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首页> 外文期刊>American Journal of Physiology >Loss of lung mitochondrial aconitase activity due to hyperoxia in bronchopulmonary dysplasia in primates.
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Loss of lung mitochondrial aconitase activity due to hyperoxia in bronchopulmonary dysplasia in primates.

机译：灵长类动物支气管肺发育不良中的高氧导致肺线粒体乌头酸酶活性下降。

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摘要

The premature primate exposed to hyperoxia provides a useful model of bronchopulmonary dysplasia. A critical target in hyperoxic injury is the mitochondrial matrix enzyme aconitase. We hypothesized that this enzyme's activity would decline in the premature baboon lung during exposure to hyperoxia. Total aconitase activity was significantly decreased in the lungs of premature baboons of 140 days gestation with exposure to 100% oxygen for 6-10 days compared with as needed [pro re nada (PRN)] oxygen exposure and fetal controls (P = 0.0001). In activity gels, lungs from 100% oxygen-exposed animals (6-10 days) showed a nearly complete loss of mitochondrial aconitase activity relative to lungs from animals exposed only to PRN oxygen. Decreased lung aconitase activity was not a nonspecific effect of hyperoxia, causing mitochondrial damage or loss, because the activity of the mitochondrial respiratory enzyme cytochrome oxidase was not different in lungs of 100% oxygen-exposed relative to PRN oxygen-exposed newborns. In 125-day-gestation premature primates (age 6-10 days), lung total aconitase activity was correlated with inspired oxygen tension (r = 0.73 for fraction of inspired oxygen > 0.35), whereas, for animals of 140 days gestation, no such correlation was found. Thus the more premature animal's lung was more susceptible to loss of aconitase.
机译：暴露于高氧血症的过早的灵长类动物提供了支气管肺发育不良的有用模型。高氧损伤的关键目标是线粒体基质酶乌头酸酶。我们假设该酶的活性在高氧暴露下会在狒狒的早产肺中降低。与需要的[pronada（PRN）]氧气暴露和胎儿对照组相比，妊娠140天的早产狒狒的肺中总乌头酸酶活性显着降低（P = 0.0001）。在活性凝胶中，相对于仅暴露于PRN氧气的动物的肺，来自100％暴露于氧气的动物的肺（6-10天）显示线粒体乌头酸酶活性几乎完全丧失。肺乌头酸酶活性降低不是高氧的非特异性作用，会引起线粒体损伤或丢失，因为相对于PRN氧暴露的新生儿，线粒体呼吸酶呼吸活动细胞色素氧化酶的活性在100％氧暴露的肺中没有差异。在妊娠125天的灵长类动物（6-10天）中，肺总乌头酸酶活性与吸入的氧气张力相关（吸入氧气的分数> 0.35时r = 0.73），而对于妊娠140天的动物则没有这样的关系。找到相关性。因此，较早的动物的肺对乌头酸酶的损失更敏感。

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