PUBLICATION

BLT-1, a specific inhibitor of the HDL receptor SR-BI, induces a copper-dependent phenotype during zebrafish development

Authors
Raldúa, D., and Babin, P.J.
ID
ZDB-PUB-071001-5
Date
2007
Source
Toxicology letters   175(1-3): 1-7 (Journal)
Registered Authors
Babin, Patrick J., Raldúa, Demetrio
Keywords
BLT-1, Copper, High-density lipoproteins, SCARB1, Scavenger receptor class B type 1, Zebrafish
MeSH Terms
  • Animals
  • Brain/abnormalities
  • Brain/drug effects
  • Chelating Agents/toxicity*
  • Copper/metabolism*
  • Copper/pharmacology
  • Cyclopentanes/toxicity*
  • Embryo, Nonmammalian/abnormalities
  • Embryo, Nonmammalian/drug effects*
  • Melanins/metabolism
  • Notochord/abnormalities
  • Notochord/drug effects
  • Phenotype
  • Protective Agents/pharmacology
  • Scavenger Receptors, Class B/antagonists & inhibitors*
  • Scavenger Receptors, Class B/metabolism
  • Skin Pigmentation/drug effects
  • Thiosemicarbazones/toxicity*
  • Zebrafish/abnormalities*
PubMed
17890024 Full text @ Toxicol. Lett.
CTD
17890024
Abstract
Block lipid transport-1 (BLT-1) is a small chemical widely used to inhibit the transfer of lipids between high-density lipoproteins (HDL) and cells mediated by scavenger receptor B, type 1 (SR-BI). This study demonstrated that BLT-1 induced in zebrafish (Danio rerio) embryos a copper-dependent phenotype with a twisted notochord, brain ventricle enlargement, and absence of melanisation, phenocopying neocuproine-treated, or calamity mutants. This finding supports an unexpected link between copper availability and SR-BI activity. The copper-chelating activity of BLT-1, revealed by its dramatic effect during embryo development, should be considered in any evaluation of the pharmacological effect of this thiosemicarbazone derivative on SR-BI activity and the potential therapeutic value of this molecule.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping