Los pesticidas que inhiben los complejos mitocondriales I y II activan la señalización de estrés integrada DELE1-HRI pero comprometen programas de muerte celular distintos en células neuronales humanas

significantly rescued viability in both treatments, demonstrating a pro-toxic autophagic program operating in parallel with apoptosis for FEN and as a principal death effector for FXX. Both pesticides converged on the DELE1-HRI-eIF2α-ATF4-CHOP integrated stress response, more pronounced for FXX. Early cytoskeletal disorganization was detectable at 6 h, preceding biochemical death markers. Mitochondrial respiratory chain-inhibiting pesticides thus engage divergent yet mechanistically interconnected cell death programs in human neurons, underscoring the value of mechanistic characterization for neurotoxic