The Effects of Benzoic Acid in C. elegans: Germ Cell Apoptosis

Abstract

Benzoic acid is widely consumed by humans everyday through means of fruit juices, soft drinks, pickles, salad dressings and more. However, the health impact of long-term benzoic acid exposure remains largely unknown. This study aims to increase this knowledge by using the model organism Caenorhabditis elegans (C. elegans), a metazoan with conserved homeostatic mechanisms similar to higher organisms, including humans. Specifically, we aim to detect if benzoic acid induces apoptosis in the gonad, the sex organ of C. elegans. Primary literature suggests that apoptosis is linked to oxidative stress and resulting mitochondrial disorders. We hypothesize that apoptosis rate is higher in C. elegans exposed to benzoic acid. Experimentally, eight groups of C. elegans, from the same MD701 strain, were synchronized into identical developmental stages and raised in identical conditions. The C. elegans groups were maintained on five different types of NGM agar plates, with four containing different concentrations of benzoic acid and one being a control treatment. In accordance with U.S. standards for the maximum allowance of benzoic acid in foods, the primary treatment was 0.1% benzoic acid. Two additional concentrations of 0.01% and 0.5% benzoic acid were tested following the primary treatment. Because significance (p<0.05) was seen with the 0.01% treatment, an additional concentration of 0.001% benzoic acid was tested. Gonadal apoptosis was assessed and apoptotic cell counts were recorded under a Zeiss Axio Observer Z1 fluorescence microscope. The results showed no significant difference in apoptotic germ cell counts in the 0.001% benzoic acid treatment, and a significantly higher number of apoptotic cells in 0.01%, 0.1%, and 0.5% benzoic acid treated C. elegans.