Acetamiprid (ACE) is a neonicotinoid insecticide with widespread global application, resulting in persistent human
exposure. The current research examined the toxicological implications of ACE exposure on human lung fibroblasts
(MRC-5 cells) and bronchial epithelial cells (BEAS-2B cells). The following implications were explored:
oxidative stress, epithelial-mesenchymal transition, apoptosis, cellular proliferation, and extracellular matrix accumulation.
The prospective protective properties of heat-killed Lactobacillus fermentum and Lactobacillus delbrueckii
(HKL) were further studied. The 14-day exposure to ACE at 4 μM triggered oxidative stress and inflammation.
ACE promoted epithelial-mesenchymal transition, as evidenced by the decline of protein and mRNA
abundances of E-cadherin alongside increased protein and mRNA quantities of α-SMA and N-cadherin in BEAS-
2B cells. Additionally, it elicited apoptosis in BEAS-2B cells and stimulated the cellular growth of MRC-5 cells.
The TGF-β1/Smad pathway was activated upon ACE exposure, leading to the accumulation of extracellular matrix.
HKL demonstrated antioxidant, anti-apoptotic, anti-proliferative, and anti-fibrotic properties, mitigating
ACE-induced toxicity. Our findings delineate the molecular mechanisms underlying epithelial-mesenchymal
transition, inflammation, oxidative stress, and extracellular matrix accumulation in ACE-induced pulmonary fi- |
