PUBLICATION

Chronic exposure to low benzo[a]pyrene level causes neurodegenerative disease-like syndromes in zebrafish (Danio rerio)

Authors
Gao, D., Wu, M., Wang, C., Wang, Y., Zuo, Z.
ID
ZDB-PUB-150910-1
Date
2015
Source
Aquatic toxicology (Amsterdam, Netherlands)   167: 200-208 (Journal)
Registered Authors
Keywords
Alzheimer’s disease, Benzo[a]pyrene, Neurodegenerative disease, Parkinson’s disease, Zebrafish
MeSH Terms
  • Animals
  • Benzo(a)pyrene/toxicity*
  • Brain/drug effects
  • Environmental Exposure*
  • Gene Expression Regulation/drug effects
  • Neurodegenerative Diseases/chemically induced*
  • Polycyclic Aromatic Hydrocarbons/toxicity
  • Syndrome
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/genetics
  • Zebrafish/physiology*
PubMed
26349946 Full text @ Aquat. Toxicol.
Abstract
Previous epidemiological and animal studies report that exposure to environmental pollutant exposure links to neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. Benzo[a]pyrene (BaP), a neurotoxic polycyclic aromatic hydrocarbon, has been increasingly released into the environment during recent decades. So far, the role of BaP on the development of neurodegenerative diseases remaind unclear. This study aimed to determine whether chronic exposure to low dose BaP would cause neurodegenerative disease-like syndromes in zebrafish (Danio rerio). We exposed zebrafish, from early embryogenesis to adults, to environmentally relevant concentrations of BaP for 230 days. Our results indicated that BaP decreased the brain weight to body weight ratio, locomotor activity and cognitive ability; induced the loss of dopaminergic neurons; and resulted in neurodegeneration. In addition, obvious cell apoptosis in the brain was found. Furthermore, the neurotransmitter levels of dopamine and 3,4-dihydroxyphenylacetic acid, the mRNA levels of the genes encoding dopamine transporter, Parkinson protein 7, phosphatase and tensin-induced putative kinase 1, ubiquitin carboxy-terminal hydrolase L1, leucine-rich repeat serine/threonine kinase 2, amyloid precursor protein b, presenilin 1 and presenilin 2 were significantly down-regulated by BaP exposure. These findings suggest that chronic exposure to low dose BaP could cause the behavioral, neuropathological, neurochemical, and genetic features of neurodegenerative diseases. This study provides clues that BaP may constitute an important environmental risk factor for neurodegenerative diseases in humans.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping