Academic Journal
Vanadium pentoxide induced oxidative stress and cellular senescence in human lung fibroblasts
| Title: | Vanadium pentoxide induced oxidative stress and cellular senescence in human lung fibroblasts |
|---|---|
| Authors: | Xiaojia He, Zachery R. Jarrell, Yongliang Liang, Matthew Ryan Smith, Michael L. Orr, Lucian Marts, Young-Mi Go, Dean P. Jones |
| Source: | Redox Biology, Vol 55, Iss , Pp 102409- (2022) |
| Publisher Information: | Elsevier, 2022. |
| Publication Year: | 2022 |
| Collection: | LCC:Medicine (General) LCC:Biology (General) |
| Subject Terms: | Environmental health, Lung fibrosis, Redox cycling, Thiol/disulfide redox, Vanadate, Medicine (General), R5-920, Biology (General), QH301-705.5 |
| More Details: | Both environmental exposure to vanadium pentoxide (V2O5, V+5 for its ionic counterparts) and fibroblast senescence are associated with pulmonary fibrosis, but whether V+5 causes fibroblast senescence remains unknown. We found in a dose-response study that 2–40 μM V+5 caused human lung fibroblasts (HLF) senescence with increased senescence-associated β-galactosidase activity and p16 expression, while cell death occurred at higher concentration (LC50, 82 μM V+5). Notably, measures of reactive oxygen species (ROS) production with fluorescence probes showed no association of ROS with V+5-dependent senescence. Preloading catalase (polyethylene-conjugated), a H2O2 scavenger, did not alleviate the cellular senescence induced by V+5. Analyses of the cellular glutathione (GSH) system showed that V+5 oxidized GSH, increased GSH biosynthesis, stimulated cellular GSH efflux and increased protein S-glutathionylation, and addition of N-acetyl cysteine inhibited V+5-elevated p16 expression, suggesting that thiol oxidation mediates V+5-caused senescence. Moreover, strong correlations between GSSG/GSH redox potential (Eh), protein S-glutathionylation, and cellular senescence (R2 > 0.99, p |
| Document Type: | article |
| File Description: | electronic resource |
| Language: | English |
| ISSN: | 2213-2317 |
| Relation: | http://www.sciencedirect.com/science/article/pii/S2213231722001811; https://doaj.org/toc/2213-2317 |
| DOI: | 10.1016/j.redox.2022.102409 |
| Access URL: | https://doaj.org/article/d7e74f3b4eab414f810dfbf6ccf8a6a0 |
| Accession Number: | edsdoj.7e74f3b4eab414f810dfbf6ccf8a6a0 |
| Database: | Directory of Open Access Journals |
| ISSN: | 22132317 |
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| DOI: | 10.1016/j.redox.2022.102409 |
| Published in: | Redox Biology |
| Language: | English |