Propylparaben-induced endoplasmic reticulum stress triggers G2/M phase cell cycle arrest and initiates caspase-3-dependent apoptosis in human lung cells.

Abstract

Listen

Translate article

Propylparaben (PrP) is commonly used as an antimicrobial agent in food, cosmetics, and pharmaceuticals. While recent studies have shown that PrP exposure can cause various disruptions in cellular physiology, the precise mechanisms behind these effects remain unclear. In this study, we sought to examine the cytotoxic effects of PrP exposure on human lung cells in a dose- and time-dependent manner. We utilized flow cytometry to analyze the expression of proteins associated with the cell cycle and apoptosis at the single-cell level. Our results showed that PrP treatment leads to a significant upregulation of genes related to ER stress. The activation of ER stress results in a decrease in cyclin B1 levels, which subsequently causes cell cycle arrest at the G2/M phase. After 48h of PrP exposure, the unfolded protein response (UPR) triggers an apoptotic signaling pathway, increasing the number of cells undergoing caspase-3-mediated apoptosis. Together, these physiological changes lead to a reduction in cell viability in the presence of PrP. These findings suggest that PrP exerts harmful effects on human lung cells by activating ER stress, which can lead to apoptosis and cell cycle arrest.