Evidence supports a role for
ceruloplasmin (ferroxidase I) in the release of
iron to the blood from mammalian cells. However, recent studies with cultured cells have suggested that it has the opposite effect, and that
iron deficiency enhances expression of
ceruloplasmin. We therefore examined in rats how nutritional
iron status would affect expression of
ceruloplasmin. Groups of male Sprague-Dawley rats were reared on a low
iron,
starch-based diet for 6-8 wk; half were supplemented by injection of
iron dextran. At killing, hematocrits of deficient rats were half normal. Supplemented rats had normal liver concentrations of
ferritin and
ferritin iron. No
ferritin was detected in the livers of the deficient rats. Northern analysis showed that
ferritin L and H mRNAs were present in the deficient livers, but expression was half that of the normal rats. There was also twice as much
copper. Levels of circulating
ceruloplasmin (measured by rocket immunoelectrophoresis) were not altered by
iron deficiency, although
p-phenylenediamine oxidase activity and plasma
copper were reduced approximately 30%. In repeated studies, no differences in the expression of hepatic
ceruloplasmin mRNA were detected. Treatment of rats of both sexes with additional
iron (25 mg as
iron dextran) 5-14 d before killing increased liver
ferritin but did not alter liver
ceruloplasmin mRNA expression or levels of circulating
ceruloplasmin. We conclude that
iron status is not an important factor in the expression of plasma
ceruloplasmin made by the liver. However, it does have modest effects on steady-state levels of liver
ferritin mRNA.