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Ascorbic acid and iron metabolism: alterations in lysosomal function.

K E Hoffman1, K Yanelli, K R Bridges

  • 1Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.

The American Journal of Clinical Nutrition
|December 1, 1991
PubMed
Summary
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Vitamin C (ascorbate) protects cells by stabilizing iron storage in ferritin. It slows ferritin shell degradation, preventing iron release and cellular damage, thus enhancing iron availability.

Area of Science:

  • Cellular metabolism
  • Biochemistry
  • Nutritional science

Background:

  • Iron is vital for cell metabolism but can cause oxidative damage.
  • Ferritin stores excess intracellular iron within its shell to prevent harm.
  • Ascorbate (Vitamin C) is known to interact with iron and ferritin.

Purpose of the Study:

  • To investigate the mechanism by which ascorbate affects ferritin's iron storage and degradation.
  • To determine how ascorbate influences iron bioavailability and cellular iron handling.

Main Methods:

  • Cells were labeled with radioactive iron (59Fe) and methionine (35S).
  • Subcellular fractionation using Sepharose CL-6B column chromatography was performed.
  • Ferritin degradation and localization within cellular compartments were analyzed.

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Main Results:

  • Ascorbate significantly retards the degradation of ferritin shells.
  • This stabilization delays the release of iron from ferritin.
  • Ascorbate prevents the shift of ferritin from the cytoplasm to lysosomes, slowing autophagic uptake.

Conclusions:

  • Ascorbate enhances iron bioavailability by stabilizing ferritin iron cores.
  • The vitamin protects cells from iron-induced oxidative stress by retarding ferritin degradation.
  • Ascorbate's effect is primarily on delaying the lysosomal degradation of ferritin clusters.