ZFIN ID: ZDB-PUB-130416-13
Global gene expression analysis reveals pathway differences between teratogenic and non-teratogenic exposure concentrations of bisphenol A and 17beta-estradiol in embryonic zebrafish
Saili, K.S., Tilton, S.C., Waters, K.M., and Tanguay, R.L.
Date: 2013
Source: Reproductive toxicology (Elmsford, N.Y.) 38: 89-101 (Journal)
Registered Authors: Tanguay, Robert L., Tilton, Susan C.
Keywords: Bisphenol A, 17β-estradiol, microarray, zebrafish, prothrombin, CREB
Microarrays: GEO:GSE38960
MeSH Terms:
  • Animals
  • Benzhydryl Compounds/toxicity*
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/metabolism
  • Estradiol/toxicity*
  • Gene Expression Profiling
  • Gene Expression Regulation, Developmental/drug effects*
  • Oligonucleotide Array Sequence Analysis
  • Phenols/toxicity*
  • Teratogens/toxicity*
  • Zebrafish
PubMed: 23557687 Full text @ Reprod. Toxicol.

Transient developmental exposure to 0.1 μM bisphenol A (BPA) results in larval zebrafish hyperactivity and learning impairments in the adult, while exposure to 80 μM BPA results in teratogenic responses, including craniofacial abnormalities and edema. The mode of action underlying these effects is unclear. We used global gene expression analysis to identify candidate genes and signaling pathways that mediate BPA's developmental toxicity in zebrafish. Exposure concentrations were selected and anchored to the positive control, 17β-estradiol (E2), based on previously determined behavioral or teratogenic phenotypes. Functional analysis of differentially expressed genes revealed distinct expression profiles at 24 hours post fertilization for 0.1 versus 80 μM BPA and 0.1 versus 15 μM E2 exposure, identification of prothrombin activation as a top canonical pathway impacted by both 0.1 μM BPA and 0.1 μM E2 exposure, and suppressed expression of several genes involved in nervous system development and function following 0.1 μM BPA exposure.