Curcumin may impair iron status when fed to mice for six months

Autor: Patricia Huebbe, Jan Frank, Kathrin Pallauf, Dawn Chin, Gerald Rimbach
Jazyk: angličtina
Rok vydání: 2014
Předmět:
Clinical Biochemistry
TBS
tris buffered saline

Pharmacology
Biochemistry
chemistry.chemical_compound
Mice
TfR1
transferrin receptor 1

Enlarged spleen
lcsh:QH301-705.5
HO1
haem oxygenase

lcsh:R5-920
biology
qRT-PCR
quantitative real-time polymerase chain reaction

Iron deficiency
γ-GCS
γ-glutamyl cysteine synthetase

NRF2
nuclear factor (erythroid-derived 2)-like 2

Zinc
medicine.anatomical_structure
Liver
FPN
ferroportin

TNFα
tumour necrosis factor α

Toxicity
Female
Safety
lcsh:Medicine (General)
Research Paper
Curcumin
Liver minerals
Iron
Spleen
Transferrin receptor
NQO1
NAD(P)H quinone oxidoreductase

Drug Administration Schedule
DMT1
divalent metal transporter 1

Hepcidins
Hepcidin
medicine
Animals
Dose-Response Relationship
Drug

Organic Chemistry
Body Weight
DMT1
medicine.disease
Iron store
IL
interleukin

Ferritin
Mice
Inbred C57BL

chemistry
Gene Expression Regulation
lcsh:Biology (General)
Immunology
Dietary Supplements
Ferritins
Splenomegaly
biology.protein
Copper
Zdroj: Redox Biology, Vol 2, Iss C, Pp 563-569 (2014)
Redox Biology
ISSN: 2213-2317
Popis: 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.
Graphical abstract A 6 month dietary supplementation with 0.2% curcumin in C57BL/6J mice led to a significant reduction in iron, but not zinc and copper stores, in the liver and the spleen, and suppressed liver hepcidin and ferritin expression. Furthermore, the expression of the iron-importing transport proteins divalent metal transporter (DMT) 1 and transferrin receptor (TfR) 1 was induced in the curcumin-fed mice. These data suggest that long-term curcumin supplementation and a Western-type diet may aggravate iron deficiency.
Highlights • 0.2% dietary curcumin for 6 months reduced iron stores in murine liver and spleen. • Curcumin chelated iron but not zinc and copper in vivo. • Liver hepcidin and ferritin expression was strongly suppressed in curcumin-fed mice. • Curcumin induced expression of hepatic iron transporters DMT1 and TfR1. • Curcumin did not affect hepatic and splenic inflammatory and oxidative markers.
Databáze: OpenAIRE