Global warming causes the release of dioxin-like deposits and increases geographical migration, increasing the risk of exposure for humans and animals. In this experiment, we used CYP1A transgenic zebrafish Tg (cyp1a: mCherry) and liver fluorescent transgenic zebrafish Tg (fabp10: Ps Red) as an animal model and exposed to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) at 26 °C and 30 °C, respectively. Morphological changes, histological changes, transcriptome and related genes expression were detected. The results showed that exposure to TCDD at 30 °C increased the mortality rate, pericardial cavity area, and reduced the number of liver cells in zebrafish larvae compared to 26 °C. Transcriptome analysis showed that, TCDD significantly altered Peroxisome Proliferators-Activated Receptors (PPARs) metabolic pathway, adipocytokine, fatty acid degradation and cell death. qRT-PCR also detected a further significant increase in the expression of ahr2, cyp-related genes (cyp1.1, cyp1b1, cyp1c1 and cyp3a65), and PPARs (pparα, pparβ and pparγ) in zebrafish larvae induced by TCDD exposure under 30 °C compared to 26 °C water temperature incubation. Our results showed that the increase of ambient temperature (from 26 °C to 30 °C) causes TCDD induced hepatotoxicity to be more intense. The observed toxic changes were likely related to lipid peroxidation.
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http://dx.doi.org/10.1016/j.envpol.2025.126039 | DOI Listing |
Environ Pollut
March 2025
College of Animal Science and Technology, Inner Mongolia Minzu University, Tongliao, Inner Mongolia, 028000, China; Inner Mongolia Key Laboratory of Toxicant Monitoring and Toxicology. Electronic address:
Global warming causes the release of dioxin-like deposits and increases geographical migration, increasing the risk of exposure for humans and animals. In this experiment, we used CYP1A transgenic zebrafish Tg (cyp1a: mCherry) and liver fluorescent transgenic zebrafish Tg (fabp10: Ps Red) as an animal model and exposed to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) at 26 °C and 30 °C, respectively. Morphological changes, histological changes, transcriptome and related genes expression were detected.
View Article and Find Full Text PDFEcotoxicol Environ Saf
March 2025
Nanjing Institute of Environmental Sciences, Ministry of Ecology and Environment, Nanjing 210042, China. Electronic address:
The increasing global spread of cyanobacteria and their toxin Cylindrospermopsin (CYN) is a growing concern.This study aimed to examine the toxic effects of CYN on the early neurodevelopment of zebrafish, and to identify the underlying mechanisms. The findings indicated that zebrafish exposed to varying concentrations of CYN exhibited general developmental toxicity, including typical malformations, diminished embryonic movement, and shortened body length.
View Article and Find Full Text PDFSci China Life Sci
March 2025
State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China.
Sound pollution (noise) is an increasing environmental concern, particularly associated with neurological and neurobehavioral abnormalities. However, the molecular mechanisms underlying noise-induced neural damage remain unclear. In this study, we conducted transcriptional profiling of zebrafish to investigate the mechanisms underlying acoustic stimulation (1,000 Hz, 130 dB).
View Article and Find Full Text PDFSci Rep
March 2025
Department of Pharmacology and Regenerative Medicine, University of Illinois College of Medicine, Chicago, IL, 60612, USA.
Edema, characterized by the accumulation of interstitial fluid, poses significant challenges in various pathological conditions. Lymphangiogenesis is critical in edema clearance, and delayed or inadequate lymphatic responses significantly hinder healing processes. However, real-time observation of dynamic changes in lymphangiogenesis during tissue repair in animal models has been challenging, leaving the mechanisms behind compensatory lymphatic activation for edema clearance largely unexplored.
View Article and Find Full Text PDFPLoS One
March 2025
Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin, United States of America.
Damage to the axons of the adult mammalian central nervous system (CNS) from traumatic injury or neurodegenerative diseases often results in permanent loss of function due to failure of axons to regenerate. Zebrafish, however, can express regeneration-associated genes to revert CNS neurons to a growth-competent state and regenerate damaged axons to functionality. An established model for CNS axon regeneration is optic nerve injury in zebrafish, where it was previously shown that thousands of genes are temporally expressed during the regeneration time course.
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