急性吸入暴露于超细碳黑会改变心脏中的线粒体基质利用率
William E Mullen1,2, Jackson E Stewart1,2, Rahatul Islam1,2
1Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia, USA.
Environmental toxicology
|October 31, 2025
概括
对黑碳空气污染的急性暴露会通过改变蛋白质乙化来触发心脏线粒体功能障碍. 这导致心脏从脂肪酸转向葡萄糖代谢.
科学领域:
- 环境健康 环境健康
- 心血管研究研究心血管研究
- 线粒体生物学 线粒体生物学
背景情况:
- 空气污染,特别是碳黑等颗粒物,与心血管死亡率有关.
- 暴露于碳黑可以诱导心脏线粒体功能障碍.
- 氨酸乙化是一种关键的翻译后修改,调节蛋白质功能.
研究的目的:
- 为了研究氨酸乙化在急性碳黑暴露后心脏线粒体功能障碍中的作用.
- 通过乙化识别受黑碳暴露影响的特定蛋白质和通路.
主要方法:
- 暴露C57BL/6J小鼠的碳黑 (10毫克/立方米3为3小时).
- 分析蛋白质乙化水平和关键代谢酶 (脂肪酸和葡萄糖氧化) 的酶活性.
- 电子传输链复杂活动的评估.
主要成果:
- 碳黑暴露增加了脂肪酸氧化蛋白的乙化,降低了它们的活性.
- 观察到有降低的卡尼丁棕转移酶1b水平.
- 增加电子运输链复合物I和V的乙化,增强复合物V的活动.
- pyruvate脱酶 (葡萄糖氧化途径) 的升级,以弥补脂肪酸代谢减少.
结论:
- 急性黑碳暴露会通过改变的氨酸乙化诱导心脏线粒体功能障碍.
- 代谢从脂肪酸转移到葡萄糖利用发生在心脏中.
- 氨酸乙化在碳黑暴露引起的线粒体功能障碍中起着调节作用.
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