纳米级SiO2对雄性大鼠睾丸组织的氧化损伤作用

目的 探讨微米和纳米级SiO2对雄性大鼠生殖功能的影响.方法 将Wistar大鼠随机分为5组[7.5 mg/ml纳米级SiO2组、1.5 mg/ml纳米级SiO2组、7.5 mg/ml微米级SiO2组、1.5 mg/ml微米级SiO2组、对照组(生理盐水)],采用非暴露式气管内注入法,按1 ml/kg体重染毒5周后,称重,计算睾丸、附睾的脏器系数,检测睾丸组织及血清中氧化和抗氧化指标[丙二醛(MDA)、超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)].结果 各染毒组睾丸组织中,MDA、GSH含量均高于对照组,SOD、GSH-Px活力均低于对照组.7.5mg/ml纳米级SiO2组血清中,MDA含量高于对照组,差异有统计学意义(P＜0.05);其余各组GSH含量和SOD、GSH-Px活力与对照组比较,差异均无统计学意义(P＞0.05).相同剂量纳米组与微米组各指标间比较,差异均无统计学意义(P＞0.05).结论 微米和纳米级SiO2对大鼠睾丸组织产生氧化损伤作用;与微米级SiO2相比,纳米级SiO2的损伤作用更为严重.     

PM_(2.5)对大鼠肝、脾、肾组织的氧化损伤效应

目的探讨PM2.5对大鼠肝、脾、肾组织抗氧化酶活力和脂质过氧化(LPO)水平的影响。方法选取32只雄性Wistar大鼠,随机分为4组,分别用0、1.5、7.5、37.5mg/kg的PM2.5经气管注入染毒后24h处死大鼠,测定肝、脾、肾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)活力,谷胱甘肽(GSH)和硫代巴比妥酸反应物(TBARS)含量。结果PM2.5染毒组大鼠肝、肾组织内SOD、CAT、GSH-Px活力和SOD/TBARS比值均较对照组降低(P<0.05,P<0.01),具有剂量-效应关系。各染毒组TBARS/GSH-Px比值较对照组显著升高(P<0.01,P<0.001)。染毒组脾、肾组织GSH含量较对照组显著下降(P<0.05,P<0.01),而染毒组肝组织GSH含量则出现先升高后降低的非线性变化特征(P<0.01,P<0.05)。染毒组肝组织LPO水平出现剂量-效应性升高(P<0.05),染毒组脾组织各种抗氧化酶活力、LPO水平和TBARS/GSH-Px比值均未见显著变化。结论PM2.5可引起大鼠肝、肾组织的氧化损伤。     

不同粒径SiO2致A549细胞毒性及氧化损伤作用实验研究

目的探讨纳米SiO2及纳米/微米复合SiO2颗粒对A549细胞的毒性效应及氧化损伤作用。方法将纳米、微米、纳米/微米复合SiO2按照不同作用浓度(0、3.13、6.25、12.5、25.0、50.0、100、200μg/ml),对A549细胞进行染毒作用24h后,采用CCK-8法测定A549细胞的抑制率,DCFH-DA荧光染色法标记检测细胞活性氧(ROS)水平,微量酶标法测定细胞乳酸脱氢酶(LDH)活力。结果与阴性对照组比较,纳米、微米、纳米/微米复合组细胞抑制率均升高(P<0.05);且纳米/微米复合组始终高于纳米组及微米组。低浓度时微米SiO2对细胞抑制率高于纳米SiO2。随着浓度的增加,纳米组高于微米组(P<0.05)。各暴露组ROS水平则呈剂量-效应关系。同浓度纳米SiO2组高于微米SiO2组,且纳米/微米复合SiO2组高于同浓度纳米组及微米组。与阴性对照组比较,染毒组LDH水平升高,存在剂量-效应关系。同浓度纳米组高于微米组,纳米/微米复合组高于纳米组及微米组(P<0.05)。结论不同粒径SiO2均可引起A549细胞抑制率升高、ROS水平升高和细胞膜损伤。且纳米/微米复合SiO2组强于纳米组及微米组,同浓度纳米SiO2组高于微米组,说明粒径越小,对细胞损伤越大,而氧化损伤可能是纳米SiO2致细胞凋亡的一个途径。     

纳米与微米级二氧化硅粉尘对小鼠氧化和抗氧化指标的影响

目的 观察纳米SiO2和微米SiO2粉尘对雄性小鼠血清中超氧化物歧化酶(SOD)同工酶活力、丙二醛(MDA)含量、总抗氧化能力(TAOC)的影响.方法 将70只昆明种小鼠随机分成7组,每组lO只,设1个对照组,6个染毒组(纳米SiO2组50、100、200mg/m3,微米SiO2组50、100、200mg/m3),染尘14 d,每天1 h,染尘结束后测定小鼠血清中SOD活力、MDA含量、TAOC水平.结果 与对照组比,纳米SiO2 50 mg/m3组SOD活力[(217.46±118.07)U/ml]明显降低,100、200 mg/m3组SOD活力明显增高,差异有统计学意义(P＜0.05);纳米SiO2 100、200 mg/m3 组MDA含量明显低于对照组,差异有统计学意义(P＜0.05).随剂SiO2染尘量增加,微米SiO2组SOD活力呈降低趋势,MDA含量呈现增高趋势,与对照组比较,差异有统计学意义(P＜0.05).各纳米SiO2组TAOC分别为(8.24±1.15)、(12.60±3.53)、(9.52±3.53)U/ml,与相应微米组SiO2相比,TAOC明显降低,差异有统计学意义(P＜0.05).结论 纳米与微米SiO2粉尘均对小鼠产生氧化损伤作用,纳米SiO2粉尘对小鼠的氧化损伤作用更严重.     

谷胱甘肽和α-硫辛酸对锰致大鼠体内过氧化反应的影响

将Wistar大鼠32只随机分为4组,即对照组、单纯染锰组、硫辛酸(LA)干预组、谷胱甘肽(GSH)干预组。对照组腹腔注射生理盐水,其余各组腹腔注射MnCl2150μmol/kg,2 h后,对照组、单纯染锰组皮下注射生理盐水,每周染毒5次;硫辛酸干预组皮下注射LA 35μmol/kg,谷胱甘肽干预组皮下注射GSH 1 mmol/kg,隔日干预,共计4周。测定肝、脑和肾组织中的谷胱甘肽(GSH)、丙二醛含量(MDA)和谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性。结果与对照组比较,单纯染锰组肝、脑、肾组织中的MDA含量均升高(P<0.05),GSH含量和GSH-Px、SOD的活性都有不同程度的降低;两干预组肾组织中MDA含量降低(P<0.01,P<0.05)。与单纯染锰组比较,GSH干预组肝组织的MDA、GSH含量降低(P<0.05),SOD、GSH-Px活性升高(P<0.05),脑和肾组织的MDA含量降低(P<0.05,P<0.01);LA干预组肝组织SOD、GSH-Px的活性升高(P<0.01),脑、肾组织的MDA含量降低(P<0.05,P<0.01)。提示GSH和LA对锰致大鼠氧化损伤有一定的拮抗作用。     

亚硒酸钠和N-乙酰半胱氨酸对锰致大鼠氧化损伤的影响

目的探讨亚硒酸钠(Na2SeO3)和N-乙酰半胱氨酸(NAC)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、Na2SeO3干预组和NAC干预组。对照组大鼠腹腔注射生理盐水,其余各组腹腔注射150μmol/kgMnCl2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,Na2SeO3干预组隔日皮下注射10μmol/kg Na2SeO3,NAC干预组隔日皮下注射1 mmol/kg NAC。每周染锰5次,1次/d,染毒4周。共计染锰20次,Na2SeO3和NAC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,染锰大鼠肝、脑和肾组织MDA含量显著升高,肝肾组织GSH含量降低。Na2SeO3和NAC干预均使脑和肾组织MDA含量显著降低。Na2SeO3干预组大鼠肾GSH含量显著增加,肝GSH-Px和SOD活力降低。NAC干预组大鼠脑SOD活力显著降低。结论锰可使大鼠产生氧化损伤,Na2SeO3和NAC对锰致大鼠氧化损伤有一定的拮抗作用。     

大鼠急性羰基镍中毒各脏器谷胱甘肽过氧化物酶水平动态观察

目的探讨大鼠急性羰基镍中毒各脏器谷胱甘肽过氧化物酶(GSH-Px)活力变化。方法 SD大鼠200只,分为低、中、高剂量羰基镍实验组、氯气染毒对照组和正常对照组,每组各40只。3个实验组分别给予20、135、250 mg/m3羰基镍染毒,氯气染毒对照组给予250 mg/m3氯气染毒,正常对照组未予特殊处理。静态吸入染毒,染毒时间为30 min,每组染毒1次,染毒后1、2、3和7 d取材,应用化学比色法测定肺、肝、肾、心和脾脏GSH-Px活力。结果在低、中、高剂量羰基镍染毒条件下,大鼠肺、肝、肾、心GSH-Px活力均有下降,以高剂量羰基镍实验组GSH-Px下降最显著(P<0.05);不同取材时间GSH-Px活力比较,染毒后3 d脏器GSH-Px活力下降最明显(P<0.05);氯气染毒后各脏器GSH-Px活力均显著下降(P<0.05)。结论急性羰基镍中毒可诱发组织氧化损伤,降低机体清除自由基的能力,并存在组织差异。     

血液灌流对急性百草枯中毒兔氧化应激和基质金属蛋白酶及其抑制物的影响

目的 观察血液灌流(hemoperfusion,HP)对急性百草枯(PQ)中毒兔氧化指标和基质金属蛋白酶(MMP)-2、MMP-9及基质金属蛋白酶组织抑制因子-1(TIMP-1)的影响,探讨HP对急性PQ中毒兔的治疗作用及机制.方法 将78只日本大耳白兔随机分成正常对照组(N组)6只、PQ中毒组(PQ组)24只、HP治疗组24只、空白对照组(HP对照组)24只.后3组动物分为1、3、7、21d4个观察时间组,N组给予5 ml生理盐水灌胃;PQ组每只兔经口一次灌胃PQ (50 mg/kg); HP治疗组兔经口一次灌胃PQ (50 mg/kg)后于1h内予活性炭HP治疗2h,HP对照组给予等量生理盐水灌注后1h内予无吸附柱灌流2h.分别测定不同处理后动物肺、肝脏、肾脏中丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力,并用免疫组化SP法检测MMP-2和MMP-9及TIMP-1表达.结果 随观察时间的延长,PQ组和HP治疗组兔肺、肝、肾组织中MDA含量呈下降趋势,SOD及GSH-Px活力呈上升趋势.PQ组与HP治疗组肺、肝、肾组织MMP-2、MMP-9、TIMP-1在第1天表达均增强,PQ组最为明显,随观察时间的延长,各种阳性表达仍呈较高水平.与N组比较,PQ中毒组和HP治疗组动物肺、肝、肾组织中SOD、GSH-Px活力明显降低,肺、肝、肾组织中MDA含量增高;肺、肝、肾组织中MMP-2、MMP-9、TIMP-1含量明显增加,差异均有统计学意义(P＜0.05,P＜0.01).与PQ组比较,HP治疗组动物肺、肝、肾组织中SOD、GSH-Px活力明显升高,MDA含量降低;肺、肝、肾组织中MMP-2、MMP-9、TIMP-1含量降低,但高于N组,差异均有统计学意义(P＜0.01).结论 急性PQ中毒引起的脏器损伤可能与氧化应激及基质金属蛋白酶异常变化有关,HP可能通过改善组织清除自由基的能力及下调兔肺、肝、肾组织中MMP-2、MMP-9和TIMP-1含量,上调组织中MMP-9/TIMP-1比值而发挥救治PQ中毒、保护脏器功能的作用.     

短期暴露于纳米SiO_2对HaCaT细胞基因组DNA甲基化的影响

目的探讨纳米SiO2对体外培养细胞基因组总体DNA甲基化水平的影响。方法分别以2.5、5、10μg/ml纳米SiO2溶液和10μg/ml微米级SiO2处理人皮肤表皮细胞系(HaCaT)24h;以3μmol/L DNA甲基化转移酶抑制剂5-脱氧杂氮胞苷(DAC)处理48 h的10μg/ml组为阳性对照,并设立溶剂对照组。应用高效毛细管电泳(HPCE)定量分析纳米SiO2处理细胞24h后,基因组DNA总体甲基化的变化,用Q-PCR和Western Blot方法检测甲基化相关蛋白mRNA和蛋白的表达变化,并用DNA甲基化转移酶活性试剂盒检测DNA甲基化转移酶的活性。结果 HPCE定量分析结果显示纳米SiO2可引起HaCaT细胞总体甲基化程度降低,呈剂量依赖性关系;与正常细胞相比,微米SiO2以及2.5、5和10μg/ml纳米SiO2组分别降低37.8%、43.9%、54.9%和52.8%,差异有显著性(P<0.05);对照组5-aza-dC处理后使HaCaT细胞甲基化程度减少27.3%。各组酶的蛋白表达与mRNA表达水平及DNMTs活性变化具有相同的变化趋势,经纳米SiO2处理的HaCaT细胞,DNMT1、DNMT3a及MBD2表达随着纳米SiO2剂量的上升而下降,DAC组表达水平最低。结论纳米SiO2能引起HaCaT细胞整体基因组DNA甲基化水平降低,可能与DNA甲基化转移酶的酶活性降低有关。     

铜绿的亚慢性健康效应研究

目的探讨长期经口暴露铜绿对大鼠健康的影响及其可能的作用机制。方法选用80只SPF级SD大鼠,雌雄各半,随机分为4组,铜绿染毒剂量分别为0、7.3、24.4和73.2mg/kg。每周大鼠经口灌胃染毒6天,第7天称重,连续13周,记录动物的外观体征、行为活动等。13周末处死动物,观察大鼠血清生化指标和尿液指标;取脑、心、肝、肾、胃和脾等脏器称重并对脏器进行病理学检查,同时测定组织匀浆中的丙二醛(MDA)水平、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力。结果大鼠的行为活动、摄食饮水、粪便尿液、组织超微结构正常,动物体重增加。与对照组比较,低剂量组雄性大鼠体重显著增加(P<0.05);高剂量组大鼠血清乳酸脱氢酶活性较对照组显著降低(P<0.05);实验组大鼠肝脏、脑、心脏SOD活力增加,心脏GSH-Px活性增强,与对照组比较,差异有统计学意义(P<0.05);中、高剂量组大鼠胃SOD、GSH-Px活性显著降低,MDA含量显著增高(P<0.05)。结论在一定的暴露剂量下,铜绿可明显增加大鼠体重,提高大鼠肝、心和脑的抗氧化酶的活性,但是过量的铜绿会对胃组织产生一定的氧化损伤。     

纳米和微米SiO2吸入染毒对大鼠氧化损伤指标的比较研究

OBJECTIVE: To compare the changes of oxidative damage in rats inhaled by nano-sized and micro-sized silicon dioxide. METHODS: 36 male rats were randomly divided into two control groups and four experimental groups which was inhaled by nano-sized and micro-sized silicon dioxide respectively at the concentration of 300 mg/m3 for 2 hours and the activities of SOD, CAT and GSH-Px and the contents of H2O2, GSH and MDA of the liver, kidney, brain were determinated 24h and 48h after inhalation. RESULTS: The contents of H2O2 in all organs in nano-sized groups increased significantly while increased in micro-size groups only in liver and kidney at 24h and in brain at 48h. On the contrary, the activities of CAT in nano-sized group were lower than those in micro-sized group. Superoxide anion contents increased only in the brain of nano-sized group. The activities of SOD decreased significantly in nano-sized groups in kidney at 24h and brain but not in micro-sized groups. The content of GSH decreased only in liver at 24h. The activities of GSH-PX decreased significantly in nano-sized compared with control group and were lower significantly in brain than those in micro-sized group. The contents of MDA increased in all nano-sized groups but only in liver and brain in micro-sized group. The total anti-oxygen activities decreased in all nano-sized groups, but only in kidney at 24h and brain in micro-sized group, especially more significantly in brain at 48h in nano-sized than micro-sized group. While the activity in kidney in nano-sized group increased at 48h comparing to at 24h. CONCLUSION: Nano-sized silicon dioxide could induce oxidative damage more easily than micro-sized silicon dioxide. Through comparing different interval, it was found that the degree of oxidative damage at 48h after inhalation inferior to that at 24h after inhalation, which could be associated with the repair of the body against the oxidative damage.     

八氯二丙醚吸入染毒对小鼠脏器组织的氧化损伤作用

[目的]研究八氯二丙醚(octachlorodipropyl ether)吸入染毒对小鼠肝、肾、脾、肺细胞的氧化损伤作用。[方法]采用静式吸入染毒法,研究不同染毒羰基含量(282、564、1128 mg/m3,连续染毒20 d,每天1h)对小鼠的氧化损伤作用,染毒结束后测定各脏器丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)及羰基含量。 [结果] 高浓度(1128 mg/m3)染毒组中,小鼠肝、脾、肺MDA、羰基含量与对照组比差异有显著性(P<0．05);肺 MDA含量、羰基含量随染毒浓度的增加而增加,且呈剂量-反应关系(P<0．05)。高浓度组肝、脾、肺SOD、GSH-Px的活性下降且与对照组比差异有显著性(P<0．05);肾脏细胞各观察指标与对照组的差异均不显著。[结论]八氯二丙醚吸入染毒可引起小鼠肝、脾、肺的氧化损伤,肺脏可能是其主要的靶器官。     

亚硒酸钠对镉和汞肝肾氧化损伤影响的实验研究

目的:观察一次染镉和汞对大鼠肝、肾组织氧化损伤作用,探讨亚硒酸钠预处理对镉和汞氧化损伤的影响。方法:Wister大鼠48只,随机分成6组,每组8只,第1组为染镉实验对照组,第2组为单纯染镉组,第3组为亚硒酸钠预处理组,第4组为染汞实验对照组,第5组为单纯染汞组,第6组为亚硒酸钠预处理干预组。第1、4组大鼠先腹腔注射生理盐水,2 h后皮下注射生理盐水。第2组大鼠先腹腔注射生理盐水,2 h后皮下注射35μmol/kg氯化镉溶液。第3组大鼠先腹腔注射10μmol/kg亚硒酸钠溶液,2 h后皮下注射35μmol/kg氯化镉溶液。第5组大鼠先腹腔注射生理盐水,2 h后皮下注射2.5 mg/kg HgCl2溶液,第6组大鼠先腹腔注射20μmol/kg亚硒酸钠溶液,2 h后皮下注射2.5 mg/kg HgCl2溶液。染毒24 h后测定肝、肾皮质镉或汞、谷胱甘肽、丙二醛含量和谷胱甘肽过氧化物酶活性。结果:与对照组比较,单纯染镉组大鼠肝GSH、MDA含量显著升高,GSH—Px活性显著下降。Na2SeO3预处理组肝、肾皮质GSH和镉含量显著降低,肝脏GSH—Px活性及肾皮质MDA含量显著升高。单纯染汞组大鼠肝、肾皮质及尿汞含量均显著高于对照组。单纯染汞组肝MDA含量显著高于对照组,GSH含量和GSH—Px活性显著低于对照组。Na2SeO3预处理组的肝脏GSH含量和GSH—Px活性均较单纯染汞组升高,有显著性差异。单纯染汞组肾皮质MDA含量显著高于对照组,GSH含量和GSH—Px活性显著降低。Na2SeO3预处理组中肾皮质MDA含量低于单纯染汞组,GSH—Px含量高于单纯染汞组。结论:给大鼠一次染镉和汞,可以对肝和肾脏产生明显的氧化损伤作用。亚硒酸钠对急性染镉和汞所致肝肾损伤具有一定的拮抗作用,其机制可能与增加内源性GSH、使GSH—Px活性增强以及清除自由基能力提高有关。     

Effect of Sulfur Dioxide Inhalation on the Glutathione Redox System in Mice and Protective Role of Sea Buckthorn Seed Oil

This study investigated the effects of sulfur dioxide (SO₂) inhalation and protection by sea buckthorn seed oil from oxidative damage caused by SO₂ in male Kunming-strain mice. One approach was set up to study the effects of SO₂ inhalation on changes of the mice antioxidant defense system. SO₂ at different concentrations (22 ± 2, 64 ± 3, and 148 ± 23 mg/m³) was administered to animals in treatment groups for 7 days, 6 h per day, while control groups were exposed to filtered air under the same condition. The activities of glutathione-S-transferase (GST) and glucose-6-phosphate dehydrogenase (G6PD) and the contents of reduced glutathione (GSH) in brain, lung, heart, liver, and kidney of mice were measured. In the case of inhalation of a SO₂ concentration of 148 ± 23 mg/m³, the activities of GST and G6PD and contents of GSH in the brain, lung, heart, liver, and kidney were significantly decreased. Dose-dependent relations were found between various SO₂-exposed concentrations and the activities of GST and G6PD and the content of GSH. Meanwhile another approach was taken to determine whether sea buckthorn seed oil could maintain the glutathione redox system and prevent the oxidative damage of lung induced by SO₂. In groups given a high dosage (6 or 8 ml/kg) intraperitoneally, the level of TBARS (thiobarbituric acid-reactive substances) was decreased significantly (p < 0.05) by the injection of sea buckthorn seed oil, and the activity of GST was increased significantly (p < 0.05). Overall GST activity and TBARS level exhibited a significant negative correlation (r = 0.891, p < 0.05). The observations showed that SO₂ inhalation resulted in a significant change in the glutathione redox system and indicated that sea buckthorn seed oil could contribute to the antioxidant effects in the case of SO₂ exposure.     

沙棘油对汞致急性肝、肾损伤的保护作用

[目的]探讨急性染汞致大鼠肝、肾毒性的作用机制,观察沙棘油（SBO）的保护作用。[方法]24只Wistar大鼠随机均分为：阴性对照组（皮下注射0．9％生理盐水）;染汞组（皮下注射2．5mg／kgHgCl：）;SBO＋HgCl2组[灌胃SBO（体积分数为95％）5mL／kg,2h后皮下注射2．5mg／kgHgCl2］。染汞后12h将大鼠移入代谢笼,收集12h尿样。染汞48h后处死,采取血样和肝肾组织。测定肝脏、肾皮质和尿汞含量;尿N-乙酰-β—D-氨基葡萄苷酶（NAG）、碱性磷酸酶（ALP）、乳酸脱氢酶（LDH）活性和尿蛋白、血清尿素氮（BUN）含量;肝、肾中谷胱甘肽（GSH）、丙二醛（MDA）、蛋白含量和超氧化物岐化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性。[结果]与对照组相比,HgCl2组、SBO＋HgCl2组的肝、肾皮质及尿汞含量均明显增加（P〈0．01）;与HgCl2组相比,SBO＋HgC｜2组尿汞含量增加（P〈0．05）。HgCl2组尿NAG、ALP、LDH活性和尿蛋白、BUN含量均明显高于对照组（P〈0．01）;SBO＋HgCl2组NAG、ALP活性和BUN含量均低于HgCl2组（分别为P〈0．05,P〈0．01和P〈0．01）。与对照组相比,HgCl2组肝、肾GSH含量、GSH—Px活性、SOD活性均下降（P〈0．01）,MDA含量增加（P〈0．05或P〈0．01）;SBO＋HgCl2组与HgCl2组相比,其肝GSH-Px活性明显增加（P〈0．01）。[结论]大鼠经一次染汞后可致急性肝、肾损伤。沙棘油具有促进汞从肾脏排出的作用,对汞致肝脏氧化损伤有一定保护作用。     

二氧化硫对小鼠超氧化物歧化酶活性的影响

[目的]观察二氧化硫（SO2）对小鼠9种脏器超氧化物歧化酶（SOD）活性的影响。[方法]采用整体动物吸入染毒方式，测定小鼠吸入SO2气体后不同脏器SOD活性的变化。[结果]小鼠吸入较低浓度的SO2后，SOD活性变化因脏器而异；肝，肾，心，脾，脑，小肠，睾丸组织的SOD活性呈下降趋势，肺和胃组织的SOD活性呈上升趋势，但在较高SO2吸入浓度下，9种脏器SOD活性显著下降。[结论]SO2吸入体内会引起机体上述组织抗氧化能力下降。造成机体的氧化损伤。     

模拟400m氦氧饱和潜水对大鼠抗氧化能力的影响

[目的]观察模拟400m氦氧饱和潜水对大鼠抗氧化能力的影响。[方法]将大鼠在加压舱4．1MPa氦氧环境中饱和暴露24h,以常压和4．1MPa常氧高氦环境作为对照。出舱后测定大鼠肝、脑和肺中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—px）活性和还原型谷胱甘肽（GSH）、丙二醛（MDA）及8-羟基脱氧鸟苷（8-OhdG）含量。[结果]4．1MPa氦氧饱和暴露后大鼠脑SOD活性和肝、脑和肺GSH—Px活性降低（P〈0．05）,脑和肺GSH含量减少（P〈0．05）。4．1MPa常氧高氦暴露后大鼠各指标未见明显改变（P〉0．05）。各组MDA和8-OhdG含量差异无统计学意义（P〉0．05）。[结论]模拟400m氦氧饱和潜水24h使大鼠产生了氧化应激反应,抗氧化能力降低,其原因可能与该环境中的高分压氧有关。     

乙二醛对小鼠谷胱甘肽过氧化物酶活力及巯基含量的影响

目的：观察乙二醛对小鼠全血及组织中谷胱甘肽过氧化物酶(GSH-Px)活力及巯基含量的影响,以探讨乙二醛毒作用机制。方法：40只昆明种小鼠随机分为对照组和低、中、高(75,150,300mg／kg)3个剂量染毒组,腹腔注射乙二醛水溶液染毒,染毒24h后测定小鼠全血、肝、脑、心、肾组织中的GSH-Px活力、总巯基(T—SH)、非蛋白巯基(NP—SH)和蛋白巯基(PB—SH)的含量。结果：乙二醛可使小鼠全血和肝、肾GSH-Px活力下降;高剂量组的脑组织及各剂量组全血中T—SH及PB—SH含量增加,而高剂量组的全血、脑和肾脏及各剂量组肝脏的NP—SH含量下降。结论：乙二醛对全血和肝脏、肾脏的GSH-Px活力及对全血、肝、脑、肾中的NP-SH含量的影响主要表现为抑制。对全血及脑中TSH及．PB—SH含量的影响表现为应激性增高。     

Enzymatic and nonenzymatic antioxidants as an adaptation to phagocyte-induced damage in Anguilla anguilla L. following in situ harbor water exposure

Anguilla anguilla L. were caged for 8 and 48 h in harbor water of Aveiro Lagoon, Portugal. Respiratory burst activity (RBA) of peritoneal, head kidney, and gill phagocytes was measured. Lipid peroxidation (LPO) was estimated in gill, kidney, and liver. Liver ethoxyresorufin-O-deethylase (EROD) activity, cytochrome P450 (Cyt P450) content, and bile metabolites were assayed. Various antioxidant enzymes, viz., glutathione peroxidase, catalase, and glutathione S-transferase and nonenzymatic antioxidant, viz., total reduced glutathione were also studied. Harbor water xenobiotics induced a significant RBA increase in gill after 8 h; whereas in peritoneum and head kidney it increased after 48 h exposure. These responses were adversely associated with tissue-specific peroxidative damage since significant LPO increase was observed in gill (8 and 48 h), kidney (48 h), and liver (48 h). The tissue most affected was gill. Moreover, liver EROD activity, Cyt P450 content and bile metabolites remain unaltered after 8 h; in contrast, 48 h exposure showed significant EROD activity decrease and pyrene-type bile metabolites increase. Decreased EROD activity may be associated with concomitant liver damage, as increased LPO was observed after 48 h. Furthermore, the tissue-specific damage corresponded to the differences in the antioxidant potentials of the tissues, since the initial exposure period caused a significant increase in liver antioxidant activities, whereas gill and kidney showed a significant decrease, demonstrating that liver is highly adaptive to oxidative damage. However, at 48 h exposure gill, kidney, and liver showed a suppressive antioxidant effect, probably due to PAHs, since a significant induction at PAH-type bile metabolites has been seen. Our results demonstrate that phagocyte activation and associated peroxidative damage are concomitantly corroborated with enzymatic and nonenzymatic antioxidant activity differences. In addition, hepatic antioxidant induction after short-term exposure may serve as a potent biomarker for water pollutants in fish.     

南瓜提取物对慢性苯染毒小鼠抗氧化酶的影响

目的：探讨南瓜提取物对慢性苯中毒所造成的机体抗氧化系统损伤的拮抗作用。方法：将小白鼠分为正常组、苯染毒组、苯＋南瓜提取物组，静式吸入染毒，60d后，取其肝、脾、脑检测组织匀浆中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）的活性及丙二醛（MDA）的含量。结果：苯染毒组小鼠机体内SOD、GSH—Px活性均降低，MDA含量升高，南瓜提取物组小鼠机体内SOD、GSH—Px活性均升高，MDA含量降低，结论：慢性苯染毒能够对机体的抗氧化酶系统产生损伤，导致机体组织内SOD、GSH—Px活性降低，MDA含量升高。而南瓜提取物能够减轻机体的氧化损伤，增强抗氧化系统的功能。