When less calcium does not mean slower contraction: Divergent effects of phenanthrene and 3-methylphenanthrene on fish ventricular cardiomyocytes.

Polycyclic aromatic hydrocarbons (PAHs) are dominant constituents of the water-soluble fraction of crude oil and are known to disrupt fish cardiac function, yet their consequences for cellular contractility remain poorly characterised. We investigated the acute effects of phenanthrene (P) and 3-methylphenanthrene (3-MP) at 1-10 μM on single rainbow trout (Oncorhynchus mykiss) ventricular cardiomyocytes, measuring sarcomere length dynamics, cytosolic Ca2+ transients, L-type Ca2+ current (ICa,L) and actin-myosin sliding velocity. P reduced the maximum velocity of sarcomere shortening from 1.57 to 1.00 μm/s and prolonged the time to peak contraction from 140.5 to 174.5 ms; 3-MP affected no sarcomere parameter. Both compounds reduced Ca2+ transient amplitude by ~50-55%, and 3-MP additionally accelerated its decay (CaD50 from 147.4 to 122.7 ms). P lowered peak ICa,L, whereas 3-MP left peak ICa,L unchanged but accelerated its inactivation. Also, both compounds significantly reduced charge, transferred by ICa,L at 0 mV. Neither compound altered actin-myosin sliding velocity. Importantly, phenanthrene and 3-methylphenanthrene produced opposite functional outcomes - slowing of contraction kinetics by phenanthrene but no mechanical effect of 3-methylphenanthrene. Even though both compounds reduced the Ca2+ transient to a similar extent, only phenanthrene slowed sarcomere shortening kinetics. This dissociation between the Ca2+-handling signature and the mechanical output points to compensatory mechanisms operating between the cytosolic Ca2+ signal and the sarcomere.