1. Free Radic Biol Med. 2006 Apr 1;40(7):1152-60.

Iron chelation in the biological activity of curcumin.

Jiao Y, Wilkinson J 4th, Christine Pietsch E, Buss JL, Wang W, Planalp R, Torti
FM, Torti SV.

Department of Cancer Biology, Wake Forest University Health Sciences,
Winston-Salem, NC 27157, USA.

Curcumin is among the more successful chemopreventive compounds investigated in
recent years, and is currently in human trials to prevent cancer. The mechanism
of action of curcumin is complex and likely multifactorial. We have made the
unexpected observation that curcumin strikingly modulates proteins of iron
metabolism in cells and in tissues, suggesting that curcumin has properties of an
iron chelator. Curcumin increased mRNA levels of ferritin and GSTalpha in
cultured liver cells. Unexpectedly, however, although levels of GSTalpha protein
increased in parallel with mRNA levels in response to curcumin, levels of
ferritin protein declined. Since iron chelators repress ferritin translation, we
considered that curcumin may act as an iron chelator. To test this hypothesis, we
measured the effect of curcumin on transferrin receptor 1, a protein stabilized
under conditions of iron limitation, as well as the ability of curcumin to
activate iron regulatory proteins (IRPs). Both transferrin receptor 1 and
activated IRP, indicators of iron depletion, increased in response to curcumin.
Consistent with the hypothesis that curcumin acts as an iron chelator, mice that
were fed diets supplemented with curcumin exhibited a decline in levels of
ferritin protein in the liver. These results suggest that iron chelation may be
an additional mode of action of curcumin.

PMID: 16545682 [PubMed - indexed for MEDLINE]