PUBLICATION
Dibutyl phthalate disrupts energy metabolism and morphology in the gills and induces hepatotoxicity in zebrafish
- Authors
- Rodrigues, K., Batista-Silva, H., de Moura, K.R.S., Van Der Kraak, G., Silva, F.R.M.B.
- ID
- ZDB-PUB-230804-45
- Date
- 2023
- Source
- Fish physiology and biochemistry 49(5): 883-893 (Journal)
- Registered Authors
- Van Der Kraak, Glen
- Keywords
- Fish, Glycogen, Glucose, Lactate, Phthalate, Toxicity
- MeSH Terms
-
- Gills/metabolism
- Animals
- Dibutyl Phthalate/metabolism
- Dibutyl Phthalate/toxicity
- Chemical and Drug Induced Liver Injury*
- Lactates/metabolism
- Lactates/pharmacology
- Energy Metabolism
- Zebrafish*/metabolism
- PubMed
- 37537493 Full text @ Fish Physiol. Biochem.
Citation
Rodrigues, K., Batista-Silva, H., de Moura, K.R.S., Van Der Kraak, G., Silva, F.R.M.B. (2023) Dibutyl phthalate disrupts energy metabolism and morphology in the gills and induces hepatotoxicity in zebrafish. Fish physiology and biochemistry. 49(5):883-893.
Abstract
This study investigated the acute effects of dibutyl phthalate (DBP) exposure on energy metabolism and gill histology in zebrafish (Danio rerio). The in vitro incubation of gill tissue with 10 μM DBP for 60 min altered tissue energy supply, as shown by decreased lactate content and lactate dehydrogenase (LDH) activity. Higher concentrations of DBP (100 μM and 1 mM) increased lactate content and LDH activity; however, they blocked glucose uptake, depleted the glycogen content in cellular stores, and induced injury to the gills, as measured by LDH release to the extracellular medium. In addition, in vivo exposure of fish to 1 pM DBP for 12 h induced liver damage by increasing alanine aminotransferase (ALT) and gamma-glutamyl transferase (GGT) activities. Gill histology indicated hyperemia, lamellar fusion, lamellar telangiectasis, and necrosis. Data indicate that acute exposure of zebrafish gills to the higher DBP concentrations studied induces anaerobic cellular activity and high lactate production, causing gill damage, diminishing cell viability, and incurring liver dysfunction.
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Human Disease / Model
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