Abstract
Bis-(2-ethylhexyl) phthalate commonly called (DEHP) is a major environmental contaminant known to interfere with various biological pathways following human exposure. Our previous research demonstrated that Bis(2-ethylhexyl) phthalates increased the oxidative stress, increased level of acetylcholinesterase in third instar larvae of Drosophila melanogaster (hsp70-lacZ) Bg. [9] This study demonstrated that apigenin, a naturally occurring flavonoid, effectively mitigates the toxic effects of DEHP in third instar larvae. In this study, apigenin was incorporated into the diet at final concentrations of 20, 40, 60, and 80 μM, along with 0.02 M Bis-(2-ethylhexyl) phthalate. The larvae were exposed to this diet for a period of 24 h. Through metabolites study and biochemical evaluations, we assessed the impact of apigenin on oxidative stress markers, enzymatic activity, and metabolic pathway alterations in the larvae exposed to Bis-(2-ethylhexyl) phthalate. Our results indicated that Bis-(2-ethylhexyl) phthalate exposure along with apigenin significantly affected oxidative stress markers, leading to increased levels of glutathione (GSH) and decreased activities of superoxide dismutase (SOD), and catalase (CAT). Furthermore, Bis-(2-ethylhexyl) phthalate along with apigenin exposure was associated with decreased in lipid peroxidation (as indicated by TBARS), protein carbonylation (PC) highlighting extensive oxidative damage. Metabolomic analysis revealed notable changes in critical metabolites, and apigenin was found to mitigate oxidative stress and also changes in the concentration of certain metabolities. This study highlights the potential of apigenin a protective compound against Bis-(2-ethylhexyl) phthalate-induced toxicity by alleviating oxidative stress and helping to restore metabolic balance.
