Revisiting the Cardiotoxic Effect of Chloroquine View Full Text


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Article Info

DATE

2019-02

AUTHORS

Marguerite Blignaut, Yolandi Espach, Mignon van Vuuren, Karthik Dhanabalan, Barbara Huisamen

ABSTRACT

PURPOSE: Cardiotoxicity is a well-known side effect of chloroquine. Several studies have proposed chloroquine as a potential anti-diabetic treatment but do not address this problem. The current study investigated the effect of ex vivo chloroquine treatment on (1) heart function and glucose uptake, (2) mitochondrial function and (3) in vivo treatment on heart function. METHODS: Control or obese male Wistar rats were used throughout. Dose responses of increasing chloroquine concentrations versus vehicle on cardiac function were measured using isolated, Langendorff-perfused hearts whilst glucose uptake and cell viability were determined in ventricular cardiomyocytes. Mitochondrial function was assessed with a Clark-type oxygraph (Hansatech) after ex vivo perfusion with 30 μM chloroquine versus vehicle. Animals were treated orally with 5 mg/kg/day chloroquine for 6 weeks. RESULTS: Acute chloroquine treatment of 10 μM was sufficient to significantly decrease heart function (p < 0.05) whilst 30 μM significantly reduced heart rate (p < 0.05). Chloroquine became toxic to isolated cardiomyocytes at high concentrations (100 μM), and had no effect on cardiomyocyte glucose uptake. Ex vivo treatment did not affect mitochondrial function, but chronic low-dose in vivo chloroquine treatment significantly decreased aortic output and total work in hearts (p < 0.005). CONCLUSION: Low and intermediate chloroquine doses administered either chronically or acutely are sufficient to result in myocardial dysfunction. More... »

PAGES

1-11

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http://scigraph.springernature.com/pub.10.1007/s10557-018-06847-9

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http://dx.doi.org/10.1007/s10557-018-06847-9

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https://app.dimensions.ai/details/publication/pub.1111369643

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30635818


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46 schema:description PURPOSE: Cardiotoxicity is a well-known side effect of chloroquine. Several studies have proposed chloroquine as a potential anti-diabetic treatment but do not address this problem. The current study investigated the effect of ex vivo chloroquine treatment on (1) heart function and glucose uptake, (2) mitochondrial function and (3) in vivo treatment on heart function. METHODS: Control or obese male Wistar rats were used throughout. Dose responses of increasing chloroquine concentrations versus vehicle on cardiac function were measured using isolated, Langendorff-perfused hearts whilst glucose uptake and cell viability were determined in ventricular cardiomyocytes. Mitochondrial function was assessed with a Clark-type oxygraph (Hansatech) after ex vivo perfusion with 30 μM chloroquine versus vehicle. Animals were treated orally with 5 mg/kg/day chloroquine for 6 weeks. RESULTS: Acute chloroquine treatment of 10 μM was sufficient to significantly decrease heart function (p < 0.05) whilst 30 μM significantly reduced heart rate (p < 0.05). Chloroquine became toxic to isolated cardiomyocytes at high concentrations (100 μM), and had no effect on cardiomyocyte glucose uptake. Ex vivo treatment did not affect mitochondrial function, but chronic low-dose in vivo chloroquine treatment significantly decreased aortic output and total work in hearts (p < 0.005). CONCLUSION: Low and intermediate chloroquine doses administered either chronically or acutely are sufficient to result in myocardial dysfunction.
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