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Peer-reviewedCC BY 4.0Molecules

Contribution of the ROS/IRE1α Signaling Pathway to Arsenic Trioxide-Induced Apoptosis and Autophagy-Associated Responses in BEAS-2B Cells

  • Jiaming Yuan1,2
  • Yanhong Chen1,3
  • Chenjuan Yao4
  • Haiyan Wei1
  • Yu Han1
  • Gang Chen1
  • Jianhua Qu1
4 affiliations
  1. 1Department of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China
  2. 2Hangzhou Fuyang District Center for Disease Control and Prevention (Hangzhou Fuyang District Health Supervision Institute), Hangzhou 311400, China
  3. 3Heqing Community Health Service Center, Pudong New Area, Shanghai 201201, China
  4. 4Department of Oral Physiology, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima 770-8504, Japan
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Abstract

Inorganic arsenic primarily originates from geological processes and human activities. Exposure to high concentrations of inorganic arsenic can cause diverse health problems, with lung injury being one of the main hazards. The present study sought to elucidate the cytotoxicity and underlying mechanisms of inorganic arsenic in BEAS-2B cells. The results showed that exposure of BEAS-2B cells to arsenic trioxide (As2O3) for 24 h resulted in a dose-dependent decline in viability. As2O3 triggered reactive oxygen species (ROS) production in BEAS-2B cells, and ROS contributed to increased p-IRE1α and p-eIF2α abundance relative to β-actin, along with GRP78 protein expression. The autophagy-associated and apoptotic responses induced by As2O3 in BEAS-2B cells were likewise associated with ROS. Further analysis revealed that increased p-IRE1α abundance relative to β-actin is involved in As2O3-triggered autophagy-associated responses and apoptosis in BEAS-2B cells. The antioxidant N-acetylcysteine (NAC) markedly attenuated As2O3-induced apoptosis and autophagy-associated responses and reduced p-IRE1α abundance relative to β-actin. Collectively, these findings indicate that the ROS/IRE1α pathway contributes to As2O3-triggered autophagy-associated responses and apoptosis in BEAS-2B cells.

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Cite

BibTeXRIS
BibTeX
@article{yuan2026contribution,
  title = {{Contribution of the ROS/IRE1α Signaling Pathway to Arsenic Trioxide-Induced Apoptosis and Autophagy-Associated Responses in BEAS-2B Cells}},
  author = {Jiaming Yuan and Yanhong Chen and Chenjuan Yao and Haiyan Wei and Yu Han and Gang Chen and Jianhua Qu},
  journal = {Molecules},
  year = {2026},
  month = oct,
  doi = {10.3390/molecules31203787},
  url = {https://www.mdpi.com/1420-3049/31/20/3787},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Contribution of the ROS/IRE1α Signaling Pathway to Arsenic Trioxide-Induced Apoptosis and Autophagy-Associated Responses in BEAS-2B Cells
AU  - Jiaming Yuan
AU  - Yanhong Chen
AU  - Chenjuan Yao
AU  - Haiyan Wei
AU  - Yu Han
AU  - Gang Chen
AU  - Jianhua Qu
PY  - 2026
DA  - 2026/10/01
JO  - Molecules
DO  - 10.3390/molecules31203787
UR  - https://www.mdpi.com/1420-3049/31/20/3787
AB  - Inorganic arsenic primarily originates from geological processes and human activities. Exposure to high concentrations of inorganic arsenic can cause diverse health problems, with lung injury being one of the main hazards. The present study sought to elucidate the cytotoxicity and underlying mechanisms of inorganic arsenic in BEAS-2B cells. The results showed that exposure of BEAS-2B cells to arsenic trioxide (As2O3) for 24 h resulted in a dose-dependent decline in viability. As2O3 triggered reactive oxygen species (ROS) production in BEAS-2B cells, and ROS contributed to increased p-IRE1α and p-eIF2α abundance relative to β-actin, along with GRP78 protein expression. The autophagy-associated and apoptotic responses induced by As2O3 in BEAS-2B cells were likewise associated with ROS. Further analysis revealed that increased p-IRE1α abundance relative to β-actin is involved in As2O3-triggered autophagy-associated responses and apoptosis in BEAS-2B cells. The antioxidant N-acetylcysteine (NAC) markedly attenuated As2O3-induced apoptosis and autophagy-associated responses and reduced p-IRE1α abundance relative to β-actin. Collectively, these findings indicate that the ROS/IRE1α pathway contributes to As2O3-triggered autophagy-associated responses and apoptosis in BEAS-2B cells.
SN  - 1420-3049
ER  -