| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2583149 | Environmental Toxicology and Pharmacology | 2015 | 7 Pages |
•Molecular mechanism of SO2 on the key gene expression of two channels was revealed.•Negative inotropic effect of SO2 related to expression of K+ and Ca2+ channels.•SO2 presumably induce cardiovascular diseases by changing the expression of channels.•SO2 at high concentrations might have potential damage on rat hearts.
Epidemiological studies have revealed an association between sulfur dioxide (SO2) exposure and cardiovascular diseases. This study is designed to investigate the SO2 effect on the expression of ATP-sensitive K+ (KATP) channel and L-type calcium (L-Ca2+) channel in rat hearts. The results show that the mRNA and protein levels of the KATP channel subunits Kir6.2 and SUR2A of rat hearts in SO2 groups were higher than those in control group. SO2 at 14 mg/m3 significantly decreased the expression of the L-Ca2+ channel subunits Cav1.2 and Cav1.3. This suggests that SO2 can activate the KATP channels by up-regulating the expression of Kir6.2 and SUR2A, while it inhibits the L-Ca2+ channels by down-regulating the expression of Cav1.2 and Cav1.3 in rat hearts. The molecular mechanism of SO2-induced negative inotropic effect might be linked to the expression changes of these subunits, which may contribute to the pathogenesis of SO2-associated cardiovascular diseases.
