Effects of carbon tetrachloride on oxidative stress, inflammatory response and hepatocyte apoptosis in common carp (Cyprinus carpio)

Rui Jia, Li Ping Cao, Jin Liang Du, Jia Hao Wang, Ying Juan Liu, G. Jeney, Pao Xu, Guo Jun Yin

Research output: Contribution to journalArticle

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Abstract

In the present study, the cellular and molecular mechanism of carbon tetrachloride (CCl4)-induced hepatotoxicity in fish was investigated by studying the effects of CCl4 on the oxidative stress, inflammatory response and hepatocyte apoptosis. Common carp were given an intraperitoneal injection of 30% CCl4 in arachis oil (0.5ml/kg body weight). At 72h post-injection, blood were collected to measure glutamate pyruvate transaminase (GPT), glutamate oxalate transaminase (GOT), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), total antioxidant capacity (T-AOC) and malondialdehyde (MDA), liver samples were taken to analyze toll-like receptor 4 (TLR4), cytochrome P450 2E1 (CYP2E1) and gene expressions of inflammatory cytokines and nuclear factor-κB (NF-κB/cREL). Cell viability and apoptosis were analyzed after treatment of the primary hepatocytes with CCl4 at 8mM. The results showed that CCl4 significantly increased the levels of GPT, GOT, MDA, TLR4 and CYP2E1, reduced the levels of SOD, GPx, CAT, GSH and T-AOC, and up-regulated the gene expressions of NF-κB/cREL and inflammatory cytokines including tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), IL-1β, IL-6 and IL-12. In vitro, CCl4 caused a dramatic loss in cell viability and induced hepatocyte apoptosis. Overall results suggest that oxidative stress lipid peroxidation, and TNF-α/NF-κB and TRL4/NF-κB signaling pathways play important roles in CCl4-induced hepatotoxicity in fish.

Original languageEnglish
Pages (from-to)11-19
Number of pages9
JournalAquatic Toxicology
Volume152
DOIs
Publication statusPublished - 2014

Fingerprint

carbon tetrachloride
Carps
Carbon Tetrachloride
apoptosis
Transaminases
Cyprinus carpio
hepatocytes
Glutamic Acid
Hepatocytes
Oxidative Stress
oxidative stress
hepatotoxicity
tumor necrosis factors
inflammation
oxalate
Apoptosis
alanine transaminase
cytochrome P-450
aspartate transaminase
tumor

Keywords

  • Apoptosis
  • Carbon tetrachloride
  • Cyprinus carpio
  • Inflammatory cytokines
  • Nuclear translocation factor

ASJC Scopus subject areas

  • Aquatic Science
  • Health, Toxicology and Mutagenesis

Cite this

Effects of carbon tetrachloride on oxidative stress, inflammatory response and hepatocyte apoptosis in common carp (Cyprinus carpio). / Jia, Rui; Cao, Li Ping; Du, Jin Liang; Wang, Jia Hao; Liu, Ying Juan; Jeney, G.; Xu, Pao; Yin, Guo Jun.

In: Aquatic Toxicology, Vol. 152, 2014, p. 11-19.

Research output: Contribution to journalArticle

Jia, Rui ; Cao, Li Ping ; Du, Jin Liang ; Wang, Jia Hao ; Liu, Ying Juan ; Jeney, G. ; Xu, Pao ; Yin, Guo Jun. / Effects of carbon tetrachloride on oxidative stress, inflammatory response and hepatocyte apoptosis in common carp (Cyprinus carpio). In: Aquatic Toxicology. 2014 ; Vol. 152. pp. 11-19.
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AU - Liu, Ying Juan

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AU - Xu, Pao

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AB - In the present study, the cellular and molecular mechanism of carbon tetrachloride (CCl4)-induced hepatotoxicity in fish was investigated by studying the effects of CCl4 on the oxidative stress, inflammatory response and hepatocyte apoptosis. Common carp were given an intraperitoneal injection of 30% CCl4 in arachis oil (0.5ml/kg body weight). At 72h post-injection, blood were collected to measure glutamate pyruvate transaminase (GPT), glutamate oxalate transaminase (GOT), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), total antioxidant capacity (T-AOC) and malondialdehyde (MDA), liver samples were taken to analyze toll-like receptor 4 (TLR4), cytochrome P450 2E1 (CYP2E1) and gene expressions of inflammatory cytokines and nuclear factor-κB (NF-κB/cREL). Cell viability and apoptosis were analyzed after treatment of the primary hepatocytes with CCl4 at 8mM. The results showed that CCl4 significantly increased the levels of GPT, GOT, MDA, TLR4 and CYP2E1, reduced the levels of SOD, GPx, CAT, GSH and T-AOC, and up-regulated the gene expressions of NF-κB/cREL and inflammatory cytokines including tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), IL-1β, IL-6 and IL-12. In vitro, CCl4 caused a dramatic loss in cell viability and induced hepatocyte apoptosis. Overall results suggest that oxidative stress lipid peroxidation, and TNF-α/NF-κB and TRL4/NF-κB signaling pathways play important roles in CCl4-induced hepatotoxicity in fish.

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