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To probe into the changes induced by infrasonic exposure on the methylation status of the genome in testes and underlying mechanisms, we inspected the percentage of unmethylated CpG sites (an index for DNA methylation level) and DNA methyltransferase activity in testes of SD rats exposed to infrasound of 8Hz at 90dB or 130dB for 1, 7, 14 and 21 days (2h/d). Compared to control groups at the same time points, significantly decreased DNA methylation level and methyltransferase activity were observed in all but experimental groups of ld and 21d at 90dB ( p

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 O 2 - (superoxide anion) were determined using lucigenin-enhanced chemiluminescence. Oxidant levels of H 2 O 2 (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 O 2 - and H 2 O 2 . 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 O 2 - or H 2 O 2 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.

Objectives To observe the changes of cardiac fibrosis and its underlying mechanism after acute myocardial infarction in rats. Methods Thirty male Sprague Dawley (SD) rats were randomised to control group, infarction group and infrasound treatment group, with 10 rats in each group. The rats in the infrasound treatment group were treated with infrasound for 7 days, 0.5 h, 2/days. The collagen expression of rat myocardium, the contents of NO and Ang-II in rat plasma and the rat heart function were observed. Results Competed with those in the infarction group, the contents of NO in rat plasma significantly decreased p Conclusions Infrasound treatment significantly assuages the cardiac fibrosis of rats after myocardial infarction, which may be relative with the changes of NO and Ang-II.