Early labeled heme synthesis in normal rats and rats with iron deficiency anemia.
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.
D000747:Anemia, Hypochromic / Q000188:drug therapy / Q000378:metabolism*; D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005998:Glycine / Q000378:metabolism; D006418:Heme / Q000096:biosynthesis*; D006454:Hemoglobins / Q000378:metabolism; D007501:Iron / Q000494:pharmacology / Q000627:therapeutic use; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D009928:Organ Specificity; D051381:Rats
D006454:Hemoglobins; D006418:Heme; D003513:Cycloheximide; D007501:Iron; D005998:Glycine