Abstract
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 PC-12 cells with varying concentrations of sodium benzoate (0.125, 0.25 or 0.5 mg/ml) in the presence of aluminum maltolate (500 μM), the cell viability was assessed by MTT assay. The type of cell death (necrosis or apoptosis) was analyzed by flow cytometry (7-ADD/An V-PE staining). Also, rhodamine 123 was used to measure the Mitochondrial Membrane Potential (MMP). The acetylcholinesterase activity (AChE) was assessed by Ellman’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 PC-12 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.
Highlights
T he origin and etiology of neurodegenerative disorders, such as Alzheimer’s and Parkinson’s Diseases (AD, PD) is multifactorial
Sodium benzoate may provide its protective effects through increased AChE activity and inhibiting apoptosis induced by aluminum toxicity
Effects on PC-12 cell line: Based on our previous study on cell viability, we used 500 μM of Aluminum maltolate (Almal) concentration, which is closest to LC50, and a co-treatment with non-cytotoxic concentration (0.125, 0.25 or 0.5 mg/mL) of sodium benzoate [19]
Summary
T he origin and etiology of neurodegenerative disorders, such as Alzheimer’s and Parkinson’s Diseases (AD, PD) is multifactorial. One of the metals that is increasing known to play a major role in cell toxicity in the central nervous system is aluminum [1]. This metal may enter the human body via food, drinking water, beverages and medications [2, 3]. There is evidence to suggest that beta amyloids can disrupt mitochondrial functions directly by inducing neuronal death [8, 9]. 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
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