Erythrocyte Shape Abnormalities, Membrane Oxidative Damage, and β-Actin Alterations: An Unrecognized Triad in Classical Autism
Figure 4
(a) Representative SDS-PAGE analyses of RBC ghosts (silver staining) in a healthy control subject (lane C−), a positive control subject (see text for definition; lane C+), and two autistic patients (lanes A1 and A2): visible reduction of intensity for β-actin in autistic patients (lanes A1 and A2) is evidenced; the electrophoretic position of bands 4.1 and 4.2 is indicated by arrowheads; (b) SDS-PAGE of immunoprecipitated β-actin (silver staining) from RBC ghosts of a healthy control subject (lane C−), a positive control individual (lane C+), and an autistic patient (lane A): visible reduction of intensity for β-actin in autistic patients (lane A); (c) immunochemical detection in the 4-HNE protein adducts in RBC ghosts: representative western blot from a healthy control subject (lane C-), a positive control individual (lane C+) and from an autistic patients (lanes A1 and A2). An increase in the 4-HNE PAs signal is evident in RBC ghosts from autistic patients (lanes A1 and A2), in particular as it concerns the β-actin band; the 4-HNE binding to bands 4.1 and 4.2 is indicated by arrowheads; and (d) immunochemical detection in the 4-HNE protein adducts in immunoprecipitated β-actin from RBC ghosts: representative western blot from a healthy control subject (lane C−), positive control individual (lane C+), and from an autistic patient (lane A): a visible increase in the 4-HNE PAs signal in β-actin from autistic patient (lane A) is evident. Molecular weight marks are indicated on the right side.
