Effect of Sodium Benzoate on Apoptosis and Mitochondrial Membrane Potential After Aluminum Toxicity in PC-12 Cell Line

Background: Sodium benzoate, a food preservative, prevents the growth of fungi and bacteria. Numerous studies have reported the protective effects of sodium benzoate on the nervous system. This study investigated the effect of sodium benzoate on cell apoptosis and mitochondrial function in an aluminum cell toxicity model. Methods: After 48 hr of treating PC12 cells with varying concentrations of sodium benzoate (0.125, 0.25 or 0.5 mg/ml) in the presence of aluminum maltolate (500 mu;M), the cell viability was assessed by MTT assay. The type of cell death (necrosis or apoptosis) was analyzed by flow cytometry (7ADD/An VPE staining). Also, rhodamine 123 was used to measure the Mitochondrial Membrane Potential (MMP). The acetylcholinesterase activity (AChE) was assessed by Ellman rsquo;s method. Results: It was observed that sodium benzoate inhibited aluminum induced cell death within 48hr. Sodium benzoate at a concentration of 0.5 mg/ml significantly reduced the apoptotic cells that had been exposed to aluminum. Exposure of PC12 cells with sodium benzoate and aluminum, increased the AChE activity, although, no significant changes in mitochondrial membrane potential were observed. Conclusion: Sodium benzoate may provide its protective effects through increased AChE activity and inhibiting apoptosis induced by aluminum toxicity. It is likely that the disruption of MMP is neither involved in the induction of apoptosis by aluminum nor in the protective effect of sodium benzoate.