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In vitro effects of bisphenol F on antioxidant system indicators in the isolated hepatocytes of rainbow trout (Oncorhyncus mykiss).

Handan AykutBurak Kaptaner
Published in: Molecular biology reports (2021)
Bisphenol F (BPF) has been used frequently in the plastics industry and the production of daily consumer products as an alternative to bisphenol A (BPA). It was aimed herein to determine the cytotoxic effects of BPF on hepatocytes isolated from the liver of rainbow trout (Oncorhyncus mykiss) using lactate dehydrogenase (LDH) assay and antioxidant defence system indicators. The cultured hepatocytes were exposed to seven concentrations (0, 15.63, 31.25, 62.50, 125, 250, and 500 µM) of BPF for 24 h. According to the LDH assay, the percentage of cytotoxicity was increased dose dependently in the cells. The malondialdehyde content, which is indicative of lipid peroxidation, was increased significantly at BPF concentrations between 15.63 and 250 µM, whereas it remained unchanged with a concentration of 500 µM. The activities of superoxide dismutase were increased, while those of catalase were decreased with all of the BPF concentrations. Elevated levels of reduced glutathione content were determined with BPF concentrations between 15.63 and 250 µM, but decreased significantly with a concentration of 500 µM. Significant increases in the activities of the glutathione peroxidase were found in hepatocytes treated with BPF at concentrations of 31.25 to 500 µM. GST activity was only significantly increased with a BPF concentration of 250 µM. The results showed that the toxic mechanism of BPF was mainly based on cell membrane damage and oxidative stress, which have an influence on antioxidant defences. Therefore, BPF should be reconsidered as a safe alternative instead of BPA in the manufacturing of industrial or daily products.
Keyphrases
  • oxidative stress
  • induced apoptosis
  • liver injury
  • high throughput
  • hydrogen peroxide
  • risk assessment
  • endoplasmic reticulum stress
  • drug induced
  • wastewater treatment
  • cell death
  • newly diagnosed
  • heat shock protein