Ayaz K L, Csallany A S
Arch Environ Health. 1978 Nov-Dec;33(6):292-6. doi: 10.1080/00039896.1978.10667350.
One hundred and twenty female mice fed diets containing various levels of vitamin E were continuously exposed to 0.5 ppm, 1.0 ppm nitrogen dioxide (NO2), and filtered air for 17 months. Blood, lung, and liver tissues were assayed for glutathione peroxidase (GSH-peroxidase) activity. Exposure to 0.5 ppm NO2 did not affect blood and lung GSH-peroxidase activity; 1.0 ppm NO2 exposure, however, caused suppression of the enzyme. A combination of vitamin E deficiency and 1.0 ppm NO2 exposure resulted in the lowest GSH-peroxidase activities in the blood and lung. High levels of vitamin E in the diet resulted in elevated GSH-peroxidase in the blood and lung. Liver GSH-peroxidase activity was unaffected by either dietary vitamin E or NO2 exposure. No inverse relationship was found between GSH-peroxidase levels and concentrations of organic solvent soluble lipofuscin pigments present in tissues.
120只喂食含有不同水平维生素E饮食的雌性小鼠，持续暴露于0.5 ppm、1.0 ppm二氧化氮（NO2）以及过滤空气中17个月。对血液、肺和肝脏组织进行谷胱甘肽过氧化物酶（GSH-过氧化物酶）活性检测。暴露于0.5 ppm NO2未影响血液和肺中GSH-过氧化物酶活性；然而，暴露于1.0 ppm NO2会导致该酶受到抑制。维生素E缺乏与暴露于1.0 ppm NO2共同作用，导致血液和肺中GSH-过氧化物酶活性最低。饮食中高水平的维生素E导致血液和肺中GSH-过氧化物酶升高。肝脏GSH-过氧化物酶活性不受饮食中维生素E或NO2暴露的影响。未发现GSH-过氧化物酶水平与组织中存在的有机溶剂可溶性脂褐素色素浓度之间存在负相关关系。
