EFFECTS OF CHRONIC ETHANOL-CONSUMPTION ON STEROL TRANSFER PROTEINS INMOUSE-BRAIN

Although lipids are essential to brain function, almost nothing is kno wn of lipid transfer proteins in the brain. Early reports indicates cr oss-reactivity of brain proteins with antisera against two native live r sterol transfer proteins, sterol carrier protein-2 (SCP-2) and the l iver form of fatty acid-binding protein (L-FABP). Herein, polyclonal a ntibodies raised against the recombinant liver sterol transfer protein s SCP-2 and L-FABP were used to identify the lipid transfer proteins i n the brains of alcohol-treated and control mice. L-FABP was not detec table in brain of either control or chronic ethanol-treated mice. In c ontrast, SCP-2 not only was present, but its level was significantly ( p < 0.05) increased 23 and 50%, respectively, in brain homogenates and synaptosomes of mice exposed to alcohol. To determine whether antibod ies against the recombinant liver SCP-2 reflected true levels of SCP-2 in brain, the cDNA sequence for brain SCP-2 was isolated from a brain cDNA library. The mouse brain SCP-2 sequence was 99.99% identical to the mouse liver SCP-2 sequence, The translated sequence differed by on ly one amino acid, and the replacement was conservative, Thus, unlike the fatty acid binding proteins, the SCP-2 moieties of brain and liver are essentially identical. Polyclonal antibodies against acyl-CoA bin ding protein, a lipid-binding protein that does not bind or transfer s terol, showed that increased levels of brain SCP-2 with chronic ethano l consumption did not represent a general increase in content of all l ipid transfer proteins. Changes in the amount of SCP-2 may contribute to membrane tolerance to ethanol.