Tanaka K, Min K S, Onosaka S, Fukuhara C, Ueda M
Toxicol Appl Pharmacol. 1985 Mar 30;78(1):63-8. doi: 10.1016/0041-008x(85)90305-9.
The origin of metallothionein (MT) in red blood cells (RBCs) from a mouse given cadmium was studied in connection with RBC kinetics. Plasma Cd concentration rapidly decreased 3 hr following 109CdCl2 (2 mg/kg, sc) administration, whereas RBC Cd increased from 2 to 4 days, followed by a gradual decrease. RBC Cd was found to be distributed more in the high-molecular-weight fraction than in the MT fraction 12 hr after administration. But, thereafter, Cd increased rapidly in the MT fraction to show changes with time similar to Cd level in RBCs. Hepatic damage induced in a mouse given 21 injections of Cd, with resultant marked elevation of plasma MT concentrations, did not cause any change in RBC Cd concentration. MT was hardly transferred to RBC when a mouse RBC suspension was incubated with mouse hepatic MT. To examine the relationship of Cd-MT and erythropoietic function, mice in the normal group, the phenylhydrazine-induced anemia group (PH), the transfusion-induced plethora group (TR), and the erythropoietin administered plethora group (TR + EP) were given 109CdCl2. Three days after administration, Cd concentration in its RBCs and its MT fraction remarkably increased in the PH group, and was greatly decreased in the TR group. A significant increase was noted in the TR + EP group as compared with the TR group. These results indicate that MT in the RBCs is formed in erythroblasts.