PUBLICATION

Exposure to mercuric chloride induces developmental damage, oxidative stress and immunotoxicity in zebrafish embryos-larvae

Authors
Zhang, Q.F., Li, Y.W., Liu, Z.H., Chen, Q.L.
ID
ZDB-PUB-161110-22
Date
2016
Source
Aquatic toxicology (Amsterdam, Netherlands)   181: 76-85 (Journal)
Registered Authors
Keywords
Developmental damage, Immunotoxicity, Mercuric chloride exposure, Oxidative stress
MeSH Terms
  • Animals
  • Antioxidants/metabolism
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/metabolism
  • Embryonic Development/drug effects
  • Glutathione/metabolism
  • Immunity, Innate/drug effects
  • Larva/drug effects
  • Larva/growth & development
  • Larva/metabolism
  • Malondialdehyde/metabolism
  • Mercuric Chloride/toxicity*
  • Oxidative Stress/drug effects*
  • Oxidoreductases/genetics
  • Oxidoreductases/metabolism
  • Real-Time Polymerase Chain Reaction
  • Water Pollutants, Chemical/chemistry
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/growth & development*
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
27821350 Full text @ Aquat. Toxicol.
Abstract
Mercury (Hg) is a widespread environmental pollutant that can produce severe negative effects on fish even at very low concentrations. However, the mechanisms underlying inorganic Hg-induced oxidative stress and immunotoxicity in the early development stage of fish still need to be clarified. In the present study, zebrafish (Danio rerio) embryos were exposed to different concentrations of Hg2+ (0, 1, 4 and 16μg/L; added as mercuric chloride, HgCl2) from 2h post-fertilization (hpf) to 168hpf. Developmental parameters and total Hg accumulation were monitored during the exposure period, and antioxidant status and the mRNA expression of genes related to the innate immune system were examined at 168hpf. The results showed that increasing Hg2+ concentration and time significantly increased total Hg accumulation in zebrafish embryos-larvae. Exposure to 16μg/L Hg2+ caused developmental damage, including increased mortality and malformation, decreased body length, and delayed hatching period. Meanwhile, HgCl2 exposure (especially in the 16μg/L Hg2+ group) induced oxidative stress affecting antioxidant enzyme (CAT, GST and GPX) activities, endogenous GSH and MDA contents, as well as the mRNA levels of genes (cat1, sod1, gstr, gpx1a, nrf2, keap1, hsp70 and mt) encoding antioxidant proteins. Moreover, the transcription levels of several representative genes (il-1β, il-8, il-10, tnfα2, lyz and c3) involved in innate immunity were up-regulated by HgCl2 exposure, suggesting that inorganic Hg had the potential to induce immunotoxicity. Taken together, the present study provides evidence that waterborne HgCl2 exposure can induce developmental impairment, oxidative stress and immunotoxicity in the early development stage of fish, which brings insights into the toxicity mechanisms of inorganic Hg in fish.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping