PUBLICATION

Effects of Metabolic Disruption on Lipid Metabolism and Yolk Retention in Zebrafish Embryos

Authors
van den Boom, R., Vergauwen, L., Knapen, D.
ID
ZDB-PUB-240612-1
Date
2024
Source
Environmental toxicology and chemistry   43(8): 1880-1893 (Journal)
Registered Authors
Knapen, Dries, Vergauwen, Lucia
Keywords
Aquatic toxicology, Developmental toxicity, Endocrineā€disrupting compounds, Toxicity mechanisms
MeSH Terms
  • Animals
  • Benzhydryl Compounds/toxicity
  • Egg Yolk/drug effects
  • Embryo, Nonmammalian*/drug effects
  • Embryo, Nonmammalian*/metabolism
  • Endocrine Disruptors/toxicity
  • Lipid Metabolism*/drug effects
  • PPAR gamma/metabolism
  • Rosiglitazone/pharmacology
  • Water Pollutants, Chemical*/toxicity
  • Zebrafish*
PubMed
38860666 Full text @ Environ. Toxicol. Chem.
CTD
38860666
Abstract
A subgroup of endocrine-disrupting chemicals have the ability to disrupt metabolism. These metabolism-disrupting chemicals (MDCs) can end up in aquatic environments and lead to adverse outcomes in fish. Although molecular and physiological effects of MDCs have been studied in adult fish, few studies have investigated the consequences of metabolic disruption in fish during the earliest life stages. To investigate the processes affected by metabolic disruption, zebrafish embryos were exposed to peroxisome proliferator-activated receptor gamma (PPARγ) agonist rosiglitazone, the PPARγ antagonist T0070907, and the well-known environmentally relevant MDC bisphenol A. Decreased apolipoprotein Ea transcript levels indicated disrupted lipid transport, which was likely related to the observed dose-dependent increases in yolk size across all compounds. Increased yolk size and decreased swimming activity indicate decreased energy usage, which could lead to adverse outcomes because the availability of energy reserves is essential for embryo survival and growth. Exposure to T0070907 resulted in a darkened yolk. This was likely related to reduced transcript levels of genes involved in lipid transport and fatty acid oxidation, a combination of responses that was specific to exposure to this compound, possibly leading to lipid accumulation and cell death in the yolk. Paraoxonase 1 (Pon1) transcript levels were increased by rosiglitazone and T0070907, but this was not reflected in PON1 enzyme activities. The present study shows how exposure to MDCs can influence biochemical and molecular processes involved in early lipid metabolism and may lead to adverse outcomes in the earliest life stages of fish. Environ Toxicol Chem 2024;00:1-14. © 2024 The Author(s). Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.
Genes / Markers
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
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Mapping