N-乙酰半胱氨酸和亚硒酸钠对镉亚慢性毒性的影响

目的探讨N-乙酰半胱氨酸(N-acetyl cysteine,NAC)和亚硒酸钠(Na2SeO3)对亚慢性染镉大鼠肝肾毒性的影响及其机制。方法32只Wistart大鼠随机分为4组,每组8只,第1组为对照组,第2组为单位染镉组,第3、4组为干预组。大鼠连续6周皮下注射7μmol/kg氯化镉,然后干预组分别腹腔注射1 mmol/kg NAC和10μmol/kg Na2SeO3,共2周;测定大鼠尿N-乙酰-β-苷酶(NAG)、碱性磷酸酶活力(ALP)和肝、肾皮质谷胱甘肽(GSH)、丙二醛(MDA)含量及谷胱甘肽过氧化物酶(GSH-Px)活力。结果亚慢性染镉使大鼠肝、肾皮质和尿镉含量显著升高,尿ALP、NAG和蛋白含量显著升高,肝、肾皮质GSH含量显著升高,GSH-Px活力显著降低。与单纯染镉组比较,NAC处理组尿镉、NAG和蛋白含量显著下降,肝、肾皮质GSH显著降低;Na2SeO3处理组尿镉、ALP及肝、肾皮质GSH含量显著下降,GSH-Px活力显著升高。结论NAC和Na2SeO3对镉致肾损伤的恢复具有促进作用,其机制可能与NAC或Na2SeO3改变体内GSH含量和GSH-Px活力有关。     

松花粉对急性汞中毒大鼠肝肾的保护作用及机制研究

目的研究松花粉对急性汞中毒大鼠肝肾的保护作用及机制。方法将大鼠随机均分为正常对照组,染汞模型组,松花粉低、中、高剂量组(2、4、8 g/kg)。通过皮下注射HgCl_2建立急性汞中毒模型,末次染汞后,各组分别灌胃给予相应药物,2次/d,共5 d。通过电感耦合等离子体质谱仪,测定肝汞、肾汞、血汞和尿汞的含量。通过试剂盒,测定尿素氮(BUN)、尿蛋白、尿乳酸脱氢酶(LDH)、尿碱性磷酸酶(ALP),血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、血清总胆红素(TBIL),以及肝、肾中的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽(GSH)和丙二醛(MDA)的含量或活性。结果与正常对照组比较,染汞模型组大鼠的肝汞、肾汞、血汞、尿汞、BUN、尿蛋白、尿LDH、尿ALP、血清ALT、血清AST、血清TBIL、肾脏MDA和肝脏MDA含量或活性均升高(P<0.01),肾脏和肝脏SOD、GSH-Px、GSH含量或活性降低(P<0.01)。与染汞模型组比较,松花粉低、中、高剂量组大鼠的尿汞含量增加(P<0.05或P<0.01),上述其余指标均能显著地向正常对照组的数值变化(P<0.05或P<0.01)。结论松花粉具有清除体内汞蓄积、修复急性汞中毒诱导的急性肝肾损伤的作用,其机制与抑制脂质过氧化损伤相关。     

牛磺酸和维生素C对锰致大鼠氧化损伤的拮抗作用

目的探讨牛磺酸(Tau)和维生素C(Vit-C)对锰致大鼠氧化损伤的影响,为阐明锰中毒的发病机制和防治提供依据。方法 Wistar大鼠32只,随机分为4组,分别为对照组、单纯染锰组、Tau和Vit-C干预组。对照组大鼠腹腔注射生理盐水,其余各组腹腔注射29.685 mg/kg Mn Cl2溶液。腹腔注射后2h,对照组和单纯染锰组大鼠隔日皮下注射生理盐水,Tau干预组隔日皮下注射125.15 mg/kg Tau,Vit-C干预组隔日皮下注射704.52 mg/kg Vit-C。每周染锰5次,1次/d,染毒4周。共计染锰20次,Tau和Vit-C干预各10次。测定肝、脑和肾组织还原型谷胱甘肽(GSH)、丙二醛(MDA)的含量和谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)的活力。结果与对照组比较,单纯染锰组大鼠肝脏、脑和肾组织MDA含量增加,肝肾组织GSH含量降低。脑组织GSH含量和GSH-Px活力有下降趋势,但统计学差异不明显。Tau干预组大鼠与单纯染锰组相比,肝脏、脑和肾组织MDA含量下降,GSH含量增加。脑和肾组织GSHPx活力增高,脑组织SOD活力增高。Vit-C干预组大鼠与单纯染锰组相比,大鼠肝脏MDA含量有下降趋势,脑和肾组织MDA含量明显下降。虽然大鼠肝脏、脑和肾组织GSH含量增加,但统计学差异不明显。仅肝组织GSH-Px活力明显增加。结论锰可使大鼠产生氧化损伤,Tau和Vit-C对锰致大鼠氧化损伤有一定的拮抗作用。     

氢水对小鼠辐射致氧化损伤的保护作用

目的探讨氢水对辐射小鼠抗氧化水平的影响。方法 60只KM小鼠随机分为对照组、单纯放射组和氢水组。对照组和单纯放射组经胃给予纯化水,氢水组给予氢水。γ线照射结束后取肝肺组织制成10%肝肺组织匀浆,检测肝肺组织中SOD、GSH-PX活力及MDA含量。结果单纯照射组照射后的肝肺组织SOD、GSH-PX活力与对照组比明显降低。MDA含量明显升高(P<0.05)。氢水组的SOD、GSH-PX活性升高,MDA含量明显降低(P<0.05)。结论氢水对小鼠因辐射引起的氧化损伤有保护作用,可能与氢水具有选择性抗氧化作用有关。     

姜黄素对汞致大鼠肾损伤保护作用的实验研究

目的探讨姜黄素对汞致大鼠肾损伤的影响,为汞中毒的发病机制和防治提供实验依据。方法 Wistar大鼠30只按体重随机分为5组,每组6只,雌雄各半。分别为对照组、低剂量染汞组、中剂量染汞组、高剂量染汞组和姜黄素预处理组。1~4组大鼠予皮下注射0.9%氯化钠溶液,第5组大鼠给予皮下注射100 mg/kg姜黄素;2 h后,第1组腹腔注射生理盐水,第2~5组大鼠分别腹腔注射2.2、4.4、8.8和8.8μmol/kg氯化汞溶液,连续干预与染毒3 d。第3天染毒2 h后将动物放入代谢笼,收集24 h尿液测定尿汞和尿蛋白含量,以及尿碱性磷酸酶(ALP)、β-N-乙酰氨基葡萄糖苷酶(NAG)和乳酸脱氢酶(LDH)活力;用乙醚将大鼠麻醉,腹主动脉采血测定血清尿素氮(BUN);切取肾皮质,测定肾皮质汞、还原型谷胱甘肽(GSH)和丙二醛(MDA)的含量及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力。结果与对照组比较,随着染汞剂量的增加,肾皮质汞、尿汞、尿蛋白和BUN含量均升高;尿NAG、LDH和ALP活力均升高;肾皮质GSH和MDA含量明显升高而GSH-Px和SOD活力显著下降,差异具有统计学意义(P0.05)。姜黄素预处理组与高剂量氯化汞染毒组比较,各项指标均有不同程度的改善,差异有统计学意义(P0.05)。结论姜黄素对汞致大鼠肾损伤具有一定的保护作用。     

小鼠丙酮预处理对丙烯腈氧化应激效应的影响

目的探讨细胞色素P450 2E1诱导对丙烯腈氧化应激效应的影响。方法将40只小鼠(雌雄各半)随机分成4组:空白对照组、(丙酮)诱导组、单纯丙烯腈染毒组(AN)和(丙酮)诱导加丙烯腈染毒组(诱导 AN)。诱导组和诱导 AN组小鼠饮用体积分数为1%的丙酮溶液预处理7 d。4组分别给予丙烯腈0、01、0和10 mg/kg,经腹腔注射染毒24 h后测定小鼠全脑和肝脏的丙二醛(MDA)和谷胱甘肽(GSH)含量以及超氧化歧化酶(SOD)活力。结果4组脑的脏器系数及肝脏的脏器系数性差异无统计学意义;AN染毒组小鼠脑组织中的MDA含量显著高于对照组,诱导 AN组的MDA水平较AN组有所降低;诱导 AN组组小鼠脑组织GSH和SOD含量均高于AN组,其中GSH水平升高具有统计学意义(P<0.05);和空白对照组相比,诱导 AN组、AN组小鼠肝组织中的MDA含量均有所增高,非酶性抗氧化剂GSH含量有所降低,特别是诱导 AN组和AN组相比又有所上升,但差异无统计学意义(P>0.05)。单纯AN组的SOD活力较单纯对照组明显降低(P<0.05),诱导 AN组的SOD活力有所回升,接近单纯对照组水平。结论CYP 2E1诱导表达可减轻丙烯腈的氧化应激损伤,提示丙烯腈原形可能是小鼠引起氧化损伤的主要机制。     

D-青霉胺和二巯丙磺酸钠对汞致大鼠肾毒性的影响

目的　研究预投D- 青霉胺 (D- penicillamine ,DPA)和二巯丙磺酸钠 (2 ,3 - Dimercato 1 Propanesulfonate ,DMPS)对汞致急性肾毒性的保护作用及其机制。方法　 48只Wistar大鼠随机分成 6组。第 1组以 5mL/kg体重皮下注射质量分数为 0 . 9%的氯化钠溶液 ,第 2、3和 4组分别皮下注射 0 .75、1.5和 2 .5mg kgHgCl2 溶液。第 5、6组大鼠分别腹腔注射2 0 0 μmoLDMPS和 2 0 0 μmoLDPA ,2h后再投与 2 5mg/kgHgCl2 溶液。染毒 12h后 ,收集 12h尿样 ,测定尿N- 乙酰 - β- D- 氨基葡萄糖苷酶 (NAG)和尿碱性磷酸酶 (ALP)活力、尿蛋白和尿汞含量。染毒 48h后 ,切取肾脏和肝脏 ,分别测定肾脏和肝脏中的丙二醛 (MDA)和谷胱甘肽 (GSH)含量、谷胱甘肽过氧化物酶 (GSH- Px)活力、肝脏汞和肾脏汞含量。结果　DMPS显著降低NAG和ALP活力和尿蛋白含量 ;DPA明显降低NAG活力和尿蛋白含量 ,对ALP没有影响。DMPS显著降低肾脏MDA含量 ,而DPA对肾脏MDA含量没有影响。DMPS-和DPA两干预组在肾脏中GSH含量和GSH -Px活力都明显高于 2 . 5mg kg染汞组 ,差异有显著性。DPA能显著降低肾脏汞含量。结论　DMPS比DPA更能有效地保护肾功能。DMPS会显著减轻汞在肾脏的氧化损伤 ,而DPA则没有影响。DMPS和DPA能明显减少肾脏GSH和GSH- Px的耗     

叶黄素对砷致小鼠肝脏损伤的拮抗作用

目的探讨叶黄素对三氧化二砷(As_2O_3)所致小鼠肝脏氧化损伤的拮抗作用。方法将60只昆明小鼠(雌雄各半)随机分为空白组、对照组、As_2O_3组、叶黄素组和As_2O_3+叶黄素组,每组12只。As_2O_3与叶黄素溶液的灌胃剂量分别为5和40 mg/kg·bw,时间分别为70和35 d。称量小鼠体重、肝重并计算肝脏系数;测定肝组织天冬氨酸转氨酶(AST)与丙氨酸转氨酶(ALT)活力、丙二醛(MDA)含量、谷胱甘肽(GSH)含量、超氧化物歧化酶(SOD)活力、总抗氧化能力(T-AOC)水平、一氧化氮(NO)含量。结果与对照组相比,As_2O_3组体重、GSH含量、SOD活力、T-AOC水平、NO含量降低,肝重、肝脏系数、AST与ALT活力、MDA含量升高(P0.05);与As_2O_3组比较,As_2O_3+叶黄素组的体重、GSH含量、SOD活力、T-AOC水平、NO含量均升高,肝重、肝脏系数、AST与ALT活力、MDA含量均降低,差异均具有统计学意义。结论叶黄素能够拮抗砷所致小鼠的肝脏毒性和氧化损伤。     

褪黑素对溴氰菊酯致大鼠血清氧化损伤的保护作用

目的 探讨褪黑素(Melatonin,MT)对溴氰菊酯(Deltamethrin,DM)诱发大鼠血清氧化性损伤的保护作用.方法 35只Wistar雄性大鼠按体重随机分为5组(每组7只),分别为橄榄油对照组、DM、MT1、MT2、MT3组.每组连续10d,腹腔注射相应剂量药物.并在第1、4、7和10天给药后4 h,对各组大鼠尾间采血.酶标仪比色测定大鼠血清上清中丙二醛(MDA)、谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活力.结果给药10 d后,与对照组相比,DM组血清中MDA含量从第4天到第10天,随给药时间的延长MDA明显升高(P<0.05).与DM组相比,MT1、MT2组和MT3组血清MDA含量在第7天和第10天明显降低(P<0.05),与对照组比较,DM组血清中GSH和GSH-Px活力第4天到第10天明显降低(P<0.05),CAT和SOD活力在第7天和第10天明显降低(P<0.05).与DM组相比,MT1组血清CAT、GSH和GSH-Px活力从第4天到第10天逐渐升高(P<0.05),SOD活力在第7天和第10天明显升高(P<0.05).与DM组相比,MT2组和MT3组血清CAT、GSH、SOD GSH-Px活力在第7天和第10天明显升高(P<0.05).结论 DM能诱发大鼠血清氧化损伤,MT对DM引起的大鼠血清的氧化损伤有抑制作用.     

川芎嗪对大鼠心肌缺血再灌注损伤保护作用的研究

目的观察川芎嗪对心肌缺血再灌注损伤的保护作用及机理。方法采用大鼠冠脉结扎30min后再通20min造成心肌缺血再灌模型。大鼠随机分对照组、缺血组、模型组(缺血再灌组)和川芎嗪保护组。观测心肌细胞膜和线粒体中过氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH·PX)、Ca2 _ATP酶和K ,Na _ATP酶活力 ,MDA及心肌钙含量。结果川芎嗪保护组心肌细胞膜SOD、GSH·PX、Ca2 _ATP酶和Na ,K _ATP酶活性较缺血再灌组均有显著性升高(P<0.05或P<0.01) ,丙二醛(MDA)和心肌钙含量却呈显著性降低。线粒体中SOD和GSH·PX活力也呈显著性升高(P<0.05),MDA却为显著性降低。结论川芎嗪对大鼠缺血再灌注损伤心肌有确切保护作用 ,其机理是通过提高对氧自由基的清除及抑制脂质过氧化。     

Simultaneous administration of sodium selenite and mercuric chloride decreases efficacy of DMSA and DMPS in mercury elimination in rats

Two chelating agents meso-2,3-dimercaptosuccinic acid (DMSA) and sodium 2,3-dimercapto-propane-1-sulphonate (DMPS) were tested for their efficiency in mercury removal from the body of rats in the presence and in the absence of selenium. Female Wistar rats were given a single intraperitoneal injection of mercuric chloride or an equimolar mixture of mercuric chloride and sodium selenite (1.5 micromol/kg body weight). The chelating agents were given orally, in excess (500 micromol DMSA/kg body weight; 300 micromol DMPS/kg body weight), 30 min after the administration of mercury and selenium. The animals were euthanized 24 h after the treatment and mercury in the kidney, liver, and 24 h urine was determined using cold vapour atomic absorption spectrometry (CV-AAS). The simultaneous administration of mercuric chloride and sodium selenite led to a redistribution of mercury in the organs, so that accumulation of mercury in the kidneys was decreased and in the liver increased. Selenite also caused decrease in the level of urinary mercury excretion. Both chelating agents were effective in mercury removal from the body, by increasing its urinary excretion. However, when animals were simultaneously treated with mercury and selenite, the rise of mercury excreted in the urine due to the treatment with chelating agents was lower when compared to animals receiving mercury without selenite. It is concluded that sodium selenite decreases the efficiency of DMSA and DMPS in mercury removal from the body of rats.     

Influence of selenium dose on mercury distribution and retention in suckling rats

It is well known that metal–metal interactions in the body are age‐dependent. We studied the influence of increasing selenium (Se) doses on mercury (Hg) distribution and retention in the postnatal period in Hg‐exposed suckling rats. Seven‐day‐old Wistar pups were pretreated with three different oral doses of Se as sodium selenite (6.45, 12.9 and 19.4 µmol Se kg^?1 b.w.) over 3 days. This was followed by simultaneous Se (as sodium selenite) and Hg (as mercury chloride) oral administration over 4 days. The molar ratio between Se and Hg given to pups was 1:1, 2:1 and 3:1, respectively. Mercury and Se were measured in brain, kidneys, liver, plasma, erythrocytes and urine of pups on the day after the last administration by atomic absorption spectrometry. Results showed that in all samples Se concentrations rose almost proportionally to the dose of Se given to pups. Mercury concentration in organs, plasma and urine decreased with higher oral doses of Se. However, Hg concentration in erythrocytes increased with increasing Se dose. There was evidently a redistribution of Hg from plasma to erythrocytes at higher ratio of Se:Hg. Approximately equimolar doses of Se and Hg are necessary to produce maximum uptake of Hg by plasma and liver and minimum retention of Hg in the kidney and erythrocytes. Copyright © 2009 John Wiley & Sons, Ltd.     

Ameliorative stroke of selenium against toxicological effects of mercuric chloride in liver of freshwater catfish Heteropneustes fossilis (Bloch)

Mercury, a prevalent and unrelenting toxin, occurs in a variety of forms in freshwater as well as, in marine life. Mercury is an important inducer of oxidative stress in fish leading to formation of reactive oxygen species. Selenium is an essential micronutrient for animals and has antagonistic effect against mercuric toxicity in fishes. Present study has been made to evaluate toxic effect of HgCl₂ (0.15 mg/L) on liver of freshwater catfish Heteropneustes fossilis (Bl.). Protective ability of selenium has been investigated by simultaneous exposure of fish with sodium selenite (0.15 mg/L) along with mercuric chloride. For present study Fishes were divided into three groups of ten fishes each the first group served as control, while the second group fish were exposed to HgCl₂. Animals of third group were treated with HgCl₂ and Na₂SeO₃. Results reveal that mercury induced lipid peroxidation and in response to this, antioxidants reduced glutathione (GSH) and Catalase (CAT) were reduced whereas, Glutathione reductase (GR) level was enhanced. These antioxidants scavenge the reactive oxygen radicals. Hg induced histopathological damage and elevation in alkaline phosphatase (ALP) and transaminases and reduction in protein and glucose contents were evidently seen in catfish liver. Intriguingly, results indicate that under stress of mercury, the fish actively generate oxidative stress and antioxidant responses, which can be used as biomarkers of pollution. Simultaneous exposure to Selenium along with Hg suppressed Hg uptake and lipid peroxidation. Histological architecture and all biochemical parameters were maintained near normal in the presence of selenium in liver of the catfish. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 927–936, 2015.     

nmhaFGF对大鼠肾脏缺血-再灌注ET-1和NO的影响

目的 探讨不同浓度非促分裂人酸性成纤维细胞生长因子(nmhaFGF)对肾脏缺血-再灌注(I-R)损伤后内皮素1(ET-1)和一氧化氮(NO)含量的影响.方法 成年SD大鼠35只随机分为假手术(切除左肾,暴露右肾)(SA)组和4个模型组(切除左肾,右肾动静脉夹闭60 min).建模后5 min经舌静脉注射nmhaFGF 10 μg/kg(A组)、20μg/kg(B组)、40μg/kg(C组)或生理盐水1.5 ml(D组).术后24 h处死,放射免疫及生化方法检测肾组织和血浆ET-1和NO含量.结果 B组皮质和外髓ET-1含量明显低于D组(P<0.05),C组肾皮质、外髓、内髓和血清中ET-1含量都明显低于D组(P<0.01);B、C组肾组织中NO含量明显高于D组(P<0.05).结论 nmhaFGF可以通过降低ET-1和升高NO水平减轻大鼠肾脏I-R损伤.     

Changes in distribution of mercury and selenium in soluble fractions of rabbit tissues after simultaneous administration

The existing states of mercury and selenium in the blood and in soluble fractions of perfused rabbit liver and kidney were studied by gel filtration on Sephadex G-200 1 hr or 24 hr after intravenous injection of mercuric chloride and/or sodium selenite. Both mercury and selenium in the plasma and stroma-free hemolysate were found to exist in the high-molecular weight fraction following simultaneous injection of mercuric chloride and sodium selenite. Patterns in gel filtration of the plasma and the stroma-free hemolysate did not show any significant change between 1 hr and 24 hr after the administration. A similar tendency as described above was obtained with the liver-soluble fraction at 24 hr after injection of mercuric chloride and sodium selenite. A possible role of the high-molecular weight complex, which is quickly formed by the interaction of mercury and selenium in blood stream, in decreasing the acute renal toxicity of inorganic mercury is discussed.     

氧化应激在燃煤污染型氟中毒大鼠中的作用

目的研究氧化应激在燃煤污染型氟中毒大鼠中的作用。方法选择SD大鼠随机分2组（每组11只，雌雄各半），设对照组、染氟组。染氟组以氟中毒病区煤烘玉米为主要饲料，复制氟中毒动物模型，检查氟斑牙、尿氟浓度及血清、肝、肾、脑组织中丙二醛（MDA）含量、超氧化物歧化酶（SOD）及谷胱甘肽还原酶（GR）活性，及血清中反映肝、肾功能的指标。结果染氟组大鼠血清、肝、肾、脑组织中MDA含量升高，SOD和GR活性明显降低（P〈0．05或P〈0．01）。同时大鼠肝、肾功能已有一定的改变。结论氟中毒大鼠机体内氧化系统与抗氧化系统失衡，氧化应激引起的氧化损伤作用在氟致大鼠肝、肾毒性中起着重要的作用。     

Selenium toxicosis assessment (in vivo and in vitro) and the protective role of vitamin B12 in male quail (Coturnix Coturnix)

The present study was undertaken to elucidate the toxicity induced by sodium selenite in male quail through in vivo and in vitro studies and the role played by vitamin B12 in alleviating selenium toxicity. Administration of selenite orally for 1 month induced hepatic oxidative damage. Selenite decreased body weight gain and increased relative liver weight. Selenite reduced hemoglobin and iron concentrations and elevated total bilirubin concentration. Serum transaminases and alkaline phosphatase activities were increased in selenium-intoxicated quails. Total protein concentration was decreased associated with the appearance of prealbumin fraction, an increased γ-globulin and a decreased α- and β-globulins. The highest level of selenium was found in liver followed by kidney, testis, faeces and blood. Supplementation of vitamin B12 orally for 1 month simultaneously with selenite caused less marked biological alteration in the investigated parameters. In vitro study using isolated quail hepatocytes incubated with sodium selenite showed a dose-dependent response for toxicity markers. These results suggest that selenosis can be reduced by vitamin B12 supplementation.     

低剂量无机汞宫内及哺乳期暴露对仔大鼠肝、肾和脑组织中谷胱甘肽抗氧化物酶系统的影响

目的　研究低剂量无机汞子宫内及哺乳期暴露对仔大鼠肝脏、肾脏及脑组织中谷胱甘肽抗氧化物酶系统的影响 ,探讨低剂量无机汞对子代发育潜在的毒性。方法　对怀孕d 0的母大鼠进行 0 .2mg·L- 1Hg2 +饮水染毒直至仔鼠出生后d 2 0断乳期。研究仔鼠肝脏、肾脏及脑区 (大脑、小脑、脑干、海马及其余脑组织 )中汞的分布及汞暴露对上述组织中总巯基含量、还原型谷胱甘肽 (GSH)水平及谷胱甘肽过氧化物酶 (GSH Px)活性的影响。结果汞暴露后仔鼠肾脏中汞的含量最高 ,其次是肝脏和脑组织。在所研究的仔鼠各脑区中 ,海马汞含量最高 ,其次是小脑和大脑。汞暴露组仔鼠肝脏和肾脏中巯基含量比对照组升高了 2倍 ,而脑区中汞暴露组巯基含量与对照组相比则降低至 1/ 2～ 1/ 3。汞暴露组仔鼠肝脏中GSH水平与对照组相比升高了6 5 % ,而在肾脏和脑组织中GSH的水平与对照组相比则显著降低 ,其中 ,汞暴露组仔鼠各脑区中GSH水平降低幅度与对照组相比均超过了 5 8%。除肝脏外 ,汞暴露组仔鼠肾脏和脑区中GSH Px活性明显下降。在脑组织中 ,除海马外 ,GSH Px活性在汞暴露组其他 4个脑区中的下降幅度均超过 80 %。结论　低剂量无机汞子宫内及哺乳期暴露对仔鼠肾脏 ,特别是对脑组织的正常发育造成了一定程度的危害 ;但上述指标对肝脏的     

HBV慢性肝病尿酶活性检测的临床意义

目的探讨尿酶(LAP、NAG、GPDA)水平对HBV慢性肝病的临床意义。方法①将研究对象分为慢性肝炎组、代偿期肝炎肝硬化组、失代偿期肝炎肝硬化组以及正常对照组,测定其晨尿中LAP、NAG、GPDA水平的变化,分析各组间LAP、NAG、GPDA活性的差异;②根据肝功损害程度将所有研究对象分为轻度、中度和重度三组,比较三组间尿LAP、NAG、GPDA水平的差异;③根据HBV DNA复制的水平,将所有研究对象分为低度和高度复制两组,分析两组间尿LAP、NAG、GPDA水平的变化。结果①代偿期及失代偿期肝硬化尿NAG、LAP和GPDA水平均明显高于正常对照组及慢性肝炎组(P<0.05和P<0.01),肝硬化失代偿期尿NAG、LAP和GPDA水平均明显高于代偿期(P<0.05);②肝功损害程度与尿NAG、LAP和GPDA活性呈正相关(P<0.05和P<0.01);③HB VDNA高度复制组和低度复制组两组比较,尿NAG、LAP和GPDA水平无显著性差异(P>0.05)。结论尿LAP、NAG、GPDA活性测定可较灵敏地反映HBV慢性肝病出现的早期肾脏损害,并可间接判断慢性肝病肝功能的损害程度;尿酶(NAG、LAP和GPDA)活性与HBV DNA复制水平无明显相关性。     

Ginkgo biloba extract protects against mercury(II)-induced oxidative tissue damage in rats.

Mercury(II) is a highly toxic metal which induces oxidative stress in the body. In this study we aimed to investigate the possible protective effect of Ginkgo biloba (EGb), an antioxidant agent, against experimental mercury toxicity in rat model. Following a single dose of 5mg/kg mercuric chloride (HgCl(2); Hg group) either saline or EGb (150mg/kg) was administered for 5days. After decapitation of the rats trunk blood was obtained and the tissue samples from the brain, lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by chemiluminescence (CL) technique. BUN, creatinin, ALT, and AST levels and tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) activity were assayed in serum samples. The results revealed that HgCl(2) induced oxidative damage caused significant decrease in GSH level, significant increase in MDA level, MPO activity and collagen content of the tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the Hg group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices. Our results implicate that mercury-induced oxidative damage in brain, lung, liver, and kidney tissues protected by G. biloba extract, with its antioxidant effects.