ROLE OF COPPER IN MITOCHONDRIAL IRON-METABOLISM

  • 1 January 1976
    • journal article
    • research article
    • Vol. 48  (1) , 77-85
Abstract
Heme synthesis by Cu-deficient cells was investigated to elucidate the nature of the defect in intracellular Fe metabolism. Fe uptake from transferrin by Cu-deficient reticulocytes [swine] was 52% of normal, and the rate of heme synthesis was 33% of normal. Hepatic mitochondria isolated from Cu-deficient animals were deficient in cytochrome oxidase activity and failed to synthesize heme from ferric iron [Fe(III)] and protoporphyrin at the normal rate. The rate of heme synthesis correlated with the cytochrome oxidase activity. Heme synthesis from Fe(III) and protoporphyrin by normal mitochondria was enhanced by succinate and inhibited by malonate, antimycin A, azide and cyanide. An intact electron transport system is apparently required for the reduction of Fe(III), thereby providing a pool of ferrous iron (Fe II) for protoheme and heme a synthesis.

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