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Exposure of Larval Zebrafish to the Insecticide Propoxur Induced Developmental Delays that Correlate with Behavioral Abnormalities and Altered Expression of hspb9 and hspb11

Authors
  • Shields, Jeremiah N.1
  • Hales, Eric C.2
  • Ranspach, Lillian E.3
  • Luo, Xixia3
  • Orr, Steven2
  • Runft, Donna4
  • Dombkowski, Alan5
  • Neely, Melody N.4
  • Matherly, Larry H.
  • Taub, Jeffrey W.5
  • Baker, Tracie R.1, 6
  • Thummel, Ryan3
  • 1 (T.R.B.)
  • 2 (S.O.)
  • 3 (X.L.)
  • 4 (M.N.N.)
  • 5 (A.D.);
  • 6 Department of Pharmacology, Wayne State University, Detroit, MI 48201, USA
Type
Published Article
Journal
Toxics
Publisher
MDPI
Publication Date
Sep 21, 2019
Volume
7
Issue
4
Identifiers
DOI: 10.3390/toxics7040050
PMID: 31546644
PMCID: PMC6958418
Source
PubMed Central
Keywords
License
Green

Abstract

Recent studies suggest that organophosphates and carbamates affect human fetal development, resulting in neurological and growth impairment. However, these studies are conflicting and the extent of adverse effects due to pesticide exposure warrants further investigation. In the present study, we examined the impact of the carbamate insecticide propoxur on zebrafish development. We found that propoxur exposure delays embryonic development, resulting in three distinct developmental stages: no delay, mild delay, or severe delay. Interestingly, the delayed embryos all physically recovered 5 days after exposure, but behavioral analysis revealed persistent cognitive deficits at later stages. Microarray analysis identified 59 genes significantly changed by propoxur treatment, and Ingenuity Pathway Analysis revealed that these genes are involved in cancer, organismal abnormalities, neurological disease, and hematological system development. We further examined hspb9 and hspb11 due to their potential roles in zebrafish development and found that propoxur increases expression of these small heat shock proteins in all of the exposed animals. However, we discovered that less significant increases were associated with the more severely delayed phenotype. This raises the possibility that a decreased ability to upregulate these small heat shock proteins in response to propoxur exposure may cause embryos to be more severely delayed.

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