Pennapa Takam, Andreas Schäffer, Sarunya Laovitthayanggoon, Wasin Charerntantanakul, Panwad Sillapawattana
{"title":"多环芳烃(PAHs)对人肺泡上皮细胞(A549)和巨噬细胞(THP-1)共培养模型的毒性效应","authors":"Pennapa Takam, Andreas Schäffer, Sarunya Laovitthayanggoon, Wasin Charerntantanakul, Panwad Sillapawattana","doi":"10.1186/s12302-024-01003-7","DOIUrl":null,"url":null,"abstract":"<div><p>Polycyclic aromatic hydrocarbons (PAHs) are particulate matter bound environmental contaminants known to cause adverse effects on human health. The toxicity of carcinogenic PAH such as benzo[a]pyrene (BaP) has been extensively investigated, whereas other PAHs have received less attention. The present work investigated the toxic effects of three less investigated PAHs with distinct molecular weights in comparison to BaP on co-culture model of human epithelial lung cells (A549) and macrophages (THP-1). Due to the involvement of more than one cell type in the response to PAH exposure, the new co-culture model is considered to be suitable for the prediction of undesired toxicological effects of PAHs. To do so, the co-culture was established and exposed to 0–400 µM of phenanthrene (PHE), fluoranthene (FLA), and, benzo [<i>ghi</i>] perylene (BghiP) for 24 h. Subsequently, cytotoxicity, micronucleus formation, and cytokine excretion were analyzed. The results revealed that the viability of A549 cells decreased after being exposed to increasing concentrations of PAHs. The formation of micronuclei in binucleated cells (BNC) was found more frequently in cells treated with PAHs in comparison to the untreated group, indicating the genotoxic effect of these compounds. Moreover, an exposure to PAHs enhanced the pro-inflammatory cytokine, i.e., interleukin-6 secretion, while diminished the anti-inflammatory cytokine, i.e., interleukin-10. In summary, PAHs possess negative effects on A549 and THP-1 co-culture model, implying an adverse effect on human health when coming into contact with these chemicals via respiration.</p></div>","PeriodicalId":546,"journal":{"name":"Environmental Sciences Europe","volume":"36 1","pages":""},"PeriodicalIF":6.0000,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1186/s12302-024-01003-7.pdf","citationCount":"0","resultStr":"{\"title\":\"Toxic effect of polycyclic aromatic hydrocarbons (PAHs) on co-culture model of human alveolar epithelial cells (A549) and macrophages (THP-1)\",\"authors\":\"Pennapa Takam, Andreas Schäffer, Sarunya Laovitthayanggoon, Wasin Charerntantanakul, Panwad Sillapawattana\",\"doi\":\"10.1186/s12302-024-01003-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Polycyclic aromatic hydrocarbons (PAHs) are particulate matter bound environmental contaminants known to cause adverse effects on human health. The toxicity of carcinogenic PAH such as benzo[a]pyrene (BaP) has been extensively investigated, whereas other PAHs have received less attention. The present work investigated the toxic effects of three less investigated PAHs with distinct molecular weights in comparison to BaP on co-culture model of human epithelial lung cells (A549) and macrophages (THP-1). Due to the involvement of more than one cell type in the response to PAH exposure, the new co-culture model is considered to be suitable for the prediction of undesired toxicological effects of PAHs. To do so, the co-culture was established and exposed to 0–400 µM of phenanthrene (PHE), fluoranthene (FLA), and, benzo [<i>ghi</i>] perylene (BghiP) for 24 h. Subsequently, cytotoxicity, micronucleus formation, and cytokine excretion were analyzed. The results revealed that the viability of A549 cells decreased after being exposed to increasing concentrations of PAHs. The formation of micronuclei in binucleated cells (BNC) was found more frequently in cells treated with PAHs in comparison to the untreated group, indicating the genotoxic effect of these compounds. Moreover, an exposure to PAHs enhanced the pro-inflammatory cytokine, i.e., interleukin-6 secretion, while diminished the anti-inflammatory cytokine, i.e., interleukin-10. 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Toxic effect of polycyclic aromatic hydrocarbons (PAHs) on co-culture model of human alveolar epithelial cells (A549) and macrophages (THP-1)
Polycyclic aromatic hydrocarbons (PAHs) are particulate matter bound environmental contaminants known to cause adverse effects on human health. The toxicity of carcinogenic PAH such as benzo[a]pyrene (BaP) has been extensively investigated, whereas other PAHs have received less attention. The present work investigated the toxic effects of three less investigated PAHs with distinct molecular weights in comparison to BaP on co-culture model of human epithelial lung cells (A549) and macrophages (THP-1). Due to the involvement of more than one cell type in the response to PAH exposure, the new co-culture model is considered to be suitable for the prediction of undesired toxicological effects of PAHs. To do so, the co-culture was established and exposed to 0–400 µM of phenanthrene (PHE), fluoranthene (FLA), and, benzo [ghi] perylene (BghiP) for 24 h. Subsequently, cytotoxicity, micronucleus formation, and cytokine excretion were analyzed. The results revealed that the viability of A549 cells decreased after being exposed to increasing concentrations of PAHs. The formation of micronuclei in binucleated cells (BNC) was found more frequently in cells treated with PAHs in comparison to the untreated group, indicating the genotoxic effect of these compounds. Moreover, an exposure to PAHs enhanced the pro-inflammatory cytokine, i.e., interleukin-6 secretion, while diminished the anti-inflammatory cytokine, i.e., interleukin-10. In summary, PAHs possess negative effects on A549 and THP-1 co-culture model, implying an adverse effect on human health when coming into contact with these chemicals via respiration.
期刊介绍:
ESEU is an international journal, focusing primarily on Europe, with a broad scope covering all aspects of environmental sciences, including the main topic regulation.
ESEU will discuss the entanglement between environmental sciences and regulation because, in recent years, there have been misunderstandings and even disagreement between stakeholders in these two areas. ESEU will help to improve the comprehension of issues between environmental sciences and regulation.
ESEU will be an outlet from the German-speaking (DACH) countries to Europe and an inlet from Europe to the DACH countries regarding environmental sciences and regulation.
Moreover, ESEU will facilitate the exchange of ideas and interaction between Europe and the DACH countries regarding environmental regulatory issues.
Although Europe is at the center of ESEU, the journal will not exclude the rest of the world, because regulatory issues pertaining to environmental sciences can be fully seen only from a global perspective.