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Cardiotoxicity: Assessing Mitochondrial Toxicity in Stem Cell-Derived Cor.4U Cardiomyocytes

Axiogenesis AG Cologne, Germany
Enzo Life Sciences, Farmingdale, New York, USA

Featured Product: Mito-ID® Extracellular O2 Sensor Kit, Mito-ID® Extracellular pH Sensor Probe

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Introduction

Mitochondrial dysfunction has been implicated in the etiology of drug-induced toxicity and of the relevant toxicities; cardiotoxicity remains the number one reason for drug withdrawal. Screening for compounds with such liabilities has been difficult due to the lack of relevant cell models and assay technologies. Axiogenesis human stem cell-derived Cor.4U® cardiomyocytes provide a homogenous, reproducible and physiologically relevant cardiomyocyte cell system that allows a specific detailed assessment of cell metabolism and mitochondrial function when combined with a suitable assay technology like Enzo’s Mito-ID® Extracellular O2 Sensor Kit and Mito-ID® Extracellular pH Sensor Probe. These assays are highly flexible 96 or 384-well fluorescence plate reader-based approaches, for the direct, real-time analysis of oxygen consumption (ETC) and glycolytic flux (ECA).

The assessment of cellular O2 consumption is based on the ability of O2 to quench the excited state of the Mito-ID® O2 Sensor Probe. As the Cor.4U cardiomyocytes respire, O2 is depleted in the surrounding media, which is seen as an increase in probe phosphorescence signal. True mitochondrial toxicity is expected to result in a decrease in oxygen consumption and a resultant increase in acidification due to glycolytic compensation while a non-specific mitochondrial insult would lead to a decrease in oxygen consumption without concomitant acidification.

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