A Study of 2,3,7,8-Tetrachlorodibenzo-p-dioxin Induced Liver Injury in Jian Carp (Cyprinus carpio var. Jian) Using Precision-Cut Liver Slices

Bull Environ Contam Toxicol. 2016 Jan;96(1):55-61. doi: 10.1007/s00128-015-1683-5. Epub 2015 Oct 27.

Abstract

The aim of this study was to establish a model for the study of liver injury induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Jian carp using precision-cut liver slices (PCLS). PCLS were treated with TCDD at concentrations of 0, 0.05, 0.1, 0.3, and 0.6 μg/L for 6 h, followed by collection of the culture supernatant and PCLS for analysis. Several biochemical indices were analyzed, including glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA). Expression of mRNA was also estimated for cytochrome P4501A (CYP1A), aryl hydrocarbon receptor2 (AhR2), and aryl hydrocarbon receptor nuclear translocator2 (ARNT2). Results showed that some significant effects (p < 0.05) in MDA, GSH-Px and PCLS viability were observed at a TCDD concentration as low as 0.05 µg/L, and the observed effects increased with exposure concentration. Following exposure to TCDD for 6 h at a concentration of 0.3 μg/L, significant increases (p < 0.01) in the content of GPT, GOT, MDA, and LDH were observed, while SOD activity, GSH-Px activity, and PCLS viability were decreased (p < 0.01 or p < 0.05). Exposure to 0.3 μg/L TCDD also resulted in increased expression of mRNA for CYP1A, AhR2, and ARNT2. Overall, these results provide evidence of TCDD-induced liver injury and oxidative stress in Jian carp. These results also support the use of PCLS as an in vitro model for the evaluation of hepatotoxicity in Jian carp.

Keywords: 2,3,7,8-Tetrachlorodibenzo-p-dioxin; ARNT2; AhR2; CYP1A; Jian Carp.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carps / metabolism*
  • Glutathione Peroxidase / metabolism
  • In Vitro Techniques / methods*
  • Liver / drug effects*
  • Liver / metabolism
  • Malondialdehyde / metabolism
  • Oxidation-Reduction
  • Oxidative Stress / drug effects*
  • Polychlorinated Dibenzodioxins / toxicity*
  • RNA, Messenger / metabolism
  • Receptors, Aryl Hydrocarbon / metabolism
  • Superoxide Dismutase / metabolism

Substances

  • Polychlorinated Dibenzodioxins
  • RNA, Messenger
  • Receptors, Aryl Hydrocarbon
  • Malondialdehyde
  • Glutathione Peroxidase
  • Superoxide Dismutase