Metabolomic analysis and oxidative stress response reveals the toxicity in Escherichia coli induced by organophosphate flame retardants tris(2-chloroethyl) phosphate and triphenyl phosphate.

Abstract Organophosphate flame retardants (OPFRs) are emerging environmental pollutants that are increasingly being used in consumer commodities. The adverse effects on biota induced by tris(2-chloroethyl) phosphate (TCEP) and triphenyl phosphate (TPHP) have become a growing concern. Unfortunately, toxic mechanisms at the molecular level for OPFRs in organisms are still lacking. Herein, Escherichia coli (E.coli) was exposed to TCEP and TPHP for 24 and 48 h to reveal oxidative stress response and molecular toxicity mechanisms. The results indicated that promotion of ROS overload occurred at higher dosages groups. The levels of SOD and CAT were significantly elevated along with the increase of MDA attributed to lipid peroxidation. Additionally, apoptosis rates increased, accompanied by a decline in membrane potential and Na+/K+-ATPase and Ca2+/Mg2+-ATPase contents, signifying that E. coli cytotoxicity induced by TCEP and TPHP was mediated by oxidative stress. Based on metabolomic analysis, different metabolic pathways were disrupted, including glycolysis/gluconeogenesis, pentose phosphate metabolism, purine metabolism, glutathione metabolism, amino acid biosynthesis, butanoate metabolism, alanine and aspartate metabolism. Most differentially expressed metabolites were downregulated, indicating an inhibitory effect on metabolic functions and key metabolic pathways. These findings generated new insights into the potential environmental risks of OPFRs in aquatic organisms.