Arsenic cardiotoxicity: An overview

Alamolhodaei, Nafiseh Sadat; Shirani, Kobra; Karimi, Gholamreza

doi:10.1016/j.etap.2015.08.030

Cited by 96 publications

(58 citation statements)

References 84 publications

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“…Environmental exposure to arsenic also causes chronic cardiotoxicity (Alamolhodaei et al, 2015). In our study, arsenic trioxide decreased the contractile function and the beating of hiPS-CMs at a concentration (10 μM) comparable to its oral C max (Yamauchi et al, 2004) and up to 20-fold C max (Fox et al, 2008) observed with intravenous administration of arsenic in the clinic.…”

Section: Bjp I Kopljar Et Alsupporting

confidence: 58%

“…towards 5-6 days). The mechanisms behind arsenic-derived cardiotoxicity are considered to be driven by increased ROS production, leading to chronic cardiotoxicity (Alamolhodaei et al, 2015). Additional suggested mechanisms, possibly secondary to ROS, involve the modulation of calcium currents and hERG trafficking (Ficker et al, 2004).…”

Section: Bjp I Kopljar Et Almentioning

confidence: 99%

“…In the present study, we evaluated the translational value of these biomarkers for cardiotoxicity in hiPS-CMs. We studied different classes of drugs (doxorubicin, arsenic trioxide and panobinostat) known to be associated with chronic cardiac adverse effects in humans (Swain et al, 2003;Sharma et al, 2013;Alamolhodaei et al, 2015). Ebastine was chosen as a negative control as it has no reported, cardiac side effects in the clinic (Moss and Morganroth, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Chronic drug‐induced effects on contractile motion properties and cardiac biomarkers in human induced pluripotent stem cell‐derived cardiomyocytes

Kopljar

Bondt

Vinken

et al. 2017

British J Pharmacology

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BACKGROUND AND PURPOSEIn the pharmaceutical industry risk assessments of chronic cardiac safety liabilities are mostly performed during late stages of preclinical drug development using in vivo animal models. Here, we explored the potential of human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs) to detect chronic cardiac risks such as drug-induced cardiomyocyte toxicity. EXPERIMENTAL APPROACHVideo microscopy-based motion field imaging was applied to evaluate the chronic effect (over 72 h) of cardiotoxic drugs on the contractile motion of hiPS-CMs. In parallel, the release of cardiac troponin I (cTnI), heart fatty acid binding protein (FABP3) and N-terminal pro-brain natriuretic peptide (NT-proBNP) was analysed from cell medium, and transcriptional profiling of hiPS-CMs was done at the end of the experiment. KEY RESULTSDifferent cardiotoxic drugs altered the contractile motion properties of hiPS-CMs together with increasing the release of cardiac biomarkers. FABP3 and cTnI were shown to be potential surrogates to predict cardiotoxicity in hiPS-CMs, whereas NT-proBNP seemed to be a less valuable biomarker. Furthermore, drug-induced cardiotoxicity produced by chronic exposure of hiPS-CMs to arsenic trioxide, doxorubicin or panobinostat was associated with different profiles of changes in contractile parameters, biomarker release and transcriptional expression. CONCLUSION AND IMPLICATIONSWe have shown that a parallel assessment of motion field imaging-derived contractile properties, release of biomarkers and transcriptional changes can detect diverse mechanisms of chronic drug-induced cardiac liabilities in hiPS-CMs. Hence, hiPS-CMs could potentially improve and accelerate cardiovascular de-risking of compounds at earlier stages of drug discovery.

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Section: Bjp I Kopljar Et Alsupporting

confidence: 58%

Section: Bjp I Kopljar Et Almentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chronic drug‐induced effects on contractile motion properties and cardiac biomarkers in human induced pluripotent stem cell‐derived cardiomyocytes

Kopljar

Bondt

Vinken

et al. 2017

British J Pharmacology

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“…Through bioinformatic analysis, we found that target binding sites exist with HSF1 and miR-199b-5p sequence. we also proved that HSF1 can promote expression of VEGF by inhibiting P53 and up-regulating HIF-1, and further advance angiogenesis, leading to a positive effect on heart failure ( Zou et al, 2011;Kang et al, 2015;Alamolhodaei et al, 2015), so we hypothesized that the role of miR-199b-5p in heart failure may be related to angiogenesis. We used lipofection to up/down regulate the expression of miR-199b-5p in mouse MMVECs, and discovered that the up-regulation group showed lower expressions of HSF1 and VEGF, and reduced cell proliferation and angiogenesis, whereas, the down-regulation group presented the contrary results.…”

Section: Introductionmentioning

confidence: 80%

Role of miR-199b-5p in regulating angiogenesis in mouse myocardial microvascular endothelial cells through HSF1/VEGF pathway

Dai

Chang

et al. 2016

Environmental Toxicology and Pharmacology

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“…However, studies have shown the presence of high levels of As, a known class 1 carcinogen when in the inorganic forms (arsenite (As III ) and arsenate (As V )) [14, 15] in different seaweed species. Seaweeds are thought to absorb As as As V through phosphate channels due to its similarities to phosphate (H 2 PO 4 − versus H 2 AsO 4 − ) [16].…”

Section: Introductionmentioning

confidence: 99%

A field deployable method for a rapid screening analysis of inorganic arsenic in seaweed

et al. 2017

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Inorganic arsenic (iAs) in 13 store-bought edible seaweed samples and 34 dried kelp (Laminaria digitata) samples was determined by a newly developed, field-deployable method (FDM) with the aid of a field test kit for arsenic in water. Results from the FDM were compared to results from speciation analysis achieved by using high performance liquid chromatography coupled to inductively coupled plasma mass spectrometry (HPLC-ICP-MS). The FDM consisted of a simple extraction method using diluted HNO3 to quantitatively extract iAs without decomposing the organoarsenicals to iAs followed by the selective volatilisation of iAs as arsine (AsH3) and subsequent chemo-trapping on a filter paper soaked in mercury bromide (HgBr2) solution. Method optimization with a sub-set of samples showed 80–94% iAs recovery with the FDM with no matrix effect from organo-arsenic species in the form of dimethylarsinic acid (DMA) on the iAs concentration. The method displayed good reproducibility with an average error of ±19% and validation by HPLC-ICP-MS showed that the results from the FDM were comparable (slope = 1.03, R2 = 0.70) to those from speciation analysis with no bias. The FDM can be conducted within an hour and the observed limit of quantification was around 0.05 mg kg−1 (dry weight). This method is well suited for on-site monitoring of iAs in seaweed before it is harvested and can thus be recommended for use as a screening method for iAs in seaweed. Graphical abstractScreening seaweed for their inorganic arsenic concentration within one hour without bias has been made possible in the field by using a field deployable arsenic kit. Its accuracy and precision was compared to HPLC-ICPMS. Electronic supplementary materialThe online version of this article (doi:10.1007/s00604-017-2151-1) contains supplementary material, which is available to authorized users.

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Arsenic cardiotoxicity: An overview

Cited by 96 publications

References 84 publications

Chronic drug‐induced effects on contractile motion properties and cardiac biomarkers in human induced pluripotent stem cell‐derived cardiomyocytes

Chronic drug‐induced effects on contractile motion properties and cardiac biomarkers in human induced pluripotent stem cell‐derived cardiomyocytes

Role of miR-199b-5p in regulating angiogenesis in mouse myocardial microvascular endothelial cells through HSF1/VEGF pathway

A field deployable method for a rapid screening analysis of inorganic arsenic in seaweed

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