Elsayed N M, Hacker A D, Kuehn K, Mustafa M G, Schrauzer G N
Toxicol Appl Pharmacol. 1983 Dec;71(3):398-406. doi: 10.1016/0041-008x(83)90027-3.
We examined the influence of dietary selenium (Se) on the pulmonary biochemical response to ozone (O3) exposure. For 11 weeks, weanling female strain A/St mice were fed a test diet containing Se either at 0 ppm (-Se) or 1 ppm (+Se). Each diet contained 55 ppm vitamin E (vit E). Mice from each dietary group were exposed to 0.8 +/- 0.05 ppm (1568 +/- 98 micrograms/m3) O3 continuously for 5 days. After O3 exposure, they were killed along with a matched number of unexposed controls, and their lungs were analyzed for various biochemical parameters. The Se contents of lung tissue and whole blood were determined, and the levels were seven- to eightfold higher in +Se mice than in -Se mice, reflecting the Se intake of the animals. In unexposed control mice, Se deficiency caused a decline in glutathione peroxidase (GP) activity relative to +Se group. After O3 exposure, the GP activity in the -Se group was associated with a lack of stimulation of glutathione reductase (GR) activity and the pentose phosphate cycle (PPC) as assessed by measuring glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) activities. In contrast, the +Se group after O3 exposure exhibited increases in all four enzyme activities. Other parameters, e.g., lung weight, total lung protein, DNA and nonprotein sulfhydryl contents, and O2 consumption, were not affected by dietary Se in the presence or absence of O3 exposure. The data indicate that dietary Se alters the GP activity, which in turn influences the GR and PPC activities in the lung evidently through a reduced demand for NADPH. The level of vit E in the lung was found to be twofold higher in the -Se group than in the +Se group, suggesting a compensatory relationship between Se and vit E in the lung. With O3 exposure, both Se and vit E contents further increased in the lungs of each dietary group. It is plausible that Se and vit E under oxidant stress are "mobilized" to the lung from other body sites.
我们研究了膳食硒(Se)对肺部对臭氧(O3)暴露的生化反应的影响。在11周的时间里,将断乳的雌性A/St品系小鼠喂食含硒量为0 ppm(-Se)或1 ppm(+Se)的试验饮食。每种饮食都含有55 ppm的维生素E(维生素E)。将每个饮食组的小鼠连续5天暴露于0.8±0.05 ppm(1568±98微克/立方米)的O3中。O3暴露后,将它们与相同数量的未暴露对照一起处死,并分析其肺部的各种生化参数。测定了肺组织和全血中的硒含量,+Se组小鼠的硒含量比-Se组高7至8倍,反映了动物的硒摄入量。在未暴露的对照小鼠中,相对于+Se组,硒缺乏导致谷胱甘肽过氧化物酶(GP)活性下降。O3暴露后,通过测量葡萄糖-6-磷酸脱氢酶(G6PD)和6-磷酸葡萄糖酸脱氢酶(6PGD)活性评估,-Se组中的GP活性与谷胱甘肽还原酶(GR)活性和磷酸戊糖途径(PPC)缺乏刺激有关。相反,O3暴露后的+Se组在所有四种酶活性上均表现出增加。在有或没有O3暴露的情况下,其他参数,例如肺重量、肺总蛋白、DNA和非蛋白巯基含量以及耗氧量,均不受膳食硒的影响。数据表明,膳食硒会改变GP活性,进而明显通过降低对NADPH的需求来影响肺部的GR和PPC活性。发现-Se组的肺中维生素E水平比+Se组高两倍,表明肺中硒和维生素E之间存在补偿关系。随着O3暴露,每个饮食组的肺中硒和维生素E含量进一步增加。在氧化应激下,硒和维生素E从身体其他部位“动员”到肺部是合理的。