Cytotoxic, genotoxic, and carcinogenic effects of acrylamide on human lung cells

While an association between acrylamide (AC) exposure and the risk of developing cancer has been shown in some studies, there are very limited data on the relationship between AC exposure and lung cancer risk. Thus, we investigated the cytotoxic, genotoxic, and carcinogenic effects of AC on human lung bronchial epithelial cell line (BEAS-2B cells). AC (5 and 10 mM) significantly decreased the cell viability for all treatment times. The comet assay results showed that AC (0.5, 1 and 5 mM) increased the DNA tail (%), tail moment and olive tail moment. By using immunofluorescence, we found that AC (0.5, 1 and 5 mM) induced the formation of both phosphorylated form of the histone H2 variant H2AX (gH2AX) and p53-binding protein 1 (53BP1) foci. AC-treated BEAS2B cells exhibited various morphological and cytoplasmic changes. The transformed cells can induce form foci and significantly increase the number of colonies in soft agar. We showed for the first time that AC could induce DNA strand breaks, cell transformation, and anchorage-independent growth in BEAS-2B cells. Therefore, AC exposure can induce carcinogenesis in lung cells and may be a risk for lung cancer formation. Further studies are necessary to make a possible risk assessment in humans.

Automated summary

Research has shown that exposure to acrylamide (AC) can induce carcinogenesis in human lung cells, causing DNA strand breaks and cell transformation, which may increase the risk of lung cancer formation. Further studies are needed to assess the potential risk in humans.