Energy metabolism disorders and oxidative stress in the SH-SY5Y cells following PM2.5 air pollution exposure

Studies have shown that PM2.5 exposure can induce neuronal apoptosis and neurobehavioral changes in animal experiments due partly to the mitochondria-mediated oxidative damage. How does it affect the mitochondrial energy metabolism as well as the neuronal damage, however, remain unclear. This study aimed to investigate the molecular processes of energy metabolism and oxidative damage induced by ambient PM2.5 exposure in SH-SY5Y cells. SH-SY5Y cells were treated with PM2.5 to establish a cytotoxicity model. A Seahorse Extracellular Flux Analyzer (XFp) was performed to evaluate the cellular mitochondrial respiratory and glycolysis after exposure to PM2.5. The dose- and time-dependent effects of PM2.5 on oxidative damage and apoptosis were analyzed. To further explore the relationship among oxidative damage, energy metabolism and apoptosis, SH-SY5Y cells were co-cultured with BHA and PM2.5 for 24 h. The results demonstrated that the basic respiration and ATP production, the typical index of mitochondrial respiration as well as glycolysis, significantly reduced in SH-SY5Y cells with dose and time dependent. At the same time, the PM2.5 could significantly decrease the cell viability and Mn-SOD activity, and increase the ROS levels and apoptosis rate as the escalation of dose and the extension of time. Importantly, the application of BHA could synchronously recover the PM2.5 induced cell energy metabolism disorder, oxidative damage, and apoptosis. It seems that the abnormal cellular energy metabolism may be caused by oxidative damage following fine particles exposure, and further led to apoptosis.