DNA polymerase β may be involved in protecting human bronchial epithelial cells from the toxic effects induced by methyl tert-butyl ether exposure. (December 2021)

• Record Type: Journal Article
• Authors: He, Z; Xian, H; Tang, M; Chen, Y; Lian, Z; Fang, D; Peng, X; Hu, D
• Is Part Of: Human & experimental toxicology. Volume 40:Number 12(2021)
• Page Start: 2135
• Page End: 2144
• Publication Date: 2021-12
• Subjects: Methyl tert-butyl ether -- toxic mechanism -- DNA polymerase β -- cell viability -- DNA damage -- oxidative stress; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/09603271211022788
• Languages: English
• ISSNs: 0960-3271

Abstract

Methyl tert-butyl ether (MTBE), a widely used gasoline additive and a ubiquitous environmental pollutant in many countries and regions, can cause various kinds of toxic effects on human health. However, the molecular mechanism underlying its toxic effects remains elusive. The present study aimed to explore the cytotoxicity, DNA damage and oxidative damage effects of MTBE on human bronchial epithelial cells (16HBE) and the possible role of DNA polymerase β (pol-β) in this process. RNA interference (RNAi) was used to obtain pol-β gene knocked-down cells (pol-β − ). CCK-8 assay was adopted to analyze the cell viability. Alkaline single-cell gel electrophoresis (SCGE) was performed to detect the DNA damage effects of MTBE. The enzyme activity of GSH-Px, SOD, CAT and the level of MDA were assessed. The data indicated that when treated with MTBE at the concentration exceeding 50 μmol/L and for the time exceeding 24 h, the pol-β − exhibited significantly decreased cell viability and increased DNA damage effects, as compared to the control ( P < 0.05). Furthermore, there was significant difference in the levels of GSH-pX, SOD, CAT and MDA between the pol-β − and the control ( P < 0.05). Our investigation suggests that MTBE can cause obvious cytotoxicity, DNA damage and oxidative damage effects on 16HBE cells. DNA polymerase β may be involved in protecting 16HBE cells from the toxic effects induced by MTBE exposure. These findings provide a novel insight into the molecular mechanism underlying the toxic effects of MTBE on human cells.