Benzo[b]fluoranthene (BbF) is a common constituent of polycyclic aromatic hydrocarbons (PAHs). While numerous studies revealed adverse effects of PAHs on human health, the health effects of individual PAHs differ, and few investigations were performed on BbF. Therefore, the present study established cytotoxicity models of human lung epithelial cells (BEAS-2B cells) and bronchial epithelial cells (16HBE cells) exposed to BbF (10, 20, and 40 μM) for 24 h to reveal the mechanisms. Results from cytotoxicity and proliferation studies demonstrated that BbF inhibited cell growth in a dose-dependent manner. Flow cytometric analysis showed that BbF induced the appearance of a sub G1 peak, S-phased arrest, and apoptosis in both cells. Mechanistic investigations illustrated that BbF promoted reactive oxygen species (ROS) production, altered the expression of oxidative stress indicators, and decreased mitochondrial membrane potential. BbF also interfered with the expression of regulators associated with mitochondria disruption pathway. Taken together, these results strongly suggested that BbF inhibited cell growth and induced apoptosis in human airway epithelial cells via ROS-mediated mitochondria disruption.

中文翻译：

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苯并[b]荧蒽通过线粒体破坏诱导人气道上皮细胞的氧化应激和细胞凋亡

苯并[b]荧蒽 (BbF) 是多环芳烃 (PAH) 的常见成分。虽然大量研究揭示了多环芳烃对人类健康的不利影响，但个别多环芳烃对健康的影响各不相同，而且很少有人对 BbF 进行调查。因此，本研究建立了人肺上皮细胞（BEAS-2B 细胞）和支气管上皮细胞（16HBE 细胞）暴露于 BbF（10、20 和 40 μM）24 小时的细胞毒性模型，以揭示其机制。细胞毒性和增殖研究的结果表明，BbF 以剂量依赖性方式抑制细胞生长。流式细胞术分析表明，BbF 在两种细胞中诱导亚 G1 峰、S 期阻滞和细胞凋亡的出现。机理研究表明 BbF 促进了活性氧 (ROS) 的产生，改变氧化应激指标的表达，降低线粒体膜电位。BbF 还干扰了与线粒体破坏途径相关的调节因子的表达。总之，这些结果强烈表明 BbF 通过 ROS 介导的线粒体破坏抑制细胞生长并诱导人气道上皮细胞凋亡。