Abstract
Highlights
- Fluoride triggered marked histological changes in the liver of Bufo gargarizans [the Asiatic toad or Chusan Island toad]
- Fluoride caused disruption of lipid metabolism.
- Fluoride resulted in impairing of antioxidant capacity.
- Fluoride induced alterations of mRNA expression of genes involved in apoptosis.
The goal of the current study was to evaluate the negative influences of fluoride on liver of Bufo gargarizans larvae. B. gargarizans larvae were treated with 42.4 mg F–/L for 0, 24, 48 and 72 h at Gosner stage 37. The morphological changes and responses of molecular biomarkers involved in lipid metabolism, oxidative stress and apoptosis were examined in liver. Disappearance of cell boundaries, degeneration of hepatic parenchyma cells and significant increase in the number of melanomacrophage centres and the quantity of lipid droplets were found in the liver treated with 42.4 mg F–/L for 72 h. In addition, in the relative expression of acetyl CoA carboxylase 1 (ACC-1), fatty acid elongase 1 (FAE-1), sterol carrier protein 2 (SCP-2), and carnitine palmitoyltransferase-1 (CPT-1), decrease was observed after 24, 48 and 72 h of 42.4 mg F–/L exposure. Furthermore, the transcript levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were downregulated in tadpoles exposed for 24, 48 and 72 h to 42.4 mg F–/L, while the transcript level of heat shock protein 90 (HSP90) was upregulated at 42.4 mg F–/L for 72 h. Also, mRNA expression of Bcl-2-associated transcription factor 1(BCLAF1) and thyroid hormone receptors (TR? and TR?) was significantly upregulated in tadpoles treated with 42.4 mg F–/L for 72 h. Therefore, our results suggested that the liver injury induced by fluoride might result from disruption of lipid metabolism, oxidative damage and apoptosis.