Inhibition of BPA degradation by serum as a hydroxyl radical scavenger and an Fe trapping agent in Fenton process.

Identification of reactive oxygen species (ROS) that contribute to bisphenol-A (BPA) degradation and monitoring of BPA at various concentrations in human serum under Fenton reaction conditions were carried out using electron spin resonance (ESR) spectrophotometry and high performance liquid chromatography with electrochemical detection (HPLC-ECD). BPA recovery decreased with increasing Fe concentration and time, both with a Fenton reaction using Fe(II), and with a Fenton-like reaction using Fe(III). In these reactions, BPA dose-dependently decreased the intensity of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO)-*OH, up to 1 microg/ml BPA, and no change in DMPO-O(2)(?-) intensity was observed. The decrease in BPA recovery was inhibited strongly by addition of serum under Fenton-like reaction conditions, and there was a negative correlation between turbidity and BPA recovery. To clarify the mechanism by which serum inhibits BPA degradation, the relationship between BPA recovery and sample turbidity, and characteristics of the precipitates were investigated using spectrophotometry and X-ray analysis. The precipitate formed in the serum-containing sample consisted of C, S, O, P and Fe. BPA degradation was also inhibited under Fenton-like reaction conditions in phosphate buffered saline (PBS), and a precipitate consisting of O, P, and Fe appeared. Precipitates also appeared in authentic albumin and gamma-globulin when sulfate was added with Fenton reagents. After precipitate removal, both Fe and protein concentrations in the supernatant of the protein solutions with sulfate decreased with increasing Fe addition. We demonstrate here that hydroxyl radical generation from Fenton or Fenton-like reactions can degrade BPA, and that serum strongly inhibits BPA degradation, not only by competing with BPA for hydroxyl radicals, but also by trapping Fe with oxidative components present in the serum.