Amperometric Cytosensor for Studying Mitochondrial Interferences Induced by Plasticizers Bisphenol B and Bisphenol A

Abstract

The widespread presence of plasticizers Bisphenol B (BPB) and Bisphenol A (BPA) in food contact materials, medical equipment, and common household products is a toxicological risk factor for health due to internal exposure after environmental dietary exposure. This work describes the use of an amperometric cytosensor (i.e., a whole cell-based amperometric biosensoristic device) for studying mitochondrial interferences of BPA and BPB (5–100 µg/mL) in the yeast Saccharomyces cerevisiae model following long-term (24 h) exposure (acute toxicity). Percentage interference (%ρ) on yeast aerobic mitochondrial catabolism was calculated after comparison of aerobic respiration of exposed and control S. cerevisiae cell suspensions. Results suggested the hypothesis of a dose-dependent co-action of two mechanisms, namely uncoupling of oxidative phosphorylation and oxidative stress. These mechanisms respectively matched with opposite effects of hyperstimulation and inhibition of cellular respiration. While uncoupling of oxidative phosphorylation and oxidative stress have been previously described as separate effects from in vitro BPA exposure using other biochemical endpoints and biological systems, effects of BPB on cellular aerobic respiration are here reported for the first time. Results highlighted a similar hyperstimulation effect after exposure to 5 µg/mL BPA and BPB. About a 2-fold higher cellular respiration inhibition potency was observed after exposures to 15, 30, and 100 µg/mL BPB compared to BPA. 2,4-Dinitrophenol (2,4-DNP) was used as model uncoupling agent. A time-dependent mechanism of mitochondrial interference was also highlighted.