饲粮维生素E水平对臭氧吸入大鼠肺生化反应的影响。

Drug-nutrient interactions Pub Date : 1988-01-01
N M Elsayed, R Kass, M G Mustafa, A D Hacker, J J Ospital, C K Chow, C E Cross
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引用次数: 0

摘要

我们研究了膳食维生素E水平对大鼠肺对臭氧(O3)吸入反应的影响。在一项研究中,我们给1个月大的Sprague-Dawley (SD)大鼠喂食含有0或50 IU维生素E/kg的试验饲料2个月,然后将每个饮食组中的一半动物间歇性地(每天8小时)暴露于0.8 ppm(1,568微克/立方米)O3中,另一半暴露于室内空气中7天。在O3暴露后,我们发现两种饮食组的大鼠肺中标记酶活性相对于相应的空气暴露对照组显著增加,但0 IU组的增加幅度大于50 IU组。在另一项研究中,我们给1个月大的SD大鼠喂食含有10、50或500 IU /kg维生素E的试验饲料2个月,然后将每组饲料中的一半动物连续暴露于0.8 ppm(1568微克/立方米)O3中,另一半暴露于室内空气中4天。与相应的空气暴露对照组相比,三种饮食组的O3暴露增加了大鼠肺部的代谢活动,但10 IU组的增加幅度大于50 IU或500 IU组,50 IU和500 IU组之间的差异很小。由于人们认为臭氧暴露后肺代谢的增加与更大的组织损伤有关,因此研究结果表明,饮食中缺乏维生素E会加剧吸入臭氧造成的肺损伤,而维生素E的存在则可以保护肺免受损伤。然而,这种保护作用的程度并没有随着膳食维生素E补充量的增加而成比例地增加,超过一定水平。
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Effect of dietary vitamin E level on the biochemical response of rat lung to ozone inhalation.

We examined the effects of dietary vitamin E level on rat lung response to ozone (O3) inhalation. In one study, we fed 1-month-old Sprague-Dawley (SD) rats a test diet containing 0 or 50 IU vitamin E/kg for 2 months, and then exposed one-half of the animals from each dietary group to 0.8 ppm (1,568 micrograms/m3) O3 intermittently (8 hours daily) and the other half to room air for 7 days. After O3 exposure, we found significant increases in marker enzyme activities in rat lungs from both dietary groups relative to corresponding air-exposed controls, but the magnitude of increases was greater for the 0 IU than the 50 IU group. In another study, we fed 1-month-old SD rats a test diet containing 10, 50, or 500 IU vitamin E/kg for 2 months and then exposed one-half of the animals from each dietary group to 0.8 ppm (1,568 micrograms/m3) O3 continuously and the other half to room air for 4 days. The O3 exposure increased the metabolic activities in rat lungs from all three dietary groups relative to corresponding air-exposed controls, but the magnitude of increases was greater for the 10 IU than the 50 IU or 500 IU group, and the difference between the 50 IU and 500 IU groups was small. Because a greater increase in lung metabolism after O3 exposure is thought to be associated with a greater tissue injury, the results suggest that an absence of dietary vitamin E exacerbates lung injury from O3 inhalation, while its presence protects from injury. However, the magnitude of this protective effect does not increase proportionately with increased dietary vitamin E supplementation beyond a certain level.

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