Biomarker responses and histological damage in the gill, liver, and gonad of Cyprinus carpio with benzo(a)pyrene exposure

Sha, Weilai; Cai, Fengsen; Liu, Yu; Wang, Ying; Liu, Chunchen; Wang, Renjun; Gao, Peike

doi:10.1007/s11356-021-15065-0

Cited by 8 publications

(1 citation statement)

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“…PAHs are widely spread organic pollutants and exposure from breathing ambient (and indoor) air, consuming food containing PAHs, smoking, or inhaling smoke from an open fireplace (Kim et al, 2011, 2013; USEPA, 2005). There was evidence suggesting an association between chronic exposure of PAHs and several health outcomes, including decreased immune function, lung infections, and asthma (Oliveira et al, 2019; Sha et al, 2021; Zhang et al, 2020). Despite the structure of PAHs similarities, only some PAHs show mutagenic potential, which in turn leads to carcinogenic effects in experimental models and/or humans (Martins et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Benzo[b]fluoranthene induced oxidative stress and apoptosis in human airway epithelial cells via mitochondrial disruption

Bao

Zhao

Liu

et al. 2023

J of Applied Toxicology

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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.

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