Effects of pentachlorophenol on the quail (Coturnix japonica) liver detoxification pathway.

Abstract

Pentachlorophenol (PCP), an extensively used pesticide and biocide, is of critical environmental concern due to its toxicity and recalcitrance to degradation. In this study, the effect of PCP on induction of transcription factors, cytochrome P450 (CYP450) genes, and the antioxidative enzyme system were investigated in the quail liver. A total of 60 (4- to 6-week-old) male quails (Coturnix japonica) were administered 0, 0.05, 0.5, and 5 mg/kg/d PCP orally for 42 d. Following exposure, both absolute and relative liver weights were significantly lower than those of the control. Using gas chromatography-mass spectrometry, PCP accumulation was, from highest to lowest, kidney > liver > muscle for all exposure groups. The expressions of CYP1A5, CYP1B1, CYP2C18, nuclear translocator 1 (ARNT1), and aryl hydrocarbon receptor 1 (AHR1) were induced after PCP treatment, and increases were found in the activities of hepatic superoxide dismutase (SOD) and catalase (CAT), and the content of hepatic malondialdehyde (MDA). In addition, exposure to PCP induced an increase in liver 8-hydroxydeoxyguanosine (8-OHdG) and significantly elevated ethoxyresorufin O-deethylase (EROD), methoxyresorufin O-demethylase (MROD), and 7-ethoxycoumarin-O-deethylase (ECOD) activity, but decreased that of glutathione peroxidase (GSH-Px), benzyloxyresorufin O-debenzylase (BROD), pentoxyresorufin O-depentylase (PROD), and erythromycin N-demethylase (END). No significant responses were observed for benzyloxy-trifluoromethyl-coumarin (BFC). The protein level of liver nuclear factor κB (NF-κB) was higher, whereas that of nuclear factor E2-related factor 2 (Nrf2) was lower for exposed quail. These results suggest that PCP affects quail oxidative stress by modulating CYP450 enzymes and nuclear transcription factors.