PUBLICATION

Monobutyl phthalate (MBP) can dysregulate the antioxidant system and induce apoptosis of zebrafish liver

Authors
Jiao, Y., Tao, Y., Yang, Y., Diogene, T., Yu, H., He, Z., Han, W., Chen, Z., Wu, P., Zhang, Y.
ID
ZDB-PUB-191126-3
Date
2019
Source
Environmental pollution (Barking, Essex : 1987)   257: 113517 (Journal)
Registered Authors
Zhang, Ying
Keywords
Apoptosis, Liver, MBP, Oxidative stress, Zebrafish
MeSH Terms
  • Alanine Transaminase
  • Animals
  • Antioxidants/metabolism
  • Apoptosis
  • Aspartate Aminotransferases
  • Dibutyl Phthalate/metabolism
  • Kelch-Like ECH-Associated Protein 1
  • Liver/drug effects
  • Liver/metabolism
  • Liver/physiology*
  • Malondialdehyde/metabolism
  • NF-E2-Related Factor 2/metabolism
  • Oxidative Stress/drug effects
  • Phthalic Acids/toxicity*
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/metabolism
  • Zebrafish/physiology
  • Zebrafish Proteins/metabolism
PubMed
31761585 Full text @ Environ. Pollut.
Abstract
In this paper, the acute toxicity of monobutyl phthalate (MBP), the main hydrolysis product of dibutyl phthalate, on adult zebrafish liver antioxidant system was studied. Compared the toxicity effect of MBP and DBP by histopathology and apoptosis experiments, we speculated that the toxic effects of DBP on animals may be caused by its metabolite MBP. The results indicated that the antioxidant Nrf2-Keap1 pathway was insufficient to resist MBP-induced hepatotoxicity and led to an imbalance of membrane ion homeostasis and liver damage. Decreased cell viability, significant tissue lesions and early hepatocyte apoptosis were observed in the zebrafish liver in MBP exposure at high concentration (10 mg/L). The activities of antioxidant enzymes and ATPases in zebrafish liver were inhibited with increased malondialdehyde (MDA) content and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Integrated biomarker response (IBR) calculation results indicated that MBP mainly inhibited catalase (CAT) activity. Simultaneously, the expression of antioxidant-related genes (SOD, CAT, GPx, Nrf2, HO-1) was down-regulated, while apoptosis-related genes (p53, bax, cas3) were significantly up-regulated.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping