Efficacy of all-trans retinoid acid in preventing nickel induced cardiotoxicity in myocardial cells of rats

Nickel, a metal commonly found in battery plants and welding factories, has potential cardiotoxicity, while all-trans retinoid acid (atRA) can promote cardiovascular repair and myocardial recovery. The purpose of this study was to investigate whether atRA could prevent cardiotoxicity induced by nickel both in vitro and in vivo. In the study, a rat myocardial cell line (H9c2) exposed to different concentrations of nickel chloride (NiCl2) displayed apoptotic features accompanied by reactive oxygen species generation. In addition, NiCl2 also caused obvious apoptosis and systolic dysfunction in primary myocardial cells. Treatment with atRA efficiently attenuated the cytotoxicities triggered by NiCl2 as it significantly mitigated ROS generation and decreased MAP kinases activity in NiCl2-treated cardiomyocytes. Additionally, NiCl2 exposure caused obvious arrhythmia in Sprague–Dawley rats with the maximum tolerance dose of NiCl2 between 2 and 3 mg/kg. A combinational intragastric administration of 40 mg/kg atRA can partially reverse NiCl2-induced arrhythmia in rats. Our results suggested that atRA might have therapeutic potential in alleviating the adverse effects of nickel on the cardiovascular system.