Impact of Benzo( a)pyrene and Pyrene Exposure on Activating Autophagy and Correlation with Endoplasmic Reticulum Stress in Human Astrocytes
Issued Date
2025-02-01
Resource Type
ISSN
16616596
eISSN
14220067
Scopus ID
2-s2.0-85218940657
Journal Title
International Journal of Molecular Sciences
Volume
26
Issue
4
Rights Holder(s)
SCOPUS
Bibliographic Citation
International Journal of Molecular Sciences Vol.26 No.4 (2025)
Suggested Citation
Siangcham T., Vivithanaporn P., Jantakee K., Ruangtong J., Thongsepee N., Martviset P., Chantree P., Sornchuer P., Sangpairoj K. Impact of Benzo( a)pyrene and Pyrene Exposure on Activating Autophagy and Correlation with Endoplasmic Reticulum Stress in Human Astrocytes. International Journal of Molecular Sciences Vol.26 No.4 (2025). doi:10.3390/ijms26041748 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/105551
Title
Impact of Benzo( a)pyrene and Pyrene Exposure on Activating Autophagy and Correlation with Endoplasmic Reticulum Stress in Human Astrocytes
Corresponding Author(s)
Other Contributor(s)
Abstract
Benzo(a)pyrene (B(a)P) and pyrene, the most prominent subtypes of polycyclic aromatic hydrocarbons (PAHs), contaminate environments as organic pollutants. They adversely affect body systems, including degeneration of the central nervous system. This study investigated the in vitro toxic effects of B(a)P and pyrene on proliferation, endoplasmic reticulum (ER) stress induction, and autophagy in human astrocytes using U-87 MG human astrocytoma cells as a model. Both B(a)P and pyrene were toxic to U-87 MG cells in a concentration-dependent manner. Astrocytic proliferation was interfered with, enhancing S-phase cell cycle arrest. B(a)P promoted the presence of autophagic vesicles and the expression of autophagic markers LC3, beclin-1, and p62, suggesting activated autophagy. B(a)P enhanced the expression of ER stress markers BiP, PERK, and IRE1. ER stress appeared to be correlated with autophagy induction, as demonstrated by experiments using chloroquine, an autophagy inhibitor. Pyrene enhanced the expression of autophagic markers and ER stress primarily via PERK activation, although autophagic vesicles were not observed. The study demonstrates that B(a)P enhances ER stress-mediated autophagy more evidently than pyrene and affected toxicity to astrocytes. These results provide a basis for understanding the toxic effects of the main PAH substances affecting astrocytes.