PUBLICATION

Mixture effect of arsenic and fluoride at environmentally relevant concentrations in zebrafish (Danio rerio) liver: Expression pattern of Nrf2 and related xenobiotic metabolizing enzymes

Authors
Mondal, P., Shaw, P., Bandyopadhyay, A., Dey Bhowmik, A., Chakraborty, A., Sudarshan, M., Chattopadhyay, A.
ID
ZDB-PUB-190614-18
Date
2019
Source
Aquatic toxicology (Amsterdam, Netherlands)   213: 105219 (Journal)
Registered Authors
Keywords
Antagonism, Co-exposure, Nrf2, Oxidative stress, Xenobiotic metabolizing enzymes, Zebrafish
MeSH Terms
  • Animals
  • Arsenic/toxicity*
  • Catalase/metabolism
  • Fluorides/toxicity*
  • Gene Expression Regulation/drug effects*
  • Glutathione/metabolism
  • Glutathione Peroxidase/metabolism
  • Liver/drug effects
  • Liver/enzymology*
  • Liver/metabolism*
  • Liver/pathology
  • NF-E2-Related Factor 2/genetics*
  • NF-E2-Related Factor 2/metabolism
  • Oxidative Stress/drug effects
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Reactive Oxygen Species/metabolism
  • Superoxide Dismutase/metabolism
  • Thiobarbituric Acid Reactive Substances/metabolism
  • Water Pollutants, Chemical/toxicity
  • Xenobiotics/metabolism*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
31195325 Full text @ Aquat. Toxicol.
CTD
31195325
Abstract
Nrf2 is a crucial transcription factor that regulates the expression of cytoprotective enzymes and controls cellular redox homeostasis. Both arsenic and fluoride are potent toxicants that are known to induce Nrf2. They are reported to coexist in many areas of the world leading to complex mixture effects in exposed organisms. The present study investigated the expression of Nrf2 and related xenobiotic metabolizing enzymes along with other stress markers such as histopathological alterations, catalase activity, reduced glutathione content and lipid peroxidation in zebrafish liver as a function of combined exposure to environmentally relevant concentrations of arsenic (37.87 μgL-1 or 5.05 × 10-7 M) and fluoride (6.8 mg L-1 or 3.57 × 10-4 M) for 60 days. The decrease in the total reduced glutathione level was evident in all treatment conditions. Hyperactivity of catalase along with conspicuous elevation in reactive oxygen species, malondialdehyde content and histo-architectural anomalies signified the presence of oxidative stress in the treatment groups. Nrf2 was seen to be induced at both transcriptional and translational levels in case of both individual and co-exposure. The same pattern was observed in case of its nuclear translocation also. From the results of qRT-PCR it was evident that at each time point co-exposure to arsenic and fluoride seemed to alter the gene expression of Cu/Zn Sod, Mn Sod, Gpx and Nqo1 just like their individual exposure but at a very low magnitude. In conclusion, this study demonstrates for the first time the differential expression and activity of Nrf2 and other stress response genes in the zebrafish liver following individual and combined exposure to arsenic and fluoride.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping