Heme synthesis from [2-14C]
glycine was studied in liver and red blood cells. In normal rats liver contained two early [14C]
heme peaks maximal at 1 and 4.5 h, followed by a long plateau of
heme labeling. These phases were present in both microsomes and mitochondria.
Cycloheximide suppressed formation of the first but not the second
heme component. All phases of hepatic
heme labeling were reduced in
iron-deficient rats, with better preservation ofthe microsomal fraction. In
iron-deficient rats responding to
iron therapy, the first peak merged with an enlarged and premature second component; the increase was most marked in mitochondria. Thus, labeled
heme metabolism was less perturbed in microsomes than mitochondria in both of these conditions. Peripheral blood also contained a [14C]
heme peak at 1 h in all experimental groups. This was highest with the increased eythroid response observed in
iron-treated rats. The first
heme peak, present in both hepatic and erythroid cells, may represent a pool of free or unassigned
heme. The later
heme component may reflect formation of hemoproteins, which could be related directly or in directly to the initial, rapid turnover
heme component.