Riboflavin supplementation does not attenuate hyperoxic lung injury in transgenic (spc-mt)hGR mice.
Riboflavin supplementation does not attenuate hyperoxic lung injury in transgenic (spc-mt)hGR mice.
复制标题
DOI：
10.3109/01902148.2010.516057
复制
发表时间：
2011-04
影响因子：
1.7
通讯作者：
Welty SE
中科院分区：
文献类型：
--
作者：
Heyob KM;Rogers LK;Tipple TE;Welty SE
本研究的目的是测试的假设，即小鼠表达由表面活性蛋白C启动子（spc-mthGR）驱动的靶向人谷胱甘肽还原酶（GR）是功能性核黄素缺乏，这种缺乏加剧高氧肺损伤。作者进一步假设，膳食补充核黄素（FADH）将提高GR的生物活性，从而增强对高氧肺损伤的抵抗力。转基因mt-spchGR小鼠和它们的非转基因同窝仔在断奶时喂食对照或补充核黄素的饮食。在6周龄时，小鼠暴露于室内空气（RA）或>95% O2长达84小时。在肺组织匀浆中测量GR活性（有和没有外源性FADH）和GR蛋白水平。测定谷胱甘肽（GSH）和谷胱甘肽二硫化物（GSSG）浓度，以确定体内GR活性的变化。通过右肺与体重的比值和支气管肺泡灌洗液蛋白浓度评估肺损伤。这些数据表明，肺II型细胞线粒体中GR活性的增强并不能保护成年小鼠免受高氧肺损伤。此外，在spc-mthGR小鼠的饮食中添加核黄素既不增强GR活性，也不提供对高氧肺损伤的保护。结果表明，调节肺II型细胞中的线粒体GR活性不是最小化高氧肺损伤的有效疗法。
The aims of this study were to test the hypothesis that mice expressing mitochondrially targeted human glutathione reductase (GR) driven by a surfactant protein C promoter (spc–mthGR) are functionally riboflavin deficient and that this deficiency exacerbates hyperoxic lung injury. The authors further hypothesized that dietary supplementation with riboflavin (FADH) will improve the bioactivity of GR, thus enhancing resistance to hyperoxic lung injury. Transgenic mt–spchGR mice and their nontransgenic littermates were fed control or riboflavin-supplemented diets upon weaning. At 6 weeks of age the mice were exposed to either room air (RA) or >95% O2 for up to 84 hours. GR activities (with and without exogenous FADH) and GR protein levels were measured in lung tissue homogenates. Glutathione (GSH) and glutathione disulfide (GSSG) concentrations were assayed to identify changes in GR activity in vivo. Lung injury was assessed by right lung to body weight ratios and bronchoalveolar lavage protein concentrations. The data showed that enhanced GR activity in the mitochondria of lung type II cells does not protect adult mice from hyperoxic lung injury. Furthermore, the addition of riboflavin to the diets of spc–mthGR mice neither enhances GR activities nor offers protection from hyperoxic lung injury. The results indicated that modulation of mitochondrial GR activity in lung type II cells is not an effective therapy to minimize hyperoxic lung injury.
登录
查看更多内容
影响因子：
3.6
作者：
SMITH, CV;HANSEN, TN;ELLIOTT, SJ
通讯作者：
ELLIOTT, SJ
DOI：
10.1165/rcmb.2006-0376oc
发表时间：
2007-10-01
影响因子：
6.4
作者：
Tipple, Trent E.;Welty, Stephen E.;Smith, Charles V.
通讯作者：
Smith, Charles V.
DOI：
10.1016/0272-0590(84)90097-6
发表时间：
1984-01-01
期刊：
FUNDAMENTAL AND APPLIED TOXICOLOGY
影响因子：
--
作者：
KEHRER, JP;PARAIDATHATHU, T
通讯作者：
PARAIDATHATHU, T
DOI：
10.1016/s0074-7696(08)60166-7
发表时间：
1978-01-01
期刊：
International review of cytology
影响因子：
--
作者：
Kosower, N S;Kosower, E M
通讯作者：
Kosower, E M
影响因子：
7.1
作者：
Hoey, Leane;McNulty, Helene;Strain, J. J.
通讯作者：
Strain, J. J.