Tissue iron overload and mechanisms of iron-catalyzed oxidative injury

Adv Exp Med Biol. 1994;366:129-46. doi: 10.1007/978-1-4615-1833-4_10.

Abstract

Tissue iron overload causes clinical syndromes that involve the heart, liver, and pancreas. While tissue iron uptake occurs by both transferrin-dependent and independent processes, tissue uptake in the iron overload syndromes occurs predominantly via transferrin-independent mechanisms. Increased redox-active iron present in hemeproteins and the cytosolic iron pool can catalyze oxidative damage to lipids, proteins, and nucleic acids, either by oxyradical dependent or independent mechanisms. Iron-catalyzed injury results in damage to cell constituents, including mitochondria, lysosomes, and the sarcolemmal membrane. These mechanisms of iron-mediated damage are involved in the pathogenesis of organ dysfunction in primary hemochromatosis, transfusion-related iron overload, ischemia-reperfusion injury, and cardiac anthracycline toxicity.

Publication types

  • Review

MeSH terms

  • Animals
  • Free Radicals
  • Hemochromatosis / metabolism*
  • Hemochromatosis / therapy*
  • Humans
  • Iron / metabolism*
  • Iron / toxicity*
  • Models, Biological
  • Oxidation-Reduction
  • Transferrin / metabolism
  • Transfusion Reaction

Substances

  • Free Radicals
  • Transferrin
  • Iron