Triclosan (TCS) and perfluorooctane sulfonate (PFOS) are known to have both endocrine disrupting and developmental toxicity effects on zebrafish embryos. Currently, potential molecular mechanisms underlying these toxicological phenomena require further studies. To address this gap in the literature, we used whole transcriptome microarrays to being to address the potential molecular mechanisms underlying developmental toxicity of TCS and PFOS on zebrafish embryos. Zebrafish embryos were exposed to 300 μg/L TCS and 500 μg/L PFOS from 4 to 120 h post fertilization (hpf). Phenotypically, the hatching rate of zebrafish embryos was significantly reduced after TCS exposure at 72 hpf. Additionally, body length was significantly decreased in the TCS treatment group at 120 hpf. Gene ontology analysis of differentially expressed genes revealed that lipid metabolism, steroid metabolism, and organ development-related biological processes were significantly enriched in TCS- and PFOS-treated zebrafish embryos. Furthermore, signaling network analysis indicated that the steroid biosynthesis process was the most significant biological process disrupted by TCS in 120 hpf zebrafish embryos, while organ development was the most significant biological process disrupted by PFOS exposure. Our findings enhance the understanding of the specific types of embryotoxicity elicited by TCS and PFOS, and also provide information that can be used to inform future mechanistic studies.
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http://dx.doi.org/10.1007/s11356-021-14527-9 | DOI Listing |
Front Cell Dev Biol
December 2024
Jiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Organs Development and Epigenetics, Key Laboratory of Jiangxi Province for Biological Invasion and Biosecurity, College of Life Sciences, Clinical Research Center of Affiliated Hospital of Jinggangshan University, Jinggangshan University, Ji'an, China.
Reproductive system diseases have become a major health challenge facing humans, so extensive investigations are needed to understand their complex pathogenesis and summarize effective treatments. In the study of reproductive diseases, mice are the most commonly used animal model. However, the cost and time required to establish mouse animal models are high.
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January 2025
Division of Pediatric Gastroenterology and Nutrition, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Coxsackie and adenovirus receptor-like membrane protein (CLMP) mutation is identified as a genetic risk factor of congenital short bowel syndrome (CSBS). However, the specific pathogenic mechanism remains unclear. This study aimed to explore the clinical manifestations, genetic characteristics, and molecular mechanisms underlying CSBS caused by CLMP mutations.
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January 2025
Biology Department, Texas A&M University, College Station, TX 7843-3258. Electronic address:
During development of the vertebrate inner ear, sensory epithelia and neurons of the statoacoustic ganglion (SAG) arise from lineage-restricted progenitors that proliferate extensively before differentiating into mature post-mitotic cell types. Development of progenitors is regulated by Fgf, Wnt and Notch signaling, but how these pathways are coordinated to achieve an optimal balance of proliferation and differentiation is not well understood. Here we investigate the role in zebrafish of Foxm1, a transcription factor commonly associated with proliferation in developing tissues and tumors.
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January 2025
Faculty and Graduate School of Fisheries Sciences, Hokkaido University, Hokkaido, Japan.
Artificially induced haploidy is lethal in vertebrates, although it is useful for genetic screening and genome editing due to its single set of genomes. Haploid embryonic stem (ES) cell lines in mammals contribute to genetic studies and the production of gametes derived from haploid ES cells. In fish breeding, doubled haploids (DHs) induced by artificially induced gynogenesis are used to generate isogenic gametes for cloning purposes.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Biochemistry and Molecular Biology, Institute of Marine and Environmental Technology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Molecular chaperones play critical roles in post-translational maintenance in protein homeostasis. Previous studies have shown that loss of Smyd1b function results in defective myofibril organization and dramatic upregulation of heat shock protein gene (hsp) expression in muscle cells of zebrafish embryos. To investigate the molecular mechanisms and functional importance of this stress response, we characterized changes of gene expression in smyd1b knockdown and knockout embryos using RNA-seq.
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