二氧化硫吸入对小鼠9种脏器谷胱甘肽过氧化物酶活性的影响

[目的 ]探索SO2 吸入染毒的氧化损伤作用及其毒理作用的机制。 [方法 ]研究SO2 吸入对小鼠肝、肺、肾、心、脾、脑、胃、小肠及睾丸 9种脏器谷胱甘肽过氧化物酶 (GSH Px)活性的影响。小鼠每天吸入染毒 6h ,连续 7d ,浓度分别为 (2 2± 2 )mg/m3 和 (64± 3 )mg/m3 。 [结果 ]在SO2 浓度为 (2 2± 2 )mg/m3 时 ,雄鼠肺中GSH Px活性显著升高 ,肾和肝略有升高 ,其余脏器均有所降低 ,其中心脏降低尤为显著 ;雌性的GSH Px活性普遍升高 ,其中肺和脑显著升高。在SO2 浓度为 (64± 3 )mg/m3 时 ,雌、雄小鼠各器官中GSH Px活性均下降 ,雄鼠在肝、肺、肾、心、脑、胃、肠及睾丸中的下降达到显著性水平 (P <0 0 5或P <0 0 1) ,且降低程度大于雌鼠。 [结论 ]SO2 可引起小鼠不同脏器细胞内抗氧化酶 (GSH Px)活性的改变 ,导致机体抗氧化损伤的能力下降 ,使之对外来化学物氧化损伤作用的敏感性增高     

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。     

二氧化硫对小鼠胃组织氧化损伤的作用

目的　了解二氧化硫 (SO2 )对哺乳动物胃组织的毒理作用及其机制。方法　采用SO2 动态吸入SO2 技术 ,使昆明小鼠吸入SO2 ,浓度为 (2 2± 2 ) ,(6 4± 3) ,(1 4 8± 2 3)mg/m3 ,每天 6h ,连续 7d ,分析该小鼠胃组织氧化损伤及抗氧化状态。结果　在SO2 浓度为 2 2mg/m3 时 ,雄鼠胃组织的超氧化物歧化酶(SOD)、过氧化氢酶 (CAT)活力及雌鼠胃组织的脂质过氧化 (LPO)水平显著升高 ;在SO2 浓度为 6 4mg/m3和 1 4 8mg/m3 时 ,雌、雄鼠胃组织的LPO水平显著升高 ,SOD酶活力和还原型谷胱甘肽 (GSH)含量显著下降。结论　吸入SO2 可引起小鼠胃组织多种抗氧化指标发生显著变化 ,表明SO2 对小鼠胃组织产生了氧化损伤作用 ;SO2 的毒理作用与其诱发产生过量自由基有关     

氧化应激效应与SO2全身性毒作用研究

目的　探讨二氧化硫 (SO2 )能否引起多种脏器氧化损伤 ,以及SO2 是否是一个全身性的毒物。方法　小鼠经SO2 吸入染毒 (56mg/m3 ,6h/d× 7d)后 ,测定其 9种脏器 (脑、肺、心、肝、胃、肠、脾、肾及睾丸 )组织的脂质过氧化(LPO)水平和抗氧化状态的变化。结果　SO2 引起 :(1)所有测试器官组织的LPO水平显著升高 ;(2 )抗氧化酶超氧化物歧化酶和谷胱甘肽过氧化物酶活性显著降低 ,但是过氧化氢酶活性除肝下降外 ,其他脏器无显著变化 ;(3 )抗氧化物质谷胱甘肽显著降低。结论　 (1)SO2 能够引起小鼠全身多种器官的氧化损伤 ,是一种全身性有毒物质 ;(2 )氧化损伤是SO2 毒性作用的机制之一。为了阐明SO2 对人和哺乳动物多种器官甚至全部器官的毒作用 ,进一步研究是必要的。     

二氧化硫吸入对小鼠各脏器过氧化氢酶活性的影响

[目的]探讨SO2对小鼠不同组织的氧化损伤及其毒作用机制。[方法]对昆明种小鼠采用动式吸入法进行22，64，148mg/m^3SO2三个浓度染毒，用分光光度法测定各器官的过氧化氢酶（CAT）活性。[结果]22mg/m^3SO2吸入时，雌雄小鼠各脏器CAT活性有上升趋势，但统计学上差异不显著；64mg/m^3SO2吸入时，各脏器CAT活性有下降趋势。 在148mg/m^3浓度时，肝，肺，肾，脑中CAT活性下降比较显著，而胃，小肠中的CAT显著升高。[结论]SO2的动式吸入可引起小鼠部分脏器CAT活性下降，对机体造成氧化损伤，且损伤程度随SO2浓度的增大而增强。     

二氧化硫对小鼠肾脏的氧化损伤作用

目的：研究SO2对小鼠肾脏的氧化损伤作用。方法：160只小鼠随机分成4组,每一组又分为对照组和染毒组,染毒组分别吸入不同浓度的SO2(7,14,28,56mg／m^3),每天4h,连续染毒7d。染毒结束后立即进行还原性谷胱甘肽(GSH)含量、谷胱甘肽过氧化物酶(GSH—Px)和超氧化物歧化酶(SOD)酶活力、脂质过氧化物产物丙二醛(MDA)含量的测定。结果:雄鼠吸入SO2浓度为7mg／m^3时,肾脏组织GSH含量显著增加,吸人SO2浓度为56mg／m^3时,GSH含量显著降低;雌鼠吸入SO2浓度为56mg／m^3时,GSH含量也显著降低。随着SO2吸入浓度的增加,雌雄小鼠GSH—Px酶活力显著降低,雄鼠变化大于雌鼠。吸入SO2浓度为7,14,28mg／m^3 SO2时,小鼠肾脏组织SOD酶活力没有明显变化,吸入SO2浓度为56mg／m^3时,SOD酶活力显著降低。吸入SO2浓度为7,14,28mg／m^3时,小鼠肾脏组织MDA含量没有明显变化,吸入SO2浓度为56mg／m^3时,MDA含量显著升高。结论:肾脏可能是SO2毒理作用的重要靶器官之一,脂质过氧化作用可能是SO2肾脏毒性的机制之一。     

二氧化硫致小鼠脑胃蛋白质氧化损伤作用

目的 探讨SO2吸入后对小鼠脑和胃蛋白的氧化损伤程度和毒作用机制.方法 将小鼠随机分为14,28,56 mg/m3 3个剂量组分别进行SO2吸入染毒,用2,4-二硝基苯肼(DNPH)比色法和氯化钾十二烷基磺酸钠(KC1-SDS)沉淀法分别测定脑组织和胃组织蛋白质的羰基含量(PCO)和DNA-蛋白质交联率(DPC).结果 SO2可导致雌、雄小鼠脑细胞PCO和DPC升高,且呈现明显的剂量-效应关系(复相关系数r2≥0.984 0);SO2浓度为14、28、56 mg/m3时,脑PCO分别升高17.4%、38.2%和72.9%,DPC分别升高15.2%、22.1%和42.8%;在SO2浓度为28,56 mg/m3时升高具有统计学意义(P＜0.05);雌性小鼠脑细胞DPC升高较雄性小鼠明显;SO2未引起雌、雄小鼠胃细胞PCO和DPC的明显改变.结论 SO2吸入可致雌、雄小鼠脑PCO和DPC升高,产生氧化损伤,但未引起小鼠胃PCO和DPC明显改变.     

甲醛染毒对大鼠子代脏器及血液细胞的影响

[目的]探讨甲醛对大鼠子代脏器及血液细胞的影响。[方法]按一代一窝繁殖法进行生殖毒性试验,选用体重110~130gWistar大鼠120只,随机分为4组,每组雌鼠20只、雄鼠10只,采用静式吸入染毒,雌、雄大鼠每天染毒1h,每周7d,连续染毒24周,高、中、低组的甲醛浓度分别为(119.6±15.4)、(25.2±4.6)、(4.8±1.3)mg/m3,对照组为室内空气;并检测仔鼠脏器系数及血常规。[结果]随着染毒浓度的增加、时间的延长,各染毒组子代大鼠体重与对照组比较呈下降趋势(P<0.05);雄性仔鼠心、肺、脑、睾丸和雌性仔鼠肺、脑的脏器系数呈上升趋势,而肝脏的脏器系数呈下降趋势(P<0.05);仔鼠血液中白细胞、中性粒细胞、单核细胞及血小板值呈现下降趋势,而嗜酸性粒细胞值呈上升趋势(P<0.05)。[结论]说明甲醛可抑制大鼠子代的生长发育,损伤肝脏、脑、肺、心及睾丸等器官,并可影响仔鼠的非特异性免疫及凝血功能。     

甲醛吸入对小鼠不同组织器官谷胱苷肽水平的影响

目的　探讨经不同浓度甲醛吸入对小鼠不同组织器官的氧化损伤作用及其分子机理。方法　用 1m g/ m3和 3m g/ m3的甲醛气体对小鼠进行染毒处理 ,测定吸入甲醛后 5种器官 (脑、心、肝、肺、肾 )的谷胱苷肽 (GSH)含量。结果　吸入 1mg/ m3甲醛的小鼠 ,心、肺、肝、肾的 GSH含量明显下降 (P<0 .0 1,P<0 .0 5 ) ,其中心最为严重 ;吸入 3mg/ m3甲醛的小鼠 ,所试全部器官的 GSH水平均显著下降 (P<0 .0 0 1,P<0 .0 1,P<0 .0 5 ) ,脑、心、肾最为严重 ,肺次之 ,肝较轻。结论　气态甲醛对机体的各组织器官均有氧化损伤作用 ,是一种全身性毒物。     

二氧化硫对小鼠肺组织氧化损伤的效应

目的研究不同浓度SO2对小鼠肺组织还原性谷胱甘肽(GSH)含量、谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)活力及脂质过氧化产物丙二醛(MDA)含量的影响。方法160只昆明小鼠随机分成4组,每一组再分为对照组和染毒组,染毒组分别吸人不同浓度(7,14,28,56mg／m^3)的SO2,4h／d,连续染毒7d。染毒结束后立即进行各项指标的测定。结果SO2吸人浓度为7mg／m^3时,雄鼠肺组织匀浆上清液GSH含量明显升高,随着SO2浓度的增加,GSH含量显著降低;雌鼠在SO2吸人浓度为7,14,28mg／m^3时均无明显变化,仅在56mg／m^3时极显著降低。在上述4种SO2浓度下,雌雄小鼠的GSH-Px活力均显著降低或极显著降低。吸人较低浓度SO2(7,14mg／m^3)时,雌雄小鼠的SOD活力和MDA含量均无明显变化,但在较高浓度(28,56mg／m^3)时则显著或极显著降低。结论SO2吸入可引起肺组织的氧化损伤,且氧化损伤作用随SO2吸人浓度的增加而加强。     

Study of the response of superoxide dismutase in mouse organs to radon using a new large-scale facility for exposing small animals to radon

We examined dose-dependent or dose rate-dependent changes of superoxide dismutase (SOD) activity using a new large-scale facility for exposing small animals to radon. Mice were exposed to radon at a concentration of 250, 500, 1000, 2000, or 4000 Bq/m(3) for 0.5, 1, 2, 4, or 8 days. When mice were exposed to radon at 2000 day?Bq/m(3), activation of SOD activities in plasma, liver, pancreas, heart, thymus, and kidney showed dose-rate effects. Our results also suggested that continuous exposure to radon increased SOD activity, but SOD activity transiently returned to normal levels at around 2 days. Moreover, we classified the organs into four groups (1. plasma, brain, lung; 2. heart, liver, pancreas, small intestine; 3. kidney, thymus; 4. stomach) based on changes in SOD activity. Thymus had the highest responsiveness and stomach had lowest. These data provide useful baseline measurements for future studies on radon effects.     

Evaluation of the redox state in mouse organs following radon inhalation

Radon inhalation activates antioxidative functions in mouse organs, thereby contributing to inhibition of oxidative stress-induced damage. However, the specific redox state of each organ after radon inhalation has not been reported. Therefore, in this study, we evaluated the redox state of various organs in mice following radon inhalation at concentrations of 2 or 20 kBq/m³ for 1, 3 or 10 days. Scatter plots were used to evaluate the relationship between antioxidative function and oxidative stress by principal component analysis (PCA) of data from control mice subjected to sham inhalation. The results of principal component (PC) 1 showed that the liver and kidney had high antioxidant capacity; the results of PC2 showed that the brain, pancreas and stomach had low antioxidant capacities and low lipid peroxide (LPO) content, whereas the lungs, heart, small intestine and large intestine had high LPO content but low antioxidant capacities. Furthermore, using the PCA of each obtained cluster, we observed altered correlation coefficients related to glutathione, hydrogen peroxide and LPO for all groups following radon inhalation. Correlation coefficients related to superoxide dismutase in organs with a low antioxidant capacity were also changed. These findings suggested that radon inhalation could alter the redox state in organs; however, its characteristics were dependent on the total antioxidant capacity of the organs as well as the radon concentration and inhalation time. The insights obtained from this study could be useful for developing therapeutic strategies targeting individual organs.     

Effects of bisphenol A on the metabolisms of active oxygen species in mouse tissues

We investigated the modifications in endogenous antioxidant capacity, including superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, oxidative stress index, reduced glutathione (GSH), glutathione disulfide (GSSG), and thiobarbituric acid-reactive substance (TBARS) in the brain, liver, kidney, and testes of mice under bisphenol A (BPA), an endocrine disrupter, treated for 5 days. BPA was administrated intraperitoneally at doses of 25 and 50mg/kg/day. The TBARS levels were not affected by BPA administrations. The SOD activities increased and the catalase activities decreased in the liver after BPA administration. The GPx activity decreased in the kidney. The levels of GSH+GSSG increased in the brain, kidney, liver, and testes, while, the levels of GSH decreased in the testes. SOD converts superoxide into hydrogen peroxide, and catalase and GPx convert hydrogen peroxide into hydrogen oxide. Our results suggest that the injection of BPA induces overproduction of hydrogen peroxide in the mouse organs. Hydrogen peroxide is easily converted to hydroxy radical. The decrease of GSH and the increase of GSSG may be caused by the hydroxy radical. BPA may show its toxicity by increasing hydrogen peroxide.     

氯化锂对小鼠脂质过氧化及抗氧化酶的影响

观察氯化锂对小鼠血液和组织中脂质过氧化及抗氧化酶的影响。「方法」以氯化锂为受试剂,昆明种小鼠为受试对象,进行小鼠血液、心、肝、肾、肺、脑、睾丸、卵巢组织中脂质过氧化产物（ＬＰＯ）,谷光甘肽过氧化物酶和超氧化物歧化酶含量测定。结论一定剂量的氯化锂可能通过刺激体内产生自由基而对细胞产生一定的损害作用。     

Oxidative damage of sulfur dioxide inhalation on lungs and hearts of mice

Effects of sulfur dioxide (SO2) on concentrations of thiobarbituric acid-reactive substances (TBARS) and reduced glutathione (GSH), activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were investigated in lungs and hearts of Kunming albino mice of both sexes. The mice of SO2 groups were exposed to various concentrations (22, 56, and 112 mg/m3) of SO2 in separate exposure chambers for 6 h/day for 7 days, whereas control groups were exposed to filtered air under otherwise the same conditions. Our results show that SO2 caused lipid peroxidation and changes of antioxidative status in both lungs and hearts of mice. Exposure to SO2 at all concentrations tested caused a significant increase of TBARS and a significant decrease in GSH content in lungs and hearts of mice, with the exception of GSH content in the hearts of female mice. For lungs, SO2 at low concentrations significantly increased SOD and GPx activities, whereas at high concentrations it significantly decreased these same activities in mice of both sexes. For hearts, SO2 at all tested concentrations significantly decreased activities of SOD from mice of both sexes, as well as that of GPx from male mice, but the decrease of GPx activities in hearts from female mice was statistically insignificant. SO2 inhalation tended to decrease activities of CAT in lungs and hearts from mice of both sexes, whereas only the decrease of CAT activities caused by SO2 in lungs from male mice was statistically significant, at 112 mg/m3. The results also show a gender difference in oxidative stress and antioxidation status caused by SO2 exposure. These results lead us to conclude that SO2 exposure can cause oxidative damage to lungs and hearts of mice, and SO2 is toxic not only to the respiratory system, but to the heart as well. Additional work is required to understand the toxicological role of SO2 on many or even all mammalian organs.     

气态甲醛对小鼠不同组织器官SOD的抑制作用

目的 探讨经不同浓度气态甲醛暴露的小鼠,不同组织器官的氧化损伤作用及其分子机理。方法 用不同剂量气态甲醛对小鼠进行染毒处理72 h,测定吸入甲醛后5种脏器(脑、心、肺、肝、肾)超氧化物歧化酶(SOD)的水平。结果 吸入1.2 mg/m3甲醛的小鼠,肝脏组织的SOD活性显著下降(P<0.01);吸入3.7 mg/m3甲醛的小鼠,肝脏、肾脏、肺组织的SOD活性均显著下降(P<0.001,P<0.01,P<0.05),其中对肝脏组织SOD的抑制作用尤为明显。结论 气态甲醛对机体组织器官有氧化损伤作用,其分子机理涉及对SOD的抑制作用。