Experimentally induced copper deficiency in the rat results in increased plasma apolipoprotein B100 (apo B100) concentration in association with increased hepatic apo B100 synthesis. This enhancement of apo B100 synthesis and plasma accumulation accounts for the rise of plasma low density lipoprotein in these animals. In the present study, we have investigated if the selective increase in hepatic apo B100 synthesis is accounted for by changes in apo B mRNA editing. Reverse transcription coupled with polymerase chain reaction amplification and primer extension analysis of apo B cDNA revealed no differences in apo B mRNA editing in either the liver or small intestine between control and copper-deficient rats. We speculate that the increase in apo B100 synthesis in the liver of copper-deficient rats reflects posttranslational alterations in gene expression accompanying changes in very low density lipoprotein assembly and secretion.