Dibutyl phthalate disrupts energy metabolism and morphology in the gills and induces hepatotoxicity in zebrafish

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 mu M DBP for 60 min altered tissue energy supply, as shown by decreased lactate content and lactate dehydrogenase (LDH) activity. Higher concentrations of DBP (100 mu M 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.

Automated summary

This study examined the immediate impacts of dibutyl phthalate (DBP) exposure on energy metabolism and gill histology in zebrafish. In vitro exposure to 10 μM DBP for 60 minutes resulted in altered energy supply in the gill tissue, with decreased lactate content and lactate dehydrogenase (LDH) activity. Higher DBP concentrations (100 μM and 1 mM) increased lactate content and LDH activity, blocked glucose uptake, depleted glycogen content, and caused gill injury and liver damage.