Back to Search Start Over

Transcriptome-based analysis reveals the toxic effects of perfluorononanoic acid by affecting the development of the cardiovascular system and lipid metabolism in zebrafish.

Authors :
Qian M
Sun W
Cheng L
Wu Y
Wang L
Liu H
Source :
Comparative biochemistry and physiology. Toxicology & pharmacology : CBP [Comp Biochem Physiol C Toxicol Pharmacol] 2025 Mar; Vol. 289, pp. 110108. Date of Electronic Publication: 2024 Dec 07.
Publication Year :
2025

Abstract

Perfluorononanoic acid (PFNA) is a perfluoroalkyl acid containing nine carbon chains, with an additional carbon‑fluorine bond that makes it more stable and toxic. Studies have shown that PFNA can harm the reproductive, immune, and nervous systems, as well as many organs, which can increase the risk of cancer. In this study, zebrafish embryos were treated with 0 and 100 μM PFNA for 72 and 96 hpf, and their angiogenesis and haematopoiesis were observed under laser confocal microscopy using Tg (fli1:EGFP) and Tg (gata1:DsRed) transgenic zebrafish. The data showed that PFNA exposure decreased heart rate and slowed blood flow in zebrafish. PFNA was found to inhibit erythropoiesis by O-dianisidine staining. RNA-seq analysis was used to compare gene expression changes in zebrafish from control and 100 μM PFNA-exposed groups at 72 hpf. KEGG results showed significant enrichment of PPAR signaling pathway, fatty acid metabolism, steroid biosynthesis and apoptosis. The RNA-seq results were validated by real-time fluorescence quantitative PCR (RT-qPCR). Oil red O staining and Filipin staining showed increased lipid accumulation after PFNA exposure, and TUNEL staining showed that PFNA exposure led to apoptosis. In conclusion, exposure to PFNA may cause toxic effects in zebrafish by affecting cardiovascular development, causing lipid accumulation and promoting apoptosis.<br />Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1532-0456
Volume :
289
Database :
MEDLINE
Journal :
Comparative biochemistry and physiology. Toxicology & pharmacology : CBP
Publication Type :
Academic Journal
Accession number :
39647647
Full Text :
https://doi.org/10.1016/j.cbpc.2024.110108