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。     

增塑剂邻苯二甲酸二异癸酯致小鼠肺组织氧化损伤作用

探究邻苯二甲酸二异癸酯(diisodecyl phthalate,DIDP)对小鼠肺组织的氧化损伤。以BALB/c小鼠为受试动物,随机分为7组,包括1个阴性对照组(生理盐水)、4个DIDP染毒组(0.15,1.5,15,150 mg·kg~(-1))、1个维生素E(100 mg·kg~(-1))组和1个高剂量DIDP(150 mg·kg~(-1))加维生素E(100 mg·kg~(-1))组,灌胃染毒14 d。处死小鼠,制备肺组织匀浆样品,以化学荧光法检测活性氧(reactive oxygen species,ROS)含量,以分光光度试剂盒法检测还原型谷胱甘肽(glutathione,GSH)的含量、以硫代巴比妥酸(TBA)法检测丙二醛(malondialdehyde,MDA)的含量、以酶联免疫吸附(EILSA)试剂盒法检测8-羟基脱氧鸟苷(8-hydroxy-deoxyguanosine,8-OHdG)的含量,同时观察肺组织的病理变化与荧光染色结果。随着DIDP染毒剂量的升高,肺组织的ROS、MDA、8-OHdG含量逐渐上升,GSH含量逐渐降低,各指标呈一定的剂量-效应关系。染毒剂量为15 mg·kg~(-1)时,ROS、GSH、8-OHdG含量差异有统计学意义(P 0.05,P 0.01);染毒剂量为150 mg·kg~(-1)时,上述指标差异均有统计学意义(P 0.05,P 0.01)。小鼠肺组织HE染色和荧光染色观察结果表明,随着DIDP染毒剂量的增加,小鼠肺细胞的病理损伤越严重。与150 mg·kg~(-1)DIDP剂量组比较,150 mg·kg~(-1)DIDP+维生素E组的ROS、MDA和8-OHdG含量均有下降,GSH含量上升(P 0.05,P 0.01);小鼠肺组织病理损伤减轻。以上结果说明,较高剂量(≥15 mg·kg~(-1))的DIDP能造成小鼠肺组织的氧化损伤,维生素E对其损伤有拮抗作用。     

浮床栽培鱼腥草对吉富罗非鱼血清免疫因子的影响

为探究构建鱼腥草-罗非鱼共生体系能否对罗非鱼(Oreochromis niloticus)产生免疫增强效应,研究池塘中浮床栽培鱼腥草(Houttuynia cordata)(种植面积分别为0、5%、10%和15%)对不同免疫反应阶段吉富罗非鱼血清免疫因子的影响,测定免疫识别阶段免疫球蛋白(Ig M)和表皮生长因子(EGF),炎症反应阶段相关因子干扰素-γ(IFN-γ)、白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8),以及效应阶段金属硫蛋白(MT)和转铁蛋白(TRF)等指标。结果表明,10%鱼腥草处理组吉富罗非鱼血清EGF、IL-8、IL-10、TNF-α和TRF含量显著高于其他处理组和对照组,5%鱼腥草处理组吉富罗非鱼血清Ig M、IFN-γ含量显著高于其他处理组和对照组,且没有造成血清MT含量的降低。吉富罗非鱼养殖池塘种植鱼腥草(5%)能显著提高其不同免疫反应阶段血清免疫因子的活性。     

PFOS致大鼠肝毒性及其作用机制研究

通过全氟辛烷磺酸(perfluomoctane sultanate,PFOS)大鼠灌胃染毒实验评价PFOS对肝功能的影响,探讨PFOS肝毒性反应的潜在机制与可能途径。将Sprague Dawley (SD)雄性大鼠随机分为3组,分别以0 mg·kg~(-1)、5 mg·kg~(-1)和10 mg·kg~(-1)PFOS灌胃染毒28 d。以HE和油红染色法观察大鼠肝脏形态改变。ELISA法测定各组谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate transaminase,AST)、碱性磷酸酶(alkaline phosphatase,ALP)含量变化。化学比色法测定肝匀浆脂代谢水平和氧化产物含量。RT-PCR法检测肝脏内氧化应激以及脂代谢相关基因表达水平。结果表明,PFOS暴露大鼠体重显著降低而肝脏系数显著增加(P0.05),与对照组相比PFOS组血清肝功能酶均出现随PFOS浓度增加而升高(P0.05)。同时大鼠肝脏谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-px)和丙二醛(malondialdehyde,MDA)水平在高剂量组显著升高(P0.05),超氧化物歧化酶(superoxide dismutase,SOD)含量先显著升高(P0.05)后显著降低(P0.05)。且肝脏中脂代谢水平也随PFOS浓度的增加而出现显著改变(P0.05)。PFOS组基因表达均较对照组显著上升(P0.05)。以上结果说明PFOS具有明显的肝毒性作用,可影响肝脂代谢水平,这可能与PFOS引起的氧化应激所导致的损伤有关。     

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。     

草甘膦对雄性大鼠睾酮合成的影响

探讨草甘膦亚慢性染毒对雄性大鼠睾酮合成的影响。雄性SD大鼠按体重随机分为对照组(0 mg·kg~(-1))、低剂量组(50 mg·kg~(-1))、中剂量组(200 mg·kg~(-1))和高剂量组(800 mg·kg~(-1)),连续灌胃染毒,第4、8和12周时分别处死一批动物,采集血液和脏器。放射免疫分析法检测大鼠血清中卵泡刺激素(follicle stimulating hormone,FSH)、黄体生成素(luteinizing hormone,LH)、睾酮(testosterone,T)、雌二醇(estradiol,E2)水平; HE染色法(苏木精-伊红染色法)观察睾丸病理学变化;免疫组化法检测3β-羟基类固醇脱氢酶(3beta-hydroxysteroid dehydrogenase,3β-HSD)、类固醇激素合成急性调节蛋白(steroid synthesis of acute regulatory protein,St AR)、细胞色素P450胆固醇侧链裂解酶(cytochrome P450 cholesterol side chain lyase,P450scc)和17β-羟基类固醇脱氢酶(17beta-hydroxysteroid dehydrogenase,17β-HSD)蛋白表达水平。随染毒剂量和时间的增加,大鼠血清FSH和T水平呈下降趋势,第12周高剂量组FSH水平明显低于对照组(P0.05),第8周和第12周高剂量组T水平明显低于对照组(P0.05),LH和E2水平各组间无统计学差异(P0.05)。组织病理学可见中、高剂量组睾丸生精小管、生精细胞、间质区结构被破坏。随草甘膦染毒剂量的增加,St AR和P450scc蛋白表达水平与对照组相比显著下降(P0.05),3β-HSD和17β-HSD蛋白表达水平在各组间无差异(P0.05)。草甘膦能降低血清T水平,抑制T合成相关蛋白St AR和P450scc的表达,干扰T的合成过程,具有雄性生殖毒性作用。     

腈菌唑手性单体对雄性丽斑麻蜥肝脏代谢功能的影响

腈菌唑(MT)是一种应用广泛的手性杀菌剂,其手性对映体为(+)-腈菌唑(MT1)和(-)-腈菌唑(MT2)。为评估腈菌唑单体暴露对丽斑麻蜥(Eremias argus)肝脏代谢功能的毒性影响,研究了MT1(5 mg·kg~(-1))和MT2(5 mg·kg~(-1))暴露28 d下蜥蜴体重、肝组织病理学和代谢相关基因表达的变化。结果显示,MT1暴露组的蜥蜴体重在28 d时出现显著下降。在MT1和MT2暴露后,蜥蜴的肝组织均出现了不同程度的病理学变化。在MT1暴露下,基因CYP1A1、CYP2D6、CYP3A4、CYP3A7和CYP2D3的表达水平未发生显著变化,而基因CYP2C8A的表达显著上调。在MT2暴露下,基因CYP3A4、CYP3A7和CYP2D3的表达未发生明显变化;基因CYP1A1和CYP2C8的表达显著下调;基因CYP2D6的表达显著上调。不同腈菌唑单体对蜥蜴体重、肝组织病理学以及代谢相关基因的表达影响不同,具有一定的对映选择性。     

氯化三丁基锡(TBTCl)对罗非鱼精巢细胞凋亡的影响

以雄性奥利亚罗非鱼为试验材料,分别以0、1、3、5和10μg·L-1氯化三丁基锡(TBTCl)通过接触染毒的方式,研究TBTCl对鱼类精巢细胞凋亡的影响.细胞凋亡分析结果表明,在同一染毒时间下,除染毒时间为24和48h,染毒浓度为1μg·L-1处理组与对照组之间细胞凋亡率差异不显著(P>0.05)以外,其余情况下各处理组与对照组之间差异均显著(P<0.05或P<0.01).各相邻2个浓度处理组之间,3μg·L-1处理组和5μg·L-1处理组之间细胞凋亡率差异均不显著(P>0.05),其余各组之间差异均显著(P<0.05或P<0.01).随着TBTCl浓度的升高,罗非鱼精巢细胞凋亡率逐渐升高,剂量-效应关系显著.精巢细胞Ca2+-ATP酶活性测定结果表明,在同一染毒时间下,除在染毒时间为24和96 h时,染毒浓度为1μg·L-1处理组与对照组之间差异不显著(P>0.05)以外,其余情况下各处理组与对照组之间差异均显著(P<0.05或P<0.01).在同一染毒时间下,各处理组之间,除染毒时间为24 h时,染毒浓度1μg·L-1处理组和3 μg·L-1处理组之间差异不显著(P>0.05)以外,其余情况下各处理组之间差异显著(P<0.01);随着染毒浓度的升高,Ca2+-ATP酶活性逐渐升高,并且剂量一效应关系显著(P<0.05或P<0.01).奥利亚罗非鱼精巢细胞凋亡率与精巢Ca2+-ATP酶活性间具有一定的协同关系.     

日粮中铜胁迫对吉富罗非鱼幼鱼抗氧化、脂质过氧化及肝脏组织结构的影响

吉富罗非鱼是我国南方沿海地区水产养殖中的主要经济鱼类之一,但近年来,随着我国城镇化和工业化进程的推进,罗非鱼养殖面临着前所未有的铜富集的挑战。为探明日粮中铜胁迫对吉富罗非鱼幼鱼抗氧化系统和肝脏组织结构的影响,将1 080条罗非鱼幼鱼暴露于6个浓度梯度(0、3、30、300、1 000、3 000 mg·kg-1)的高铜日粮中,通过60 d的暴露试验,实时测定罗非鱼血清与肝脏抗氧化能力,监测肝脏病理变化。结果表明,在本试验条件下,罗非鱼幼鱼血清和肝脏中MDA的含量随日粮中铜含量的增加和胁迫时间的延长显著升高,而SOD、GSH-PX和Cu Zn-SOD的活性表现出先升高后降低的趋势;各组间肝脏表现出不同程度的病变,主要是浊肿变性和脂肪变性,且第Ⅲ、Ⅳ、Ⅴ组肝脏病变严重。综上,日粮中铜胁迫对吉富罗非鱼幼鱼的抗氧化机能有较明显的抑制作用,长时间的暴露能严重损伤其肝脏的组织结构,因此,建议吉富罗非鱼幼鱼日粮中铜的实际含量应控制在42.36 mg·kg-1以下。     

基于PBPK模型的大鼠体内镉分布的比较:联合暴露及单独暴露

环境中同时存在着多种重金属元素,联合暴露与单独暴露时,重金属在体内的蓄积分布情况也可能有所差异。为探究重金属元素(汞、铬、砷、铅)对镉(Cd)在体内分布的影响,建立了大鼠在Cd暴露下的药代动力学(PBPK)模型,并进行了包括Cd在内5种重金属的联合毒性实验,比较了Cd单独给药与重金属混合物给药2种方式下大鼠肝脏、肾脏中的Cd浓度水平。结果表明,联合暴露高(Hg Cl23.67 mg·kg~(-1),NaAsO_2 3.67 mg·kg~(-1),CdCl_2 10.55 mg·kg~(-1),K_2Cr_2O_7 6.40 mg·kg~(-1),Pb(OOCCH_3)_2·3H_2O 133.33 mg·kg~(-1))、中(HgCl_20.367 mg·kg~(-1),NaAsO_2 0.367 mg·kg~(-1),CdCl_2 1.055 mg·kg~(-1),K2Cr2O70.640 mg·kg~(-1),Pb(OOCCH_3)_2·3H_2O 13.333 mg·kg~(-1))、低(HgCl_2 0.0367 mg·kg~(-1),Na As O20.0367 mg·kg~(-1),Cd Cl20.1055 mg·kg~(-1),K_2Cr_2O_7 0.0640 mg·kg~(-1),Pb(OOCCH3)2·3H2O 1.3333 mg·kg~(-1))剂量组大鼠肝脏中Cd浓度分别为13.37、0.78和0.06μg·g~(-1);肾脏中Cd浓度分别为14.41、1.64和0.15μg·g~(-1)。与对照组相比,暴露组中Cd浓度有显著升高,且不同剂量组之间均有显著性差异。同剂量Cd单独暴露的PBPK模拟结果显示,肝脏及肾脏中的Cd浓度水平落在联合毒性实验结果的浓度范围内,初步推断其他4种重金属的联合暴露并没有影响Cd在大鼠肾脏和肝脏中的浓度分布。     

Lead-induced alterations in protein-deficient rat liver–role of zinc

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.     

Potential hepatoprotective effects of vitamin E and Nigella sativa oil on hepatotoxicity induced by chronic exposure to malathion in human and male albino rats

Malathion is an organophosphorus (OP) insecticide and has a wide range of use in agriculture, veterinary medicine, and public health. Malathion and other OP insecticides produce hepatotoxic effects. The objective of the present study was to investigate the protective effects of Nigella sativa oil and α-tocopherol (vitamin E) on the hepatotoxicity induced by malathion on workers involved in the formulation of pesticides, chronically exposed to malathion, and in male albino rats orally administrated malathion. This study was conducted on both human and experimental animals, the human study was conducted on 30 control subjects working as administrators and 45 subjects working in formulation of pesticides and exposed to malathion (≥3 years), all were males with age ranges from 30 to 60 years. The 45 males working in pesticides formulation were classified into three groups; (1) 15 workers exposed to pesticides (2) 15 workers exposed to pesticides and received vitamin (E), in a dose of 10 mg kg?1 day^?1 orally for 60 days, and (3) 15 workers exposed to pesticides and received 100 mg kg^?1 day^?1 of N. sativa oil for 60 days. The animal experiment was conducted on 40 adult male albino rats weighing 150–200 g. They were divided into four groups (10 rats in each group). First group served as the control group, the second group received malathion in a dose of 50 mg kg^?1 orally per day for 60 days, the third group received malathion (in the same dose and route of administration) and vitamin E in a dose of 10 mg kg^?1 day^?1 orally for 60 days, and the fourth group received malathion (in the same dose and route of administration) and N. sativa oil in a dose of 100 mg kg^?1 day^?1 orally for 60 days. Liver function tests (alanine aminotransferase [ALT], aspartate aminotransferase [AST], serum alkaline phosphatase [ALP], albumin, globulin, albumin/globulin ratio, and total proteins), antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD), and total glutathione peroxidase (GPx)), and lipid peroxidation [MDA] were analyzed in both human and animal experiments. The results of both human and animal study revealed that, exposure to malathion produced significant increases in AST, ALT, and lipid peroxidation. There were significant decrease in albumin, albumin/globulin ratio, total protein, and antioxidant enzymes. There was no significant change in ALP. In addition exposed workers showed significant decreases in serum globulin. Nigella sativa oil or vitamin E administration showed significant improvement of liver function tests, lipid peroxidation, and antioxidant enzymes impairment induced by malathion. Thus, dietary supplement, N. sativa oil, or vitamin E may represent a potential therapeutic agent in reducing malathion-induced hepatotoxicity.     

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.     

Vitamin E-mediated protection on methomyl-induced alterations in rat liver

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.     

全氟辛烷磺酸(PFOS)对三角帆蚌肝胰腺的氧化性损伤

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。     

Sub-chronic exposure to carbendazim induces biochemical and hematological alterations in male goats

The present investigation reports the effect of repeated (90 days) administration of carbendazim on the biochemical and hematological parameters in male goats. Carbendazim administered orally at a daily dose of 50 mg kg^?1 body weight for 90 consecutive days resulted in increased plasma concentration of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), gamma-glutamyl transferase (GGT), creatinine and albumin, while alkaline phosphatase (ALP) and glucose levels were decreased. Decrease in total leukocyte (TLC) and neutrophil count and increase in lymphocyte count was observed in the treatment group. The findings of the present investigation indicate that sub-chronic exposure to carbendazim in male goats causes hepatic and slight kidney dysfunctions.     

Hepatoprotective effects of taurine against mercury induced toxicity in rats

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.     

盐酸小檗碱对小鼠脾细胞的DNA损伤和氧化性损伤研究

为了探讨盐酸小檗碱对小鼠的DNA损伤和氧化性损伤。随机选取30只小鼠分成对照组以及7.5,15,30,60与120 mg?kg^-1实验组,处理后,应用小鼠脾细胞进行彗星实验与抗氧化酶实验。测定DNA损伤情况以及超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、过氧化物酶（POD）活性以及丙二醛（MDA）含量变化。对盐酸小檗碱的DNA损伤与氧化性损伤作用进行比较研究。研究结果表明：彗星实验中,随着盐酸小檗碱浓度的增加,尾部DNA含量、尾长与尾矩均增加,与阴性对照组相比差异有统计学意义（p<0.05或p<0.01）,且呈剂量-效应关系;超氧化物歧化酶(SOD)与过氧化氢酶(CAT)活性随盐酸小檗碱剂量增加逐渐降低,丙二醛(MDA)含量明显下降,过氧化物酶(POD)活性在7.5 mg?kg^-1时上升,而后逐渐下降。在60 mg?kg^-1和120 mg?kg^-1时,有极显著性差异（p<0.01）产生。由此可见,盐酸小檗碱对小鼠脾细胞有一定的损伤作用,能够引起小鼠脾细胞的DNA损伤和氧化性损伤。     

Dioxin alters inflammatory responses to lipopolysaccharide

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has well characterized effects on specific immune responses, but the effects on the innate immune system are less understood. The effect of TCDD on inflammatory responses induced by lipopolysaccharide (LPS) was evaluated in C57BL/6J female mice. Mice were treated with 30?µg?kg^?1 TCDD or vehicle once, p.o., and 4 days later, animals received LPS (0.05?×?10⁷?EU?kg^?1, i.p.) or vehicle. Inflammatory mediators and the liver injury marker, alanine aminotransferase (ALT), were measured, and liver histology was evaluated. TCDD-treated animals had higher plasma ALT activity than vehicle-treated animals, but the effect was mild and time-dependent. Few changes in liver histopathology were observed, mainly represented in greater steatosis in TCDD/LPS-treated mice compared to mice treated with LPS or TCDD alone. LPS produced a time-dependent increase in the plasma concentrations of interleukins (IL)-6, -10, and -12 and interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and monocyte chemoattractant protein (MCP)-1. With the exception of IL-12, concentrations of each of these mediators were higher in plasma of mice co-treated with TCDD and LPS compared to either agent alone. The dose–response curve for the concentration of IL-6 in plasma suggested that dioxin increased the potency of LPS to cause the release of this cytokine but not the maximal response. Co-treatment with TCDD and LPS also led to greater expression of mRNA for IL-10 and IFN-γ compared to either TCDD or LPS alone. These results suggest that TCDD changes the inflammatory cytokine profile induced by LPS and that LPS enhances the hepatic steatotic response to TCDD.