Sodium Benzoate Promotes Fat Accumulation and Aging via the SKN-1/Nrf2 Signaling Pathway: Evidence from theCaenorhabditis elegansModel

Abstract

Sodium benzoate (SB) is widely used in food products, cosmetics, and medical solutions due to its antimicrobial properties. While it is generally considered safe and has potential neuroprotective benefits, SB has also been linked to adverse effects, including hepatic oxidative stress and inflammation. However, the potential effects of SB on obesity and aging remain poorly understood. In this study, we investigated the effects of SB on fat accumulation and aging using the nematode Caenorhabditis elegans (C. elegans) as a model system. Wild-type worms were exposed to various SB concentrations (0%, 0.0004%, 0.0008%, 0.004%, and 0.1%) and 0.016% glucose as a positive control for 72 hours in liquid or on NGM agar plates. Fat accumulation was assessed through the Oil Red O staining, which revealed that SB induced more fat accumulation compared to vehicle control, even at low concentrations, including the dosage of 0.0004%. Lifespan analysis also demonstrated that SB significantly accelerated aging in wild-type worms in a dose-dependent manner. Further investigations found that SKN-1 (an Nrf2 homolog) is necessary for SB-induced fat accumulation and aging. Moreover, SB inhibited the nuclear localization of SKN-1 under oxidative stress conditions. These findings suggest that SB may induce fat accumulation and aging by inhibiting the oxidative stress-mediated SKN-1 signaling pathway.