Sevanian A, Elsayed N, Hacker A D
J Toxicol Environ Health. 1982 Oct-Nov;10(4-5):743-56. doi: 10.1080/15287398209530292.
The effect of vitamin E deficiency in male Sprague-Dawley rats upon lipid peroxidation in lung tissue was examined by measuring malonaldehyde and lipid epoxide production. In addition to controls, some animals were also exposed to 3 +/- 0.1 ppm NO2 continuously for 7 d in order to study the effects of oxidant stress on lung lipid peroxidation and vitamin E content. The observed changes in malonaldehyde and epoxide content could serve as good indices of lipid peroxidation, particularly under conditions of vitamin E deprivation. The responses measured indicated an inverse relation in the lung between tissue vitamin E content and quantity of lipid peroxidation products. Measurement of lipid epoxides served as a reliable indicator of lung tissue lipid peroxidation. Finally, NO2 inhalation appeared to elicit a response characterized by increased assimilation of vitamin E into lung tissue.
通过测量丙二醛和脂质环氧化物的生成,研究了雄性斯普拉格-道利大鼠维生素E缺乏对肺组织脂质过氧化的影响。除了对照组外,一些动物还连续7天暴露于3±0.1 ppm的二氧化氮中,以研究氧化应激对肺脂质过氧化和维生素E含量的影响。观察到的丙二醛和环氧化物含量变化可作为脂质过氧化的良好指标,特别是在维生素E缺乏的情况下。所测量的反应表明,肺组织中维生素E含量与脂质过氧化产物数量呈负相关。脂质环氧化物的测量是肺组织脂质过氧化的可靠指标。最后,吸入二氧化氮似乎引发了一种反应,其特征是维生素E在肺组织中的同化增加。