Abstract
BACKGROUND: The intensification of aquaculture has led to increased use of chemical agents, such as trichlorfon, for controlling parasitic infections in farmed fish. While effective, this organophosphate compound may exert toxic effects even at sublethal concentrations, posing risks to economically important species such as tambaqui (C. macropomum). This study investigated the molecular effects of trichlorfon on the expression of genes involved in stress response, energy metabolism, and apoptosis in juvenile tambaqui. METHODS: Fish were exposed to two sublethal concentrations of trichlorfon (30% and 50% LC(50-96 h), equivalent to 0.261 and 0.435 mg/L) for 48, 72, and 96 h. Expression levels of fkbp5, p53, pim-2, pir, me1, bbox1, and higd1a were quantified in liver tissue using qPCR. RESULTS: fkbp5 and p53 were strongly upregulated at 48 h, indicating acute stress and genotoxic activation. me1 and pim-2 were also upregulated, reflecting activation of compensatory energy metabolism and anti-apoptotic survival pathways. bbox1 showed an early induction followed by collapse at 96 h, while higd1a and pir exhibited delayed overexpression at 96 h, suggesting mitochondrial hypoxia and inflammation. CONCLUSIONS: Trichlorfon triggers a multifaceted toxic response characterized by initial activation of compensatory pathways (stress response, antioxidant defense, and anti-apoptotic mechanisms) followed by late-phase metabolic collapse, mitochondrial hypoxia, and inflammation, with both time- and dose-dependent effects. These findings demonstrate that even sublethal concentrations disrupt hepatic homeostasis and support the use of these genes as molecular biomarkers for environmental monitoring in aquaculture.