased level of antioxidant system (GSH, GPx, CATand SOD) has been promoted Results suggested that taurine played a vital role in reducing the mercury toxicity in intoxicated animals.  相似文献   

14.
The effects of interactions between coconut products and caffeine on the induction of drug-metabolizing enzyme in Wistar albino rats were studied. Twenty rats were randomly divided into four groups: (Group 1) control received via oral route a placebo (4 mL distilled water). Groups 2–4 were treated for a 14-day period, respectively, with 50 mg caffeine/kg body weight (BW), 50 mg caffeine/kg plus 50 mg coconut water/kg, or 50 mg caffeine/kg plus 50 mg coconut milk/kg in a 4 mL volume via gastric intubation. One day after the after the final exposure, the animals were euthanized by inhalation of an overdose of chloroform. The blood of each rat was collected by cardiac puncture, and the liver of each was harvested and processed to examine several biochemical parameters, including total protein and RNA levels, protein/RNA ratios, and the activities of alanine and aspartate aminotransferases (ALT and AST, respectively). Results showed that while ingestion of coconut milk and coconut water increased the values of protein and protein/RNA ratios, there was a decrease in ALT and AST activities. These effects were opposite to those produced by caffeine alone and may prevent the adverse effects attributed to caffeine.  相似文献   

15.
This study was designed to determine the protective effects of zinc (Zn) using liver marker enzymes in the serum and liver along with hepatic elemental profile in lead (Pb)-treated protein-deficient (PD) Sprague–Dawley male rats. Zn in the form of zinc sulfate at a dose of 227?mg?L?1 in drinking water was administrated to control, PD as well as Pb-treated PD rats for 8 weeks. Pb treatment was given orally as lead acetate at a dose level of 100?mg?kg?1 body weight to control and PD rats. The effects of different treatments were studied on the activities of enzymes that included alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum. The status of different elements (Cl, K, Mn, Fe, Cu, Zn, Se, Rb, Pb) in liver was also studied. Rats given PD diet and Pb showed significant inhibition in serum ALP activity associated with significant elevation in both AST and ALT activities. Serum ALP activity showed a significant inhibition week 1 until week 8 in Pb-treated PD rats. In contrast, serum AST activity was elevated both at 3 and 8 weeks while serum ALT activity was elevated at 8 weeks in Pb-treated PD rats. Pb treatment to PD rats elevated hepatic ALP, AST and ALT activities but depressed hepatic AST. Zn supplementation to Pb-treated PD rats restored the altered enzyme activities. The levels of K, Fe, Cu, Zn, Se and Rb were altered in protein deficiency. Furthermore, treatment with Pb to these animals depressed the Cu levels. Zn treatment to Pb-treated PD animals tended to restore the levels of altered elements. Hence, the present study clearly suggests that Zn plays an important role in regulating the liver marker enzymes and essential elements under conditions of Pb toxicity and protein deficiency.  相似文献   

16.
The present study was undertaken to determine the toxicity of the methyl orange by using the changes of some antioxidant and detoxification enzyme activities in Gammarus pulex. Lethal Concentration (LC) value of Methyl Orange (MO) was determined. Three sublethal doses of MO (1/4; 1/8 and 1/16 of LC value) were exposed to G. pulex for 24 and 96?h. Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GSH-PX), Cytochrome p450 (CYP1A1), Glutathione S-transferase (GST) activities as well as Glutathione (GSH) and Malondialdehyde (MDA) levels were determined by using The enzyme-linked immunosorbent assay (ELISA) kit. The CAT and CYP1A1 activities were decreased in all the groups exposed to different doses of MO. GST activity and GSH, MDA levels were increased all the groups exposed to different doses of MO. The GSH-PX activities were changed in all the groups. MO affected SOD activity at different levels and in different concentrations. In our study, it has been found that exposure duration didn’t significantly affect the biochemical biomarkers except for GST and GSH. In conclusion, alterations in antioxidant and detoxification enzymes and lipid peroxidation may potentially be used as sensitive biomarkers for risk assessment of dyes in the environment and may contribute to the establishment of discharge regulations.  相似文献   

17.
苯并(a)芘对鲫鱼(Carassius auratus)肝脏抗氧化酶的影响   总被引:13,自引:0,他引:13  
研究了苯并(a)芘(BaP)暴露对鲫鱼肝脏抗氧化酶的影响.共设置4个处理组,浓度分别为每千克体重0.01mg、0.1mg、1mg和10mg,暴露方式采用腹腔注射,分别在暴露后6h、12h、48h和96h测定肝脏超氧化物歧化酶(SOD)、过靴氢酶(CAT)和谷胱甘肽过氧化物酶(GPX)活性.结果显示,所有暴露浓度对SOD活性明显抑制,各处理组活性在暴露后6h均低于对照组,在暴露后12h至48h有所回升,暴露后96h又降至对照水平以下.0.01mg kg^-1、0.1mg kg^-1处理组CA3、活性在暴露期间无显著改变,1mg kg^-1、10mg kg^-1处理组CAT活性在暴露后12h显著升高,暴露后96h回落至对照水平以下,此时10mg kg^-1处理组与对照组差异显著.对照组GPX活性在暴露后出现波动,0.1mg kg^-1处理组在暴露后96h显著低于对照组,而其它处理组活性与对照组在暴露期间无显著差异.结果表明,BaP能对鲫鱼肝脏抗氧化酶产生影响,多种抗氧化酶活性相结合可作为BaP暴露的生物标志物.图3参18  相似文献   

18.
Radical scavenging activity of ethanolic extract of Trianthema triquetra root was investigated against CCl4 in rats. The rats were treated with T. triquetra (100 mg, 200 mg/kg b.w.) for a period of 7 days. Antihepatotoxic effect was studied by assaying the activities of thiobarbituric acid (TBARS), reduced glutathione (GSH), glutathione peroxidase (GPx),catalase (CAT), super oxide dismutase (SOD) and vitamin C (Vit. C). Lipid peroxidation is evidenced by an increase in the value of TBARS and also a distinct diminution in the level of GSH, Vit. C at 200 mg/kg b.w. The activity of antioxidant enzymes, such as GPx, CAT SOD and Vit. E is significantly recovered towards an almost normal level in animals coadministrated with T. triquetra. The maximum protection against CCl4 induced hepatic injury was afforded by the dose of 200 mg/kg b.w. of Trianthema triquetra.  相似文献   

19.
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.  相似文献   

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