ArticleJournal of occupational health2016
2,5-hexanedione induced apoptosis of rat bone marrow mesenchymal stem cells by reactive oxygen species.
Article in Journal of occupational health, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Proapoptotic effects of 2,5‑hexanedione on pheochromocytoma cells via oxidative injury.Molecular medicine reports · 2019Article
- Hypoxia induces senescence of bone marrow mesenchymal stem cells via altered gut microbiota.Nature communications · 2018Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesn-Hexane, a common industrial organic solvent, causes multiple organ damage, especially neurotoxicity, which is proved to be caused by its metabolite 2,5-hexanedione (2,5-HD). We previously showed that 2,5-HD induced apoptosis of rat bone marrow mesenchymal stem cells (BMSCs). In the current study, we explored the mechanism of 2,5-HD-induced apoptosis, especially the role played by reactive oxygen species (ROS).
methodsIntracellular ROS levels after 2,5-HD treatment were measured by the dichloro-dihydro-fluorescein diacetate (DCFH-DA) method, and the antioxidant N-acetyl cysteine (NAC) was used to scavenge ROS. Apoptosis, mitochondrial membrane potential (MMP), and caspase-3 activity were measured after 2,5-HD exposure with or without NAC pretreatment.
resultsIn rat BMSCs, 20 mM 2,5-HD significantly increased ROS levels and apoptosis. In addition, MMP activity was decreased and caspase-3 activity was increased. With NAC pretreatment, ROS increases were prevented, cells were rescued from apoptosis, and both MMP and caspase-3 activity returned to normal levels. Western blotting analysis of malondialdehyde-modified proteins and superoxide dismutase (SOD) 1 showed that after 2,5-HD exposure, BMSCs had oxidative damage and abnormal SOD1 expression. These returned to normal when cells were pretreated with NAC in addition to 20 mM 2,5-HD. Furthermore, the expressions of NF-κB p65/RelA and phospho-NF-κB p65/RelA (Ser536) were suppressed after 2,5-HD exposure and restored by NAC pretreatment.
conclusions2,5-HD-induced apoptosis in rat BMSCs is potentially mediated by excessive ROS production.
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