The molecular mechanisms of sodium metabisulfite on the expression of KATP and L-Ca2+ channels in rat hearts

•Experimental evidence of toxicological mechanism of SMB on hearts is provided.•In-depth study about mechanisms of toxicity of SO2-induced cardiovascular disease.•We examine changes about mRNA and protein expression of KATP and L-Ca2+ channels.•SMB at high concentrations might have potentially damaging effects on hearts. Sodium metabisulfite (SMB) is used as an antioxidant and antimicrobial agent in a variety of drugs and foods. However, there are few reported studies about its side effects. This study is to investigate the SMB effects on the expression of ATP-sensitive K+ (KATP) and L-type calcium (L-Ca2+) channels in rat hearts. The results show that the mRNA and protein levels of the KATP channel subunits Kir6.2 and SUR2A were increased by SMB; on the contrary, SMB at 520mg/kg significantly decreased the expression of the L-Ca2+ channel subunits Cav1.2 and Cav1.3. This suggests that SMB can activate the expression of KATP channel by increasing the mRNA and protein levels of Kir6.2 and SUR2A, while it inhibits the expression of L-Ca2+ channels by decreasing the mRNA and protein levels of Cav1.2 and Cav1.3 in rat hearts. Therefore, the molecular mechanism of the SMB effect on rat hearts might be related to the increased expression of KATP channels and the decreased expression of L-Ca2+ channels.