Perturbations in glycerophospholipid levels of PC12 cells after exposure to PCB95 based on targeted lipidomics analysis.

Polychlorinated biphenyls (PCBs) are a group of organic chlorine chemicals that can induce various adverse health effects in animals and humans. The toxicology of PCBs is a significant public health concern because of their long-term presence in the environment. Among the 209 PCB congeners, PCB95 has been reported to be neurotoxic, however, there has been limited researches on evaluating whether and how PCB95 affects cellular lipids, the most abundant components of the brain. In this study, PCB95 was found to inhibit cell proliferation at concentrations of 0.1 μM, 2 μM and 10 μM for 120 h. Additionally, there may be a shift in apoptosis to necrosis at 2 μM PCB95 exposure for 24 h. However, lipid peroxidation was found not dominant for PCB95 exposure, especially at the concentrations of 0.1 μM and 2 μM. Because of playing vital roles in cell metabolism, 20 glycerophospholipids in PC12 cells were investigated after exposure to PCB95 for 120 h. The distinctions in the orthogonal projection to latent structures-discriminant analysis (OPLS-DA) models indicated that different concentrations of PCB95 leaded to aberrant glycerophospholipid metabolism. Based on the principles of t-test P-value < 0.05, variable importance at projection (VIP) value >1 and fold change >1, PC (14:0/14:0) and PC (16:0/14:0) were screened as potential biomarkers from all the target glycerophospholipids. This study is the first time that identifies the effects of PCB95 on specific glycerophospholipids in PC12 cells, and the observed changes in glycerophospholipids provides the basis for further evaluation of PCB95-induced neurotoxicity mechanisms.