PUBLICATION

Fluoride exposure abates pro-inflammatory response and induces in vivo apoptosis rendering zebrafish (Danio rerio) susceptible to bacterial infections

Authors
Singh, R., Khatri, P., Srivastava, N., Jain, S., Bramchari, V., Mukhopadhyay, A., Mazumder, S.
ID
ZDB-PUB-170223-6
Date
2017
Source
Fish & shellfish immunology   63: 314-321 (Journal)
Registered Authors
Keywords
Apoptosis, DNA repair, Fluoride, Oxidative stress, Pro-inflammatory cytokine, Zebrafish
MeSH Terms
  • Animals
  • Antioxidants/metabolism*
  • Cytokines/genetics*
  • Cytokines/metabolism
  • DNA Repair/drug effects*
  • Fish Proteins/genetics
  • Fish Proteins/metabolism
  • Fluorides/immunology
  • Fluorides/toxicity*
  • Gene Expression/drug effects*
  • Interferon-gamma/genetics
  • Interferon-gamma/metabolism
  • Interleukin-1beta/genetics
  • Interleukin-1beta/metabolism
  • Tumor Necrosis Factor-alpha/genetics
  • Tumor Necrosis Factor-alpha/metabolism
  • Water Pollutants, Chemical/immunology
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/immunology*
PubMed
28223109 Full text @ Fish Shellfish Immunol.
Abstract
The present study describes the immunotoxic effect of chronic fluoride exposure on adult zebrafish (Danio rerio). Zebrafish were exposed to fluoride (71.12 mg/L; 1/10 LC50) for 30 d and the expression of selected genes studied. We observed significant elevation in the detoxification pathway gene cyp1a suggesting chronic exposure to non-lethal concentration of fluoride is indeed toxic to fish. Fluoride mediated pro-oxidative stress is implicated with the downregulation in superoxide dismutase 1 and 2 (sod1/2) genes. Fluoride affected DNA repair machinery by abrogating the expression of the DNA repair gene rad51 and growth arrest and DNA damage inducible beta a gene gadd45ba. The upregulated expression of casp3a coupled with altered Bcl-2 associated X protein/B-cell lymphoma 2 ratio (baxa/bcl2a) clearly suggested chronic fluoride exposure induced the apoptotic cascade in zebrafish. Fluoride-exposed zebrafish when challenged with non-lethal dose of fish pathogen A. hydrophila revealed gross histopathology in spleen, bacterial persistence and significant mortality. We report that fluoride interferes with system-level output of pro-inflammatory cytokines tumour necrosis factor-α, interleukin-1β and interferon-γ, as a consequence, bacteria replicate efficiently causing significant fish mortality. We conclude, chronic fluoride exposure impairs the redox balance, affects DNA repair machinery with pro-apoptotic implications and suppresses pro-inflammatory cytokines expression abrogating host immunity to bacterial infections.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping