Key result
Phenanthrene exposure reduces Ca2+ transient amplitude and inhibits INCX in zebrafish ventricular myocytes.
Why the study?
Phenanthrene, a common polycyclic aromatic hydrocarbon, affects cardiac function in vertebrates but its impact on calcium handling and NCX current in ventricular myocytes was unclear.
Phenanthrene disrupts calcium handling in zebrafish ventricular myocytes by reducing calcium transient amplitude and inhibiting the Na+/Ca2+ exchanger, potentially impacting cardiac contractility.
Phenanthrene disrupts Ca²⁺ handling in zebrafish myocytes; leaves open relevance to human PAH cardiotoxicity.
Phenanthrene is a polycyclic aromatic hydrocarbon (PAH) that is derived from fossil fuels and is present in most PAH mixtures found in water, air and soil. It has been shown to affect cardiac function of vertebrates, including fish. We investigated the effects of phenanthrene on intracellular calcium transient ([Ca2+]i) and the Na+/Ca2+ exchanger (NCX) current (INCX) in zebrafish (Danio rerio) ventricular cardiomyocytes using Fluo-4 AM imaging and whole-cell patch-clamp, respectively. Phenanthrene exposure (25 µM) reduced the amplitude and slowed the rate of decay of Ca²⁺ transients. Phenanthrene also inhibited INCX with equal efficacy in forward- and reverse-mode. We conclude that phenanthrene disrupts Ca²⁺ handling in zebrafish ventricular myocytes, which could impact cardiac contractility.
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Vehniäinen et al. (2026) studied this question. Phenanthrene was evaluated on Intracellular calcium transient ([Ca2+]i) and Na+/Ca2+ exchanger (NCX) current (INCX). Phenanthrene exposure (25 µM) reduced the amplitude and slowed the rate of decay of Ca²⁺ transients and inhibited INCX in zebrafish ventricular myocytes.
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