Fipronil, malathion,
and permethrin are widely used insecticides
in agriculture, public areas, and residential spaces. The globally
abused application of these chemicals results in residues surpassing
established maximum residue levels, giving rise to potential toxicity
in unintended organisms. Long-term exposure and the persistent accumulation
of these insecticides in animals and humans pose threats such as neurotoxicity,
liver and kidney damage, and microbiota dysbiosis. Despite the known
risks, the specific impact of these insecticides on gut microbiota
and their metabolic processes, as well as the subsequent effects on
host health, remain largely unknown. This study aimed to address this
gap by utilizing nonpathogenic
Escherichia coli
as a representative of human gut bacteria and examining its growth
and metabolic perturbations induced by exposure to fipronil, malathion,
and permethrin. Our research showed that exposure of
E. coli
to fipronil, malathion, and permethrin at
physiologically relevant concentrations resulted in significant growth
inhibition. Furthermore, we have observed the biodegradation of fipronil
and permethrin by
E. coli
, while no
biodegradation was found for malathion. Thus,
E. coli
is capable of degrading fipronil and permethrin, thereby enabling
the removal of those substances. Next, we studied how insecticides
affect bacterial metabolism to understand their influence on the functions
of the microbes. Our metabolomics analysis revealed chemical-dependent
alterations in metabolic profiles and metabolite compositions following
insecticide exposure. These changes encompassed shifts in carboxylic
acids and derivatives, organooxygen compounds, as well as indoles
and their derivatives. To gain a deeper insight into the systematic
changes induced by these insecticides, we conducted a metabolic pathway
analysis. Our data indicated that fipronil, compared with malathion
and permethrin, exhibited opposite regulation in glycine, serine,
and threonine metabolism and valine, leucine, and isoleucine biosynthesis.
In summary, our study demonstrates the capability of
E. coli
to degrade fipronil and permethrin, leading
to their removal, while malathion remains unaffected. Additionally,
we reveal chemical-dependent alterations in bacterial metabolism induced
by insecticide exposure, with specific impacts on metabolic pathways,
particularly in pathways related to amino acid metabolism.