Transcriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP)
Abstract Background Tris (2-chloroethyl) phosphate (TCEP), a widely used flame retardant, is widespread in the environment and potentially harmful to organisms. However, the specific mechanisms of TCEP-induced neurological and reproductive toxicity in fish are largely unknown. Turbot (Scophthalmus m...
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2025-01-01
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author | Xiaoqian Zhou Weifeng Liu Bailin Cong Aifang Deng Jing Lin Linlin Zhao Shenghao Liu |
author_facet | Xiaoqian Zhou Weifeng Liu Bailin Cong Aifang Deng Jing Lin Linlin Zhao Shenghao Liu |
author_sort | Xiaoqian Zhou |
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description | Abstract Background Tris (2-chloroethyl) phosphate (TCEP), a widely used flame retardant, is widespread in the environment and potentially harmful to organisms. However, the specific mechanisms of TCEP-induced neurological and reproductive toxicity in fish are largely unknown. Turbot (Scophthalmus maximus) is cultivated on a large scale, and the emergence of pollutants with endocrine disrupting effects seriously affects its economic benefits. This study aimed to investigate the toxic effects of TCEP on turbot by integrating physio-biochemical and transcriptomic analyses. Results TCEP exposure induced severe neuroendocrine disrupting effects in turbot. Firstly, the hormone levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E2), and 11-ketotestosterone (11-KT) were significantly decreased under prolonged TCEP stress, which may have a negative impact on normal reproductive function. We identified and summarized representative differentially expressed genes (DEGs) and their functions, such as endocrine system and oxidative stress. Pathway enrichment showed that the toxicological characteristics of TCEP on turbot were neuroendocrine regulation disorders, including oxidative phosphorylation, apoptosis, steroid biosynthesis, GnRH signaling pathway and so on. Weighted gene co-expression network analysis (WGCNA) also revealed key genes involved in these pathways. Among these genes, those encoding the components of the electron transport chain presented an initial increase in expression followed by a decrease, indicating that TCEP stress might affect mitochondrial function and lead to cell damage. This finding was also supported by the upregulation of apoptosis-related gene expression. Moreover, acute exposure to TCEP regulated MAPK-mediated transduction and regulation of GnRH signaling, thereby altering the expression of hypothalamic-pituitary-gonadal (HPG) axis-related genes. Conclusions These findings revealed the endocrine disrupting effects of TCEP on turbot and identified biomarkers related to reproductive toxicity, providing early warning for the monitoring of healthy aquaculture. |
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spelling | doaj-art-de17573c095a48449081afe063a519b82025-01-19T12:11:33ZengBMCBMC Genomics1471-21642025-01-0126111410.1186/s12864-024-11061-zTranscriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP)Xiaoqian Zhou0Weifeng Liu1Bailin Cong2Aifang Deng3Jing Lin4Linlin Zhao5Shenghao Liu6School of Advanced Manufacturing School of Ocean, Fuzhou UniversityLaboratory for Marine Ecology and Environmental Science and Technology, First Institute of Oceanography, Ministry of Natural ResourcesSchool of Advanced Manufacturing School of Ocean, Fuzhou UniversityLaboratory for Marine Ecology and Environmental Science and Technology, First Institute of Oceanography, Ministry of Natural ResourcesLaboratory for Marine Ecology and Environmental Science and Technology, First Institute of Oceanography, Ministry of Natural ResourcesLaboratory for Marine Ecology and Environmental Science and Technology, First Institute of Oceanography, Ministry of Natural ResourcesLaboratory for Marine Ecology and Environmental Science and Technology, First Institute of Oceanography, Ministry of Natural ResourcesAbstract Background Tris (2-chloroethyl) phosphate (TCEP), a widely used flame retardant, is widespread in the environment and potentially harmful to organisms. However, the specific mechanisms of TCEP-induced neurological and reproductive toxicity in fish are largely unknown. Turbot (Scophthalmus maximus) is cultivated on a large scale, and the emergence of pollutants with endocrine disrupting effects seriously affects its economic benefits. This study aimed to investigate the toxic effects of TCEP on turbot by integrating physio-biochemical and transcriptomic analyses. Results TCEP exposure induced severe neuroendocrine disrupting effects in turbot. Firstly, the hormone levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E2), and 11-ketotestosterone (11-KT) were significantly decreased under prolonged TCEP stress, which may have a negative impact on normal reproductive function. We identified and summarized representative differentially expressed genes (DEGs) and their functions, such as endocrine system and oxidative stress. Pathway enrichment showed that the toxicological characteristics of TCEP on turbot were neuroendocrine regulation disorders, including oxidative phosphorylation, apoptosis, steroid biosynthesis, GnRH signaling pathway and so on. Weighted gene co-expression network analysis (WGCNA) also revealed key genes involved in these pathways. Among these genes, those encoding the components of the electron transport chain presented an initial increase in expression followed by a decrease, indicating that TCEP stress might affect mitochondrial function and lead to cell damage. This finding was also supported by the upregulation of apoptosis-related gene expression. Moreover, acute exposure to TCEP regulated MAPK-mediated transduction and regulation of GnRH signaling, thereby altering the expression of hypothalamic-pituitary-gonadal (HPG) axis-related genes. Conclusions These findings revealed the endocrine disrupting effects of TCEP on turbot and identified biomarkers related to reproductive toxicity, providing early warning for the monitoring of healthy aquaculture.https://doi.org/10.1186/s12864-024-11061-zTurbotTris (2-chloroethyl) phosphate (TCEP)TranscriptomicsReproductive toxicity |
spellingShingle | Xiaoqian Zhou Weifeng Liu Bailin Cong Aifang Deng Jing Lin Linlin Zhao Shenghao Liu Transcriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP) BMC Genomics Turbot Tris (2-chloroethyl) phosphate (TCEP) Transcriptomics Reproductive toxicity |
title | Transcriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP) |
title_full | Transcriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP) |
title_fullStr | Transcriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP) |
title_full_unstemmed | Transcriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP) |
title_short | Transcriptomics-based analysis of neurotoxic and reproductive effects in turbot (Scophthalmus maximus) after exposure to tris (2-chloroethyl) phosphate (TCEP) |
title_sort | transcriptomics based analysis of neurotoxic and reproductive effects in turbot scophthalmus maximus after exposure to tris 2 chloroethyl phosphate tcep |
topic | Turbot Tris (2-chloroethyl) phosphate (TCEP) Transcriptomics Reproductive toxicity |
url | https://doi.org/10.1186/s12864-024-11061-z |
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