title: Curcumin may impair iron status when fed to mice for six months.
abstract: Curcumin has been shown to have many potentially health beneficial properties in vitro and in animal models with clinical studies on the toxicity of curcumin reporting no major side effects. However, curcumin may chelate dietary trace elements and could thus potentially exert adverse effects. Here, we investigated the effects of a 6 month dietary supplementation with 0.2% curcumin on iron, zinc, and copper status in C57BL/6J mice. Compared to non-supplemented control mice, we observed a significant reduction in iron, but not zinc and copper stores, in the liver and the spleen, as well as strongly suppressed liver hepcidin and ferritin expression in the curcumin-supplemented mice. The expression of the iron-importing transport proteins divalent metal transporter 1 and transferrin receptor 1 was induced, while hepatic and splenic inflammatory markers were not affected in the curcumin-fed mice. The mRNA expression of other putative target genes of curcumin, including the nuclear factor (erythroid-derived 2)-like 2 and haem oxygenase 1 did not differ between the groups. Most of the published animal trials with curcumin-feeding have not reported adverse effects on iron status or the spleen. However, it is possible that long-term curcumin supplementation and a Western-type diet may aggravate iron deficiency. Therefore, our findings show that further studies are needed to evaluate the effect of curcumin supplementation on iron status.
authors.affiliation: Institute of Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Hermann-Rodewald-Strasse 6-8, D-24118 Kiel, Germany.
authors.forename: Dawn
authors.initials: D
authors.lastname: Chin
authors.affiliation: Institute of Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Hermann-Rodewald-Strasse 6-8, D-24118 Kiel, Germany.
authors.forename: Patricia
authors.initials: P
authors.lastname: Huebbe
authors.affiliation: Institute of Biological Chemistry and Nutrition, University of Hohenheim, Garbenstrasse 28, D-70599 Stuttgart, Germany.
authors.forename: Jan
authors.initials: J
authors.lastname: Frank
authors.affiliation: Institute of Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Hermann-Rodewald-Strasse 6-8, D-24118 Kiel, Germany.
authors.forename: Gerald
authors.initials: G
authors.lastname: Rimbach
authors.affiliation: Institute of Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Hermann-Rodewald-Strasse 6-8, D-24118 Kiel, Germany.
authors.forename: Kathrin
authors.initials: K
authors.lastname: Pallauf
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D003300:Copper / Q000378:metabolism; D003474:Curcumin / Q000008:administration & dosage / Q000009:adverse effects*; D019587:Dietary Supplements / Q000009:adverse effects; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D005293:Ferritins / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D064451:Hepcidins / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D013154:Spleen / Q000378:metabolism*; D013163:Splenomegaly / Q000139:chemically induced / Q000378:metabolism; D015032:Zinc / Q000378:metabolism
chemical_list: D064451:Hepcidins; D003300:Copper; D005293:Ferritins; D007501:Iron; D003474:Curcumin; D015032:Zinc
keywords: Curcumin; DMT1, divalent metal transporter 1; Enlarged spleen; FPN, ferroportin; HO1, haem oxygenase; IL, interleukin; Iron store; Liver minerals; NQO1, NAD(P)H quinone oxidoreductase; NRF2, nuclear factor (erythroid-derived 2)-like 2; Safety; TBS, tris buffered saline; TNFα, tumour necrosis factor α; TfR1, transferrin receptor 1; Toxicity; qRT-PCR, quantitative real-time polymerase chain reaction; γ-GCS, γ-glutamyl cysteine synthetase