Mechanism of dimethyl sulfate-induced acute injury in human bronchial epithelial cells via oxidative stress-mitochondrial apoptosis pathway
CHEN Xiaoxiang
KONG Deqin
LIU Rui
ZHANG Qian
LI Ludi
LIU Bingjie
WU Hao
CAO Meng
AN Guangzhou
YU Weihua
LIU Jiangzheng
HAI Chunxu
Abstract：Objective To investigate the acute toxic effects of dimethyl sulfate(DMS)on human bronchial epithelial cells(BEAS-2B)and its underlying mechanisms.Methods An in vitro model of acute lung injury(ALI)was established by treating BEAS-2B cells with DMS.Cell viability after DMS exposure at different concentrations and time points was assessed using the CCK-8 assay.Changes in cell morphology were observed under an optical microscope.The apoptosis rate was measured by Annexin V/PI double staining.Mitochondrial membrane potential changes,malondialdehyde(MDA)content,intracellular total reactive oxygen species(ROS)and mitochondrial reactive oxygen species(mtROS)levels,reduced glutathione(GSH)and oxidized glutathione(GSSG)content,as well as total superoxide dismutase(SOD)and catalase(CAT)activity were detected using corresponding assay kits.Results Compared to the control group,the relative cell viability in DMS-treated groups significantly decreased(P<0.01)and progressively declined with increasing exposure time and concentration(P<0.01).The apoptosis rate significantly increased(P<0.01),and the mitochondrial transmembrane potential was markedly reduced(P<0.01).Intracellular MDA content initially increased without statistical significance but rose rapidly at later stages(P<0.01),showing a significant time-and dose-dependent effect.Both intracellular total ROS and mtROS levels significantly increased(P<0.01).In the early exposure stage,GSH content significantly increased while GSSG rose slowly.With prolonged exposure,GSH content decreased rapidly,while GSSG content increased sharply(P<0.01).Under low-concentration DMS exposure,total SOD activity increased over time but was inhibited at high concentrations.The change in CAT activity showed an opposite trend to total SOD(P<0.01).Conclusion An in vitro model of DMS-induced acute injury in BEAS-2B cells is successfully established.This model can be used to simulate the pathological process of ALI in humans caused by short-term,high-dose inhalation of DMS.Acute DMS exposure significantly reduces cell viability and induces severe apoptosis.The mechanism may be related to mitochondrial membrane potential disruption,excessive ROS generation,disruption of intracellular redox balance,and severe oxidative damage,ultimately leading to apoptosis and loss of cell viability.
Keywords：dimethyl sulfatereactive oxygen speciesmitochondriaoxidative stresssuperoxide dismutasecatalaseglutathionemalondialdehyde
Publication Date：2026-05-31
Online Publishing Date：2026-08-26(First online date of this platform, not the publication date of the document)
Pages：9( 651-659 )