ArticleToxicology research2025
Benzo(a)pyrene triggers cytotoxicity by disrupting cell cycle dynamics and activating Caspase-3-mediated apoptosis in multiple human cell lines.
Article in Toxicology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benzo(a)pyrene (B(a)P), a polycyclic aromatic hydrocarbon (PAH), is a known endocrine disruptor linked to various environmentally induced diseases. While recent studies have explored its role in short- and long-term disease development, there is limited research on B(a)P's cytotoxic effects across different cell types. This study aims to evaluate the cytotoxicity of B(a)P exposure in several human cell lines under controlled conditions. We employed flow cytometry (FACS) for quantitative cytotoxicity analysis at the single-cell level. Our findings revealed that B(a)P exhibited minimal cytotoxicity in lung and liver cells, but potent toxicity in breast cells. Notably, B(a)P-induced cytotoxicity in breast cells was associated with increased cleaved caspase-3 expression, leading to cell death. This process was further linked to cell cycle arrest, as indicated by altered cyclin B1 expression in a B(a)P-dependent manner, resulting in reduced cell viability. In summary, these results suggest that breast cells are particularly sensitive to B(a)P-induced cytotoxicity, which is driven by apoptosis and cell cycle disruption.
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