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二氧化氮对大鼠肺、肝和肾膜成分的亚急性影响。

Subacute effects of nitrogen dioxide on membrane constituents of lung, liver, and kidney of rats.

作者信息

Takahashi Y, Mochitate K, Miura T

出版信息

Environ Res. 1986 Oct;41(1):184-94. doi: 10.1016/s0013-9351(86)80180-3.

DOI:10.1016/s0013-9351(86)80180-3
PMID:3019657
Abstract

Male Wistar rats were exposed to 0.4, 1.2, and 4.0 ppm nitrogen dioxide (NO2) for up to 14 weeks to examine subacute effects of NO2 on membrane constituents of lung, liver, and kidney. In the lung, cytochrome P-450 decreased to 59% (P less than 0.01) and 57% (P less than 0.01) of the control values after 1 and 10 weeks of exposure to 4.0 ppm NO2, respectively, and remained at control levels at other exposure periods. The activity of succinate-cytochrome c reductase also decreased to 75% (P less than 0.01) of the control values after 2, 4, and 14 weeks of exposure to 4.0 ppm NO2, respectively. Exposures to 0.4 and 1.2 ppm NO2 resulted in similar patterns of alterations in these enzymes. In the liver, cytochrome P-450 decreased to 72% (P less than 0.01), 70% (P less than 0.05), and 73% (P less than 0.05) of the control values after 1, 5, and 8 weeks of exposure to 4.0 ppm NO2, respectively, and remained at control levels at other exposure periods. The activity of NADPH-cytochrome P-450 reductase also decreased in a fashion similar to cytochrome P-450. Exposures to 0.4 and 1.2 ppm NO2 resulted in similar patterns of alterations in these enzymes. In addition, cytochrome b5 showed a reduced value between 5 and 12 weeks of exposures to 1.2 and 4.0 ppm NO2 and then recovered. In the kidney, all components of the microsomal electron-transport systems increased during 12-week exposures to 1.2 and 4.0 ppm NO2. These results show that subacute exposures to 0.4-4.0 ppm NO2 caused a periodic reduction in microsomal cytochrome P-450 and mitochondrial succinate-cytochrome c reductase in the lung and in components of the microsomal electron-transport systems in the liver, whereas exposures to 1.2 and 4.0 ppm NO2 resulted in induction of the microsomal electron-transport systems in the kidney.

摘要

将雄性Wistar大鼠暴露于0.4、1.2和4.0 ppm的二氧化氮(NO₂)中长达14周,以研究NO₂对肺、肝和肾膜成分的亚急性影响。在肺中,暴露于4.0 ppm NO₂ 1周和10周后,细胞色素P - 450分别降至对照值的59%(P < 0.01)和57%(P < 0.01),在其他暴露时间段保持在对照水平。琥珀酸 - 细胞色素c还原酶的活性在暴露于4.0 ppm NO₂ 2周、4周和14周后也分别降至对照值的75%(P < 0.01)。暴露于0.4和1.2 ppm NO₂导致这些酶的变化模式相似。在肝脏中,暴露于4.0 ppm NO₂ 1周、5周和8周后,细胞色素P - 450分别降至对照值的72%(P < 0.01)、70%(P < 0.05)和73%(P < 0.05),在其他暴露时间段保持在对照水平。NADPH - 细胞色素P - 450还原酶的活性也以与细胞色素P - 450相似的方式降低。暴露于0.4和1.2 ppm NO₂导致这些酶的变化模式相似。此外,细胞色素b5在暴露于1.2和4.0 ppm NO₂的5至12周期间显示值降低,然后恢复。在肾脏中,在暴露于1.2和4.0 ppm NO₂的12周期间,微粒体电子传递系统的所有成分均增加。这些结果表明,亚急性暴露于0.4 - 4.0 ppm NO₂会导致肺中微粒体细胞色素P - 450和线粒体琥珀酸 - 细胞色素c还原酶以及肝脏中微粒体电子传递系统成分的周期性减少,而暴露于1.2和4.0 ppm NO₂会导致肾脏中微粒体电子传递系统的诱导。

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