首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  完全免费   2篇
  综合类   2篇
  2020年   1篇
  2015年   1篇
排序方式: 共有2条查询结果,搜索用时 27 毫秒
1
1.
Particulate matter exposure has been described to elevate the risk of lung and cardiovascular diseases. An increasing number of recent studies have indicated positive correlations between PM2.5 (the fraction of airborne particles with an aerodynamic diameter less than 2.5 μm) exposure and the risk of liver diseases. However, research on the effects of PM2.5 exposure on liver fat synthesis, secretion, and clearance mechanisms under normal diet conditions is limited, and whether these effects are age-dependent is largely unknown. Female C57BL/6 mice at different ages (4 weeks (4 w), 4 months (4 m), and 10 months (10 m)) were treated with 3 mg/kg body weight of PM2.5 every other day for 4 weeks. Subsequently, the ultrastructural changes of liver, the expression of genes involved in oxidative damage and lipid metabolism in the liver were examined. Observation of hepatic ultrastructure showed more and larger lipid droplets in the livers of 4-week-old and 10-month-old mice exposed to PM2.5. Further analysis showed that PM2.5 exposure increased the expression of genes related to lipid synthesis, but decreased the expression of genes involved in lipid transport and catabolism in the livers of 10-month-old mice. Our findings suggest that exposure to PM2.5 disrupts the normal metabolism of liver lipids and induces lipid accumulation in the liver of female mice in an age-dependent manner, with older mice being more susceptible to PM2.5.  相似文献
2.
Since a real atmospheric scenario usually represents a system involving multiple pollutants, air pollution studies typically focused on describing adverse effects associated with exposure to individual pollutants cannot reflect actual health risk. Particulate matter (PM10) and sulfur dioxide (SO2) are two major pollutants derived from coal combustion processes and co-existing in coal-smoke air pollution, but their potentially synergistic toxicity remains elusive thus far. In this study, we investigated the cytotoxic responses of PM10 and SO2, singly and in binary mixtures, using human non-small cell lung cancer A549 cells, followed by clarifying the possible mechanisms for their interaction. The results indicated that the concomitant treatment of PM10 and SO2 at low concentrations led to synergistic injury in terms of cell survival and apoptosis occurrence, while PM10 and SO2 alone at the same concentrations did not cause damage to the cells. Also, radical oxygen species (ROS) production followed by nuclear factor kappa B (NF-κB) activation was involved in the above synergistic cytotoxicity, which was confirmed by the repression of the actions by an ROS inhibitor (NAC). This implies that assessment of health risk should consider the interactions between ambient PM and gaseous copollutants.  相似文献
1
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号