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. 2022 Dec 7;299(1):102780. doi: 10.1016/j.jbc.2022.102780

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© 2022 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Oxidative stress depolarizes the mitochondria and can be a significant arrhythmogenic factor.A, local perfusion of the center (D = 5 mm) of NRVM monolayers with a thiol oxidizing agent (diamide, 1 mM) causes ΔΨ depolarization and inexcitability (in separate experiments). Error bars for action potential amplitude (APA) show the SEM (N = 4). Inset: A monolayer 20 min after local perfusion with diamide; mitochondria are loaded with TMRM at 2 μM in dequenching mode; the bright region indicates depolarized mitochondria. B, optical mapping of V_m shows the initiation and maintenance of a reentrant wave. Reentry occurred in 8 out of 10 monolayers perfused with diamide versus none in control monolayers (p < 0.001). A change from blue to red indicates the depolarization of the cell membrane. NRVM, neonatal rat ventricular myocyte; TMRM, tetramethylrhodamine methyl ester.