Drug accumulation-elimination kinetics and hepatic detoxification response in Acanthopagrus schlegelii juvenile after enrofloxacin bath administration

To elucidate the potential residual risk and physiological effects of enrofloxacin bath treatment on black porgy (Acanthopagrus schlegelii) juvenile, we subjected the juveniles to a 24-hour bath administration with enrofloxacin at concentrations of 5 and 10 mg·L⁻¹, and determined the drug residues in the liver, gills, and muscle, as well as the hepatic biochemical indexes within 7 d of depuration. The results revealed distinct dose-dependent and organ-specific accumulation of enrofloxacin in the juveniles. The liver was identified as the primary accumulation organ, exhibiting the highest residue levels, area under the curve (AUC_0-t), and mean residence time (MRT). Critically, the elimination half-life of enrofloxacin in muscle was longer than that in liver and gill tissues, suggesting that muscle is a long-term risk organ for drug residues. Enrofloxacin bath administration disrupted the hepatic detoxification system by markedly suppressing cytochrome P450 (CYP450) contents and elevating glutathione S-transferase (GST) activities. Enrofloxacin administration further disrupted the hepatic antioxidant defense system, evinced by sustained inhibition of superoxide dismutase (SOD) activities and significant up-regulation of catalase (CAT) activities and malondialdehyde (MDA) contents. The integrated biomarker response (IBRv2) index shows that the toxicity of enrofloxacin exhibited a significant dose-dependent effect, and a relatively high integrated toxic load was still observed even after 7 d of depuration. Although the enrofloxacin residues in various tissues of juvenile could decrease to below the maximum residue limit (MRL) of 100 μg·kg⁻¹ within 48–72 h, the disorder of detoxification metabolism and oxidative damage in the liver could persist for more than 7 d. The study indicates that the accumulation and elimination of enrofloxacin residues in A. schlegelii juvenile after bath administration were tissue-specific, and the recovery of liver physiological functions lagged significantly behind the elimination of drug residues.