Sulfur dioxide induces apoptosis via reactive oxygen species generation in rat cardiomyocytes

Abstract

Epidemiological evidence suggests that the incidence and mortality of cardiovascular diseases are closely related to sulfur dioxide (SO₂). In the present study, H9C2 cells were incubated with 100 μM NaHSO₃ with or without pretreatment of an antioxidant, N-acetyl-l-cysteine (NAC). The changes of apoptosis rate, mitochondrial membrane potential (MMP), ATP content, caspase-3 activity, and reactive oxygen species (ROS) were detected. Rats were inhaled 7 mg/m³ SO₂ and/or intraperitoneal injected with 50 mg/kg (bw) of NAC for 30 days. RT-PCR and Western blot were used to detect the mRNA and protein levels of apoptosis-related genes. We found that the apoptosis of H9C2 cells was induced by NaHSO₃, which decreased the content of MMP and ATP, and induced the expression of caspase-3. NAC can inhibit the apoptosis induced by NaHSO₃ treatment. SO₂ and NaHSO₃ decreased the expression of Bcl-2 and the ratio of Bcl-2/Bax, increased the expression of Bax and P53 accumulation and phosphorylation, and activated caspase-9 and caspase-3. Whereas NAC can reduce the changes of apoptosis-related proteins in rat heart. Our results suggest that SO₂ induces ROS-mediated P53 and caspase-dependent mitochondrial signaling pathways in H9C2 cells and rat hearts. Antioxidant therapy can reduce the adverse reactions of SO₂ and lead to a decline in the cardiovascular disease induced by SO₂.

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