Aging is an organ-specific process: Changes in homeostasis of iron and redox proteins in the rat

Baruch E. Bulvik, Eduard Berenshtein, Abraham Marim Konijn, Leonid Grinberg, Vladimir Vinokur, Ron Eliashar, Mordechai Chevion*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Organ-specific changes of iron- and redoxrelated proteins occur with age in the rat. Ferritin, the major iron storage and detoxifying protein, as well as the proteins of the methionine-centered redox cycle (MCRC) were examined in old and young animals, and showed organ-dependent changes. In spleens and livers of aged rats, ferritin (protein) levels were greater than in young ones, and their iron saturation increased, rendering higher ferritin-bound iron (FtBI). Iron saturation of the ferritin molecule in the tongues and sternohyoids of old rats was lower but ferritin level was higher than in young rats, resulting in increased FtBI with age. Ferritin level in the esophagus of older rats was lower than in young rats but its molecular iron content higher thus the total FtBI remained the same. In the larynx, both ferritin and its iron content were the same in young and old animals. MCRC proteins were measured in livers and spleens only. With aging, methionine sulfoxide reductase A and B (MsrA and MsrB) levels in livers and spleens decreased. Thioredoxin1 (Trx) and Trx-reductase1 were elevated in old spleens, but reduced in livers. Aged spleens showed reduced Msr isozyme activity; but in the liver, its activity increased. mRNA changes with age were monitored and found to be organ specific. These organ-specific changes could reflect the different challenges and the selective pathways of each organ and its resultant capacity to cope with aging.

Original languageAmerican English
Pages (from-to)693-704
Number of pages12
Issue number3
StatePublished - Jun 2012
Externally publishedYes


  • Aging
  • Ferritin
  • Iron
  • Methionine-centered redox cycle
  • Organ specific
  • Redox state


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