Hypoxia-inducible factor 1α modulates acrolein-induced cellular damage in bronchial epithelial cells.

Acrolein, a highly reactive α,β-unsaturated aldehyde, is a widespread environmental pollutant. It is generated during the incomplete combustion of materials such as tobacco smoke, petrol, coal, forest fires, and plastics, as well as from the overheating of frying oils. Acrolein is known to induce cellular damage and oxidative stress. This study investigates the critical role of hypoxia-inducible factor 1α (HIF-1α), which is a transcription factor required to regulate cell survival and angiogenesis, in protecting bronchial epithelial cells from acrolein-induced cytotoxicity and DNA damage under normoxic and hypoxic conditions. To our knowledge, no prior study has comprehensively evaluated the effects of HIF-1α on cellular responses to acrolein under normoxic and hypoxic conditions in vitro. Therefore, the goal of this study was to explore how silencing HIF-1α influences cellular responses to acrolein, and our study focused on changes in cytotoxicity, metabolic activity, DNA damage, and oxidative stress using the BEAS-2B cell line. We observed enhanced cell damage and reduced viability in cells exposed to acrolein when silenced with HIF-1α, particularly in hypoxic environments. While results indicate that silencing HIF-1α significantly increases cytotoxicity and DNA damage under hypoxia compared to normoxic conditions, oxidative stress indicator levels did not rise noticeably under hypoxia following HIF-1α silencing. This research warrants further investigation to indicate the importance of HIF-1α in adapting to environmental and hypoxic stressors, which are commonly found in chronic lung diseases and ischemic conditions.