Objectives Rats were exposed to infrasound for several weeks, and adverse effects on the cardiovascular system were demonstrated using morphology, histopathology, and histochemistry. The aim of the present study was to examine the effects of acute infrasound exposure on oxidative damage and investigate the underlying mechanisms in rat cardiomyocytes.
Methods Neonatal rat cardiomyocytes were cultured and exposed to infrasound at 5 Hz and 130 dB. The infrasound applicator was composed of a signal generator power amplifier, dynamoelectric loudhailer, microphone, low frequency sound information data processing system, computer simulation analysis, and infrasound chamber. Antioxidant expression of CAT (catalase), GPx (glutathione peroxidase), SOD1 (copper zinc superoxide dismutase 1) and manganese SOD2 (superoxide dismutase 2) in rat cardiomyocytes was measured using semi-quantitative RT-PCR and western immunoblotting. Levels of the oxidant O2 - (superoxide anion) were determined using lucigenin-enhanced chemiluminescence. Oxidant levels of H2O2 (hydrogen peroxide) were assessed using the Amplex Red Hydrogen Peroxide/Peroxidase Assay Kit.PPAR-γ (peroxisome proliferator-activated receptor-γ) expression was measured using RT-PCR and western immunoblotting. Cardiac cell viability was observed with the MTT (3,4,5-Dimethylthiazol-2-yl-2,5-diphenyltetrazolium) cytotoxicity test.
Results In the present study, we found that expression of CAT, GPx, SOD1 and manganese SOD2 and their activities in rat cardiomyocytes were significantly decreased compared to those in the various time controls, along with significantly higher levels of the oxidants O2 - and H2O2. Decreases in cardiac cell viability was not observed in controls. A significant reduction in cardiac cell viability was observed in the infrasound group, while significantly increased cardiac cell viability was observed in the infrasound exposure and rosiglitazone pretreatment groups. Rosiglitazone significantly upregulated CAT, GPx, SOD1 and SOD2 expression and their activities in rat cardiomyocytes exposed to infrasound, while the levels of O2 - or H2O2 were decreased. Semi-quantitative RT-PCR and western immunoblotting analyses demonstrated a potential link between downregulation of PPAR-γ expression and infrasound-induced oxidative stress in rat cardiomyocytes.
Conclusions These findings support the hypothesis that infrasound can induce oxidative damage in rat cardiomyocytes by inactivating PPAR-γ.