Ambient PM2.5 has been proved to be an independent risk factor for cardiovascular diseases; however, little information is available on the age-dependent effects of PM2.5 on the cardiovascular system and the underlying mechanisms following chronic exposure. In this study, multi-aged mice were exposed to PM2.5 via the newly developed real-ambient PM2.5 exposure system to investigate age-related effects on the heart after long-term exposure. First, the chemical and physical properties of PM2.5 used in the exposure system were analyzed. The heart rate of conscious mice was recorded, and results showed that exposure of aged mice to PM2.5 for 26 weeks significantly increased heart rate. Histological analysis and ELISA assays indicated that aged mice were more sensitive to PM2.5 exposure in terms of inducing cardiac oxidative stress and inflammation. Furthermore, untargeted metabolomics revealed that taurine was involved with the PM2.5-induced cardiac dysfunction. The reduced taurine concentration in the heart was examined by LC-MS and imaging mass spectrometry; it may be due to the increased p53 expression level, ROS and inflammatory cytokines. These results emphasize the age-dependent effects of PM2.5 on the cardiovascular system and suggest that taurine may be the novel cardiac effect target for PM2.5-induced heart dysfunction in the aged.
Keywords: Age-dependent effect; Cardiac dysfunction; Non-targeted metabolomics; PM(2.5) exposure; Taurine.
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