ArticleToxicology in vitro : an international journal published in association with BIBRA2016
Monomethylarsonous acid, but not inorganic arsenic, is a mitochondria-specific toxicant in vascular smooth muscle cells.
Article in Toxicology in vitro : an international journal published in association with BIBRA, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Essential and Non-Essential Metals and Metalloids and Their Role in Atherosclerosis.Cardiovascular toxicology · 2025Review
- Loss-of-function mitochondrial DNA polymerase gamma variants cause vascular smooth muscle cells to secrete a diffusible mitogenic factor.Frontiers in physiology · 2024Article
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Relationship Analysis of Inorganic Arsenic Exposure and Metabolic Syndrome Based on Propensity Score Matching in Xinjiang, China.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Identification and Genome Analysis of an Arsenic-Metabolizing Strain ofBioMed research international · 2022Article
- Origins, fate, and actions of methylated trivalent metabolites of inorganic arsenic: progress and prospects.Archives of toxicology · 2021Review
- Evaluation of different types of arsenic methylation and its relationship with metabolic syndrome in an area chronically exposed to arsenic.Environmental analysis, health and toxicology · 2020Article
- Subcellular Organelle Toxicity Caused by Arsenic Nanoparticles in Isolated Rat Hepatocytes.The international journal of occupational and environmental medicine · 2020Article
- Article
- Serum folate and cobalamin levels and urinary dimethylarsinic acid in US children and adults.Environmental science and pollution research international · 2018Article
- Treatment of Arsenite Intoxication-Induced Peripheral Vasculopathy with Mesenchymal Stem Cells.International journal of molecular sciences · 2018Article
- Mitochondrial toxicity of organic arsenicals: membrane permeability transition pore opening and respiratory dysfunction.Toxicology research · 2018Article
- Arsenite and methylarsonite inhibit mitochondrial metabolism and glucose-stimulated insulin secretion in INS-1 832/13 β cells.Archives of toxicology · 2018Article
- Arsenic Methylation Capacity and Metabolic Syndrome in the 2013-2014 U.S. National Health and Nutrition Examination Survey (NHANES).International journal of environmental research and public health · 2018Article
- Review
- MitochondrialThe Journal of biological chemistry · 2017Article
- Hyperglycemia enhances arsenic-induced platelet and megakaryocyte activation.Journal of translational medicine · 2017Article
- Glycolysis selectively shapes the presynaptic action potential waveform.Journal of neurophysiology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic exposure has been implicated as a risk factor for cardiovascular diseases, metabolic disorders, and cancer, yet the role mitochondrial dysfunction plays in the cellular mechanisms of pathology is largely unknown. To investigate arsenic-induced mitochondrial dysfunction in vascular smooth muscle cells (VSMCs), we exposed rat aortic smooth muscle cells (A7r5) to inorganic arsenic (iAs(III)) and its metabolite monomethylarsonous acid (MMA(III)) and compared their effects on mitochondrial function and oxidative stress. Our results indicate that MMA(III) is significantly more toxic to mitochondria than iAs(III). Exposure of VSMCs to MMA(III), but not iAs(III), significantly decreased basal and maximal oxygen consumption rates and concomitantly increased compensatory extracellular acidification rates, a proxy for glycolysis. Treatment with MMA(III) significantly increased hydrogen peroxide and superoxide levels compared to iAs(III). Exposure to MMA(III) resulted in significant decreases in mitochondrial ATP, aberrant perinuclear clustering of mitochondria, and decreased mitochondrial content. Mechanistically, we observed that mitochondrial superoxide and hydrogen peroxide contribute to mitochondrial toxicity, as treatment of cells with MnTBAP (a mitochondrial superoxide dismutase mimetic) and catalase significantly reduced mitochondrial respiration deficits and cell death induced by both arsenic compounds. Overall, our data demonstrates that MMA(III) is a mitochondria-specific toxicant that elevates mitochondrial and non-mitochondrial sources of ROS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.