Retracted: Cardiac mitochondrial oxidative stress and dysfunction induced by arsenic and its amelioration by diallyl trisulphide

Sumedha, Naorem Chanu; Miltonprabu, Selvaraj

doi:10.1039/c4tx00097h

Cited by 17 publications

(7 citation statements)

References 40 publications

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“…iAs is a multi-target toxin that acts through a variety of mechanisms. In various cell types, exposure to iAs III has been linked to defects in mitochondrial function, including damage to mitochondrial DNA, increased production of reactive oxygen species, decreased expression of Krebs cycle enzymes, and decreased mitochondrial membrane potential (Partridge et al 2007; Sumedha and Miltonprabu 2015; Prakash et al 2015). Fu and coworkers were the first to show that a prolonged (96-h ) iAs III exposure suppresses mitochondrial respiration in the INS-1 832/13 β-cell line while inhibiting GSIS (Fu et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Arsenite and methylarsonite inhibit mitochondrial metabolism and glucose-stimulated insulin secretion in INS-1 832/13 β cells

et al. 2017

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Growing evidence suggests that exposure to environmental contaminants contributes to the current diabetes epidemic. Inorganic arsenic (iAs), a drinking water and food contaminant, is one of the most widespread environmental diabetogens according to epidemiological studies. Several schemes have been proposed to explain the diabetogenic effects of iAs exposure; however, the exact mechanism remains unknown. We have shown that in vitro exposure to low concentrations of arsenite (iAs) or its trivalent methylated metabolites, methylarsonite (MAs) and dimethylarsinite (DMAs), inhibits glucose-stimulated insulin secretion (GSIS) from isolated pancreatic islets, with little effect on insulin transcription or total insulin content. The goal of this study was to determine if exposure to trivalent arsenicals impairs mitochondrial metabolism, which plays a key role in the regulation of GSIS in β cells. We used a Seahorse extracellular flux analyzer to measure oxygen consumption rate (OCR), a proxy for mitochondrial metabolism, in cultured INS-1 832/13 β cells exposed to iAs, MAs, or DMAs and stimulated with either glucose or pyruvate, a final product of glycolysis and a substrate for the Krebs cycle. We found that 24-h exposure to 2 μM iAs or 0.375-0.5 μM MAs inhibited OCR in both glucose- and pyruvate-stimulated β cells in a manner that closely paralleled GSIS inhibition. In contrast, 24-h exposure to DMAs (up to 2 µM) had no effects on either OCR or GSIS. These results suggest that iAs and MAs may impair GSIS in β cells by inhibiting mitochondrial metabolism, and that at least one target of these arsenicals is pyruvate decarboxylation or downstream reactions.

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Section: Discussionmentioning

confidence: 99%

Arsenite and methylarsonite inhibit mitochondrial metabolism and glucose-stimulated insulin secretion in INS-1 832/13 β cells

et al. 2017

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“…Arsenic is a naturally occurring element in the earth’s crust, which is mostly in the form of trivalent or pentavalent compounds in the natural world. Exposure to arsenic may cause many diseases, such as diabetes, − cardiovascular diseases, − and kinds of cancers. − International Agency for Research on Cancer (IARC) has identified arsenic and its compounds as explicit human carcinogens. , Excessive arsenic content in water resources is one of the important ways for human arsenic exposure. With the rapid development of industries, a large amount of high-arsenic wastewater was discharged into rivers and lakes; arsenic contamination in drinking water has been a global health problem for the past few decades. − Moreover, arsenic is also emitted into the environment by burning arsenic coal, , leading to excessive exposure of arsenic to the inhabitants of relevant areas.…”

Section: Introductionmentioning

confidence: 99%

Ultra-Performance Liquid Chromatography-Tandem Mass Spectrometry for the Analysis of Complex Compounds in Serum and Its Application in Accurate Detection of Early Arsenic Exposure

et al. 2021

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With the acceleration of industrialization, environmental arsenic pollution is threatening human health. However, by the time clinical symptoms appear, arsenic toxicity has usually caused irreversible damage to the body, so it is important to establish a rapid and accurate screening method for early arsenic exposure. In this work, 32 female C57BL/6 mice were exposed to different concentrations of inorganic arsenic in drinking water for a week. By analyzing the changes in serum, more than 20 compounds were detected to increase or decrease with the increase of arsenic intake. The abnormal increase in inosine, xanthine, xanthosine, and hypoxanthine and the abnormal purine pathway were found at the same time. Dimethylarsenic acid, an important inorganic arsenic metabolite in the body, was also found in serum. Combined with statistical analysis, early arsenic exposure can be easily and quickly detected, and the potential health risks of short-term exposure can be revealed simultaneously.

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“…41 It has been suggested that the loss of mitochondrial membrane potential and ROS overproduction (from the malfunctioned mitochondria) are the major mechanisms for arsenic toxicity and that mitochondria is supposed to be a specific target for its toxicity. 37,42 Arsenic is metabolized (methylated) in rodents. Monomethylarsonous acid, one of the metabolites, which distrib- Arsenic Nanoparticles-induced Hepatotoxicity ute irregularly in different tissues (RBC, liver, and kidney), is an ultimate toxicant to mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Subcellular Organelle Toxicity Caused by Arsenic Nanoparticles in Isolated Rat Hepatocytes

Jahangirnejad

Goudarzi

Kalantari‬

et al. 2020

Int J Occup Environ Med

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Background: Arsenic, an environmental pollutant, is a carcinogenic metalloid and also an anticancer agent. Objective: To evaluate the toxicity of arsenic nanoparticles in rat hepatocytes. Methods: Freshly isolated rat hepatocytes were exposed to 0, 20, 40, and 100 µM of arsenic nanoparticles and its bulk counterpart. Their viability, reactive oxygen species level, glutathione depletion, mitochondrial and lysosomal damage, and apoptosis were evaluated. Results: By all concentrations, lysosomal damage and apoptosis were clearly evident in hepatocytes exposed to arsenic nanoparticles. Evaluation of mitochondria and lysosomes revealed that lysosomes were highly damaged. Conclusion: Exposure to arsenic nanoparticles causes apoptosis and organelle impairment. The nanoparticles have potentially higher toxicity than the bulk arsenic. Lysosomes are highly affected. It seems that, instead of mitochondria, lysosomes are the first target organelles involved in the toxicity induced by arsenic nanoparticles.

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Retracted: Cardiac mitochondrial oxidative stress and dysfunction induced by arsenic and its amelioration by diallyl trisulphide

Abstract: Mitochondria are the particular target of arsenic (As) in the cell.

Cited by 17 publications

References 40 publications

Arsenite and methylarsonite inhibit mitochondrial metabolism and glucose-stimulated insulin secretion in INS-1 832/13 β cells

Arsenite and methylarsonite inhibit mitochondrial metabolism and glucose-stimulated insulin secretion in INS-1 832/13 β cells

Ultra-Performance Liquid Chromatography-Tandem Mass Spectrometry for the Analysis of Complex Compounds in Serum and Its Application in Accurate Detection of Early Arsenic Exposure

Subcellular Organelle Toxicity Caused by Arsenic Nanoparticles in Isolated Rat Hepatocytes

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