Effects of aerobic exercise on histopathology and toxicology of ZnO and nano ZnO in male rats

The effects of four weeks of aerobic exercise on histopathological and toxicological effects induced by nano ZnO and ZnO powders in male rats were evaluated. Tissue sections of liver and kidneys of ZnO and nano ZnO rats showed some histopathological changes, which were partly reverted by exercise. ZnO and nano ZnO treatments caused an increase in the level of tumor necrosis factor-α, while the mean of Interleukin 10 was declined. Exercise training enhanced the mean value of and declined mean level of in rats treated with ZnO and nano ZnO. The ZnO and ZnO groups demonstrated the highest means of insulin resistance, low density lipoprotein, cholesterol, triglyceride levels and lower mean value of compared to the other groups, while exercise resulted in improvement in mean of these factors.     

邻苯二甲酸二乙基己酯(DEHP)对THP-1细胞IL-1β和MMP-8表达及ROS的影响

为探讨邻苯二甲酸二乙基己酯((DEHP)的细胞免疫毒性作用与机制,采用RT-PCR和ELISA方法,考察了0.05～1μmol·L-1浓度范围内的DEHP对THP-1细胞白细胞介素-1β(IL-1β)及基质金属蛋白酶-8(MMP-8)基因和蛋白表达的影响;采用免疫印迹WesternBlot方法检测DE-HP对ERK1/2磷酸化水平的影响;以2,'7-'二氯荧光素二乙酸酯(DCFH-DA)为荧光探针检测1～50μmol·L-1DEHP对细胞内活性氧(ROS)产生的影响。结果显示,0.05和0.2μmol·L-1DEHP在6h内显著诱导IL-1β和MMP-8基因表达(P<0.05或0.01);0.05～1μmol·L-1DEHP刺激细胞48h,可诱导IL-1β蛋白表达,并表现出明显的剂量-效应关系,线性拟合的确定系数为0.937;0.05μmol·L-1DEHP刺激细胞6或12h,显著诱导MMP-8蛋白表达(P<0.05);0.2μmol·L-1DEHP在15～30min内快速诱导ERK1/2磷酸化;1～50μmol·L-1DEHP浓度依赖性刺激细胞中ROS的产生;ERK/MAPK抑制剂PD98059显著抑制DEHP诱导的MMP-8分泌,但对IL-1β分泌未表现出抑制作用。研究表明,DEHP可能是经ERK/MAPK信号路径诱导MMP-8基因和蛋白的表达,经其他路径诱导IL-1β基因和蛋白的表达,诱导细胞内ROS的产生,从而激发炎症反应,进而损害免疫系统功能引发哮喘等炎症性疾病。此研究结果可为DEHP的暴露风险评估提供参考。     

节球藻毒素对小鼠肝脏微结构的影响研究

作为新型生物毒素,节球藻毒素(NOD)常见于爆发水华的水体中,是泡沫节球藻分泌的具有高肝毒性的次生代谢产物.由于其毒性高、暴露途径广且不易降解而日趋受到人们的重视.为了阐明NOD的肝毒性机理,本研究以模式生物小鼠为载体,研究亚慢性NOD诱导下小鼠肝脏在形态学、病理学上的微结构变化.结果表明,10 μg·kg-1.D-NOD下暴露21 d可诱导小鼠肝脏出现“草莓状表面”的肉眼可见的形态学改变.在H&E染色下,观察到在NOD暴露21d可诱导小鼠肝脏出现微小结节、细胞嗜酸性病变、炎症细胞浸润、慢性淤胆及脂肪病变等病理学现象.当暴露时间延长到28 d时,嗜酸性病变恶化并出现嗜酸小体在TEM观察下,小鼠肝细胞在NOD的诱导下出现肝细胞核皱缩、染色质凝集或边集、线粒体嵴横纹加深及分布散乱、内质网肿胀、核糖体脱粒等现象,并且在胞质中多有观察到微泡性脂肪变性及吞噬小泡.上述变化充分说明,在亚慢性暴露条件下,NOD依然具有强烈肝毒性.引起NOD慢性肝中毒的主要原因是肝细胞嗜酸性病变及炎症的诱发,并在暴露时间延长后进一步恶化,肝板结构破坏更加严重.     

NLRP3 inflammasome activation determines the fibrogenic potential of PM2.5 air pollution particles in the lung

Airborne fine particulate matter(PM_2.5) is known to cause respiratory inflammation such as chronic obstructive pulmonary disease and lung fibrosis. NLRP3 inflammasome activation has been implicated in these diseases; however, due to the complexity in PM_2.5compositions, it is difficult to differentiate the roles of the components in triggering this pathway. We collected eight real-life PM_2.5samples for a comparative analysis of their effects on NLRP3 inflammasome ...     

Immunotoxic potential of aeration lagoon effluents for the treatment of domestic and hospital wastewaters in the freshwater mussel Elliptio complanata

Municipal wastewaters are major sources of pollution for the aquatic biota. The purpose of this study was to determine the levels of some pharmaceutical products and the immunotoxic potential of a municipal wastewater aeration lagoon for the treatment of the domestic wastewaters of a small town with wastewater inputs from a 400-bed hospital complex. Endemic mussels were collected, caged and placed in the final aeration lagoon and at sites 1 km upstream and 1 km downstream of the effluent outfall in the receiving river for a period of 14 days. The results showed that the final aeration lagoon contained high levels of total coliforms, conductivity and low dissolved oxygen (2.9 mg/L) as well as detectable amounts of trimethoprim, carbamazepine, gemfibrozil, and norfloxacin at concentrations exceeding 50 ng/L. The lagoon effluent was indeed toxic to the mussel specimens, as evidenced by the appearance of mortality after 14 days (10% mortality), decreased mussel weight-to-shell-length ratio and loss of hemocyte viability. The number of adhering hemocytes, phagocytic activity, total nitrite levels and arachidonic cyclooxygenase activity were significantly higher in mussels placed in the final aeration lagoon. A multivariate analysis also revealed that water pH, conductivity, total coliforms and dissolved oxygen were the endpoints most closely linked with phagocytic activity, the amount of adhering hemocytes and loss of hemocyte viability. In conclusion, exposure of mussels to treated aerated lagoon wastewater is deleterious to freshwater mussels where the immune system is compromised.     

聚苯乙烯微塑料对糖尿病小鼠肾脏的影响

以糖尿病小鼠为模式生物,探究了100nm和5μφ的聚苯乙烯微塑料(PSMPs)(200μg/L)通过饮水暴露28d后对小鼠肾脏的毒性.结果表明,糖尿病小鼠对PSMPs的暴露更加敏感,100nm和5μm PSMPs暴露导致糖尿病小鼠肾脏出现明显的炎性细胞浸润和淤血等病理损伤,且 100nm PSMPs对肾脏造成的病理损伤...     

Inhalation of two putative Gulf War toxins by mice

We employed our inhalation methodology to examine whether biomarkers of inflammation and oxidative stress would be produced in mice following inhalation of aerosols containing carbonaceous particles or the vapor of pesticides prevalent during the first Gulf War. Exposure to two putative Gulf War Illness toxins, fine airborne particles and the pesticide malathion, increased biomarkers of inflammation and oxidative stress in Friend virus B (FVB) female mice. Mice inhaling particles 24 h before had increased lung lavage and plasma Leukotriene B4 (LTB₄) (a biomarker of inflammation) and PGF_2α (a biomarker of oxidative stress) levels, lung lavage protein and lung lavage lactic dehydrogenase (LDH) levels. These changes were a function of particle density and exposure time. Compared to particle inhalation, mice inhaling malathion 24 h before had small increase in plasma LTB₄ and PGF_2α levels but no increase in lung lavage LTB₄, lung lavage protein, lung lavage LDH, and lung lavage alveolar macrophage (AM) levels compared to unexposed control mice. AM from particle-exposed mice contained phagocytosed particles, while AM from malathion-exposed mice showed no abnormalities. Our results indicate that inhaling particles or malathion can alter inflammatory and oxidative biomarkers in mice and raise the possibility that these toxins may have altered inflammation and oxidative stress biomarkers in Gulf War-exposed individuals.     

甲醛经口染毒致小鼠脏器损伤和炎症反应的研究

为探讨在单独染毒和卵清蛋白(OVA)联合致敏的条件下,甲醛灌胃染毒对小鼠造成的毒性效应,将雄性Balb/c小鼠随机分为7组:对照组(蒸馏水组);OVA致敏组;2mg/(kg·d) FA(甲醛)组;20mg/(kg·d) FA组;200mg/(kg·d) FA组;200mg/(kg·d)FA+ OVA组;200mg/(kg·d) FA+ OVA +MT(褪黑素)组,以蒸馏水和不同浓度甲醛溶液灌胃,连续21d. OVA致敏组,200mg/(kg·d) FA+ OVA组,200mg/(kg·d) FA+ OVA +MT组在第6,13,20d进行腹腔注射OVA致敏;此外,200mg/(kg·d) FA+ OVA +MT组,每天用1.0mg/mL褪黑素灌胃小鼠(小鼠灌胃剂量10mg/(kg·d)),连续21d.检测肝,肾和肺组织中活性氧自由基(ROS),丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,并采用ELISA法检测肝组织中IL-4和IFN-γ的水平.结果表明,与对照组相比,甲醛浓度为200mg/(kg·d),小鼠肝脏ROS含量增加(P<0.05),MDA含量增加以及小鼠肾脏GSH含量降低,均有显著性差异(P<0.05).OVA作为致敏剂,甲醛浓度为200mg/(kg·d)时,肝组织中IL-4(Interleukin-4)含量增加(P<0.01),10mg/(kg·d)褪黑素能够降低200mg/(kg·d)甲醛+OVA染毒小鼠肝脏内ROS含量(P<0.05).综上,200mg/(kg·d)甲醛灌胃染毒能使小鼠产生氧化损伤和炎症反应, ROS, MDA水平上升(P<0.05),GSH水平下降(P<0.05),肝脏中细胞因子IL-4水平上升(P<0.01), IFN-γ水平下降(P<0.05).     

大气细颗粒物与糖尿病

随着我国社会经济和城市化的快速发展,大气颗粒物是影响我国城市空气质量的首要污染物,大气细颗粒物污染已严重威胁我国居民健康。本文简要综述了PM2.5诱导的氧化应激和炎症反应在糖尿病的发生和发展中的分子作用机制。