ArticleBirth defects research. Part A, Clinical and molecular teratology2010
Arsenate-induced apoptosis in murine embryonic maxillary mesenchymal cells via mitochondrial-mediated oxidative injury.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 31 citations in OpenAlex.
- Maternal Immune Stimulation With Interferon-Gamma Limits Embryonic Valproic Acid Induced Apoptotic Gene Expression.Birth defects research · 2025Article
- Research progress on the regulatory mechanism of cell senescence in arsenic toxicity: a systematic review.Toxicology research · 2024Review
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Microarray analysis of apoptosis gene expression in liver injury induced by chronic exposure to arsenic and high-fat diet in male mice.Environmental science and pollution research international · 2019Article
- Impact of prenatal arsenate exposure on gene expression in a pure population of migratory cranial neural crest cells.Reproductive toxicology (Elmsford, N.Y.) · 2019Article
- Alpha lipoic acid (ALA) modulates expression of apoptosis associated proteins in hippocampus of rats exposed during postnatal period to sodium arsenite (NaAsOToxicology reports · 2015Article
- N-Acetyl cysteine reverses social isolation rearing induced changes in cortico-striatal monoamines in rats.Metabolic brain disease · 2013Article
- Epigenetic regulation of Sox4 during palate development.Epigenomics · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundArsenic is a ubiquitous element that is a potential carcinogen and teratogen and can cause adverse developmental outcomes. Arsenic exerts its toxic effects through the generation of reactive oxygen species (ROS) that include hydrogen peroxide (H(2)O(2)), superoxide-derived hydroxyl ion, and peroxyl radicals. However, the molecular mechanisms by which arsenic induces cytotoxicity in murine embryonic maxillary mesenchymal (MEMM) cells are undefined.
methodsMEMM cells in culture were treated with different concentrations of pentavalent sodium arsenate [As (V)] for 24 or 48 hr and various end points measured.
resultsTreatment of MEMM cells with the pentavalent form of inorganic arsenic resulted in caspase-mediated apoptosis, accompanied by generation of ROS and disruption of mitochondrial membrane potential. Treatment with caspase inhibitors markedly blocked apoptosis. In addition, the free radical scavenger N-acetylcysteine dramatically attenuated arsenic-mediated ROS production and apoptosis, and exposure to arsenate increased Bax and decreased Bcl protein levels in MEMM cells.
conclusionsTaken together, these findings suggest that in MEMM cells arsenate-mediated oxidative injury acts as an early and upstream initiator of the cell death cascade, triggering cytotoxicity, mitochondrial dysfunction, altered Bcl/Bax protein ratios, and activation of caspase-9.
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