A hypothetical biochemical pathway that could explain the PON1 alterations observed in the CCl
-administered rats. Free radical-induced liver impairment would result in a decrease in PPARδ gene expression and, as a consequence, in PON1 gene expression. It would also induce an inhibition of ABCA1, a decrease in HDL synthesis and, therefore, a decrease in serum PON1 concentration. Serum lactonase activity would be decreased secondarily to these changes and, as well, due to a direct inhibition by free radicals. Intrahepatic PON1 levels would be increased as a consequence of a decreased protein degradation.