Mitochondrial ROS, ER Stress, and Nrf2 Crosstalk in the Regulation of Mitochondrial Apoptosis Induced by Arsenite.
Nrf2
arsenic
arsenite
endoplasmic reticulum stress
mitochondrial ROS
toxicity
Journal
Antioxidants (Basel, Switzerland)
ISSN: 2076-3921
Titre abrégé: Antioxidants (Basel)
Pays: Switzerland
ID NLM: 101668981
Informations de publication
Date de publication:
23 May 2022
23 May 2022
Historique:
received:
20
04
2022
revised:
17
05
2022
accepted:
20
05
2022
entrez:
28
5
2022
pubmed:
29
5
2022
medline:
29
5
2022
Statut:
epublish
Résumé
Long-term ingestion of arsenicals, a heterogeneous group of toxic compounds, has been associated with a wide spectrum of human pathologies, which include various malignancies. Although their mechanism of toxicity remains largely unknown, it is generally believed that arsenicals mainly produce their effects via direct binding to protein thiols and ROS formation in different subcellular compartments. The generality of these mechanisms most probably accounts for the different effects mediated by different forms of the metalloid in a variety of cells and tissues. In order to learn more about the molecular mechanisms of cyto- and genotoxicity, there is a need to focus on specific arsenic compounds under tightly controlled conditions. This review focuses on the mechanisms regulating the mitochondrial formation of ROS after exposure to low concentrations of a specific arsenic compound, NaAsO
Identifiants
pubmed: 35624898
pii: antiox11051034
doi: 10.3390/antiox11051034
pmc: PMC9137803
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : Ministry of Education, Universities and Research
ID : 2017FJSM9S
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