Objective To study the effect of benzoapyrene (BaP) on energy metabolism of human neuroblastoma SH-SY5Y cells, and further explore the potential neurotoxicity of BaP.
Methods SH-SY5Y cells were exposed to different concentrations of BaP for 24 h. Cell viability was determined by MTT assay. Malondialdehyde (MDA) content was measured by MDA assay kit, manganese (Mn)-superoxide dismutase (SOD) content by SOD typing test kit, and cell oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) by Seahorse XFp cell energy analyzer.
Results As the concentration of BaP increased, the cell viability decreased (Ptrend < 0.01), the intracellular MDA level increased (Ptrend < 0.01), and the Mn-SOD level decreased (Ptrend < 0.01). The cells treated with 1.0, 10.0, and 100.0 μmol/L BaP showed significantly higher MDA levels and significantly lower Mn-SOD levels than the control cells (P < 0.05). As the concentration of BaP increased, the basal OCR, ATP-linked OCR, maximal respiration, glycolysis, glycolytic capacity, and glycolytic reserve displayed a downward trend (Ptrend < 0.01), the basal OCR and ATP-linked OCR of the exposed groups were significantly lower than those of the control group (P < 0.05), and the maximal respiration, spare respiratory capacity, glycolysis, glycolytic capacity, and glycolytic reserve of the 10.0 and 100.0 μmol/L BaP groups were significantly lower than those of the control group (P < 0.05). Optical density of MTT and Mn-SOD level of the BaP exposed groups were positively correlated with basal OCR, ATP-linked OCR, maximal respiration, spare respiratory capacity, glycolysis, glycolytic capacity, and glycolytic reserve (P < 0.05). Intracellular MDA level was negatively correlated with various cellular bioenergy indicators (P < 0.05).
Conclusion BaP can cause oxidative damage in SH-SY5Y cells, reduce mitochondrial respiratory function, and impair the spare respiratory capacity and glycolytic function of SH-SY5Y cells at higher concentrations.
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