Trimethylamine N-oxide does not impact viability, ROS production and mitochondrial membrane potential of adult rat cardiomyocytes

Trimethylamine N-oxide (TMAO) is an organic compound derived from dietary choline and L-carnitine. It behaves as an osmolyte, a protein stabilizer and an electron acceptor, showing different biological functions in different animals. Recent works point out that in humans high circulating levels of TMAO are related with the progression of atherosclerosis and other cardiovascular diseases. Nevertheless, studies on a direct role of TMAO on cardiomyocytes parameters are still limited. This work focuses on the effects of TMAO on isolated adult rat cardiomyocytes. TMAO both 100μM and 10mM, from 1 to 24 h of treatment, does not affect cell viability, sarcomere length, intracellular ROS and mitochondrial membrane potential. Furthermore, the simultaneous treatment with TMAO and known cardiac insults, H2O2 or Doxorubicin, does not affect the effect of the treatment. In conclusion, TMAO cannot be considered a direct cause or an exacerbating risk factor of cardiac damage at the cellular level in acute conditions.