PUBLICATION

Bis(2-ethylhexyl)-tetrabromophthalate Poses a Higher Exposure Risk and Induces Gender-Specific Metabolic Disruptions in Zebrafish Liver

Authors
Fu, K., Zhu, B., Sun, Y., Zhou, Y., Pang, H., Ren, X., Guo, Y., Shi, X., Han, J., Yang, L., Zhou, B.
ID
ZDB-PUB-240307-3
Date
2024
Source
Environmental science & technology   58(11): 4937-4947 (Journal)
Registered Authors
Zhou, BingSheng
Keywords
bis(2-ethylhexyl)-tetrabromophthalate, gender-specific effects, metabolic disorder, nonalcoholic fatty liver, toxicokinetic
MeSH Terms
  • Animals
  • Female
  • Flame Retardants*/analysis
  • Flame Retardants*/toxicity
  • Lipid Metabolism
  • Liver/metabolism
  • Male
  • Zebrafish*
PubMed
38446036 Full text @ Env. Sci. Tech.
Abstract
Bis(2-ethylhexyl)-tetrabromophthalate (TBPH), a typical novel brominated flame retardant, has been ubiquitously identified in various environmental and biotic media. Consequently, there is an urgent need for precise risk assessment based on a comprehensive understanding of internal exposure and the corresponding toxic effects on specific tissues. In this study, we first investigated the toxicokinetic characteristics of TBPH in different tissues using the classical pseudo-first-order toxicokinetic model. We found that TBPH was prone to accumulate in the liver rather than in the gonad, brain, and muscle of both female and male zebrafish, highlighting a higher internal exposure risk for the liver. Furthermore, long-term exposure to TBPH at environmentally relevant concentrations led to increased visceral fat accumulation, signaling potential abnormal liver function. Hepatic transcriptome analysis predominantly implicated glycolipid metabolism pathways. However, alterations in the profile of associated genes and biochemical indicators revealed gender-specific responses following TBPH exposure. Besides, histopathological observations as well as the inflammatory response in the liver confirmed the development of nonalcoholic fatty liver disease, particularly in male zebrafish. Altogether, our findings highlight a higher internal exposure risk for the liver, enhancing our understanding of the gender-specific metabolic-disrupting potential associated with TBPH exposure.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping