Objectives: We studied whether BPA can induce similar effects on membrane as those observed in autistic subjects.
Methods: Lymphoblasts from normal subjects were obtained from Autism Genetic Resource Exchange (AGRE) and incubated with various concentrations of BPA in serum- free medium for 24 h. Membrane fluidity was measured at 370C using diphenylhexatraiene (DPH) as a fluorescent probe. Since fluidity of the membrane is related to the temperature, the temperature-dependent effects of BPA on membrane fluidity were also studied at varying temperatures from 100C – 500C. In order to study the effect of BPA on membrane phospholipids, the cell lipids were extracted with chloroform (C)/methanol (M) (2:1, V/V), organic layer was dried and phospholipids were separated on silica gel 60 plates using C: M: H2O (65/25/4, V/V) as solvent system. Different phospholipids fractions were quantitated by measuring the inorganic phosphorus.
Results: BPA decreased membrane fluidity of lymphoblasts in a concentration-dependent manner. The effect of BPA on membrane fluidity was observed at all temperatures studied i.e., 10-50 0C. The measurement of different phospholipids fractions showed that BPA significantly decreases the levels of phosphatidylcholine and phosphatidylethanolamine in the lymphoblasts.
Conclusions: These results suggest that BPA exposure can decrease membrane fluidity and levels of PE. These effects of BPA were similar to those reported previously in the membranes from autistic subjects. It is proposed that BPA exposure may act as an environmental stressor in genetically susceptible individuals resulting in clinical symptoms of autism.