Curcumin

I ve been reading about the incredible properties of curcumin that are very similar to those of resveratrol. That prompted me to look about its properties relating to thalassemia. I was right:

Curcumin contributes to in vitro removal of non-transferrin bound iron by deferiprone and desferrioxamine in thalassemic plasma.
http://www.ncbi.nlm.nih.gov/pubmed/17897073

Proteomic analysis of plasma protein in β-thalassemia/HbE patients treated with curcumin
http://www.fasebj.org/cgi/content/meeting_abstract/23/1_MeetingAbstracts/858.1

The antioxidant effect of curcumin is red blood cells of Beta Thalassemia patients
http://mulinet10.li.mahidol.ac.th/e-thesis/4337486.pdf

Improvement in oxidative stress and antioxidant parameters in beta-thalassemia/Hb E patients treated with curcuminoids.
http://www.ncbi.nlm.nih.gov/pubmed/19900435

Efficacy of curcuminoids in alleviation of iron overload and lipid peroxidation in thalassemic mice.
http://www.ncbi.nlm.nih.gov/pubmed/19534681

Studies on curcumin and curcuminoids: XXVI. Antioxidant effects of curcumin on the red blood cell membrane
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T7W-3VYTWGN-1Y&_user=10&_coverDate=04/30/1996&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1365048461&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=53b0cff9afafb5bc0f8ce80d008f7f0d

Hepatoprotective potential of crocin and curcumin against iron overload induced biochemical alterations in rat
http://www.academicjournals.org/ajbr/PDF/Pdf2009/May/May%20Issue/EL-Maraghy%20et%20al.pdf

Curcumin inhibits growth of Saccharomyces cerevisiae through iron
chelation.
Minear S, O'Donnell AF, Ballew A, Giaever G, Nislow C, Stearns T,
Cyert MS
Eukaryot Cell 2011 Sep 9.

Curcumin, a polyphenol derived from turmeric, is an ancient
therapeutic, used in India for centuries to treat a wide array of
ailments.
Interest in curcumin has increased recently, with on-going clinical
trials exploring curcumin as an anti-cancer therapy and as a
protectant against neurodegenerative diseases.
In vitro, curcumin chelates metal ions.
However, curcumin's mechanism of action on mammalian cells remains
unclear, although diverse physiological effects have been documented
for this compound.
These studies use yeast as a model eukaryotic system to dissect the
biological activity of curcumin.
We find that yeast mutants deleted for genes required for iron and
copper homeostasis are hyper-sensitive to curcumin and that iron
supplementation rescues this sensitivity.
Curcumin penetrates yeast cells, concentrates in the ER-membranes, and
reduces the intracellular iron pool.
Curcumin-treated, iron-starved cultures are enriched in unbudded
cells, suggesting that the G1 phase of the cell cycle is lengthened.
A delay in cell cycle progression could, in part, explain the anti-
tumorigenic properties associated with curcumin.
We also demonstrate that curcumin causes a growth lag in cultured
human cells that is remediated by addition of exogenous iron.
These findings suggest that curcumin-induced iron starvation is
conserved from yeast to humans and underlies its medicinal properties.


Eukaryotic cell [Eukaryot Cell]

Phytother Res. 2018 May 28. doi: 10.1002/ptr.6118. [Epub ahead of print]
An investigation of the effects of curcumin on iron overload, hepcidin level, and liver function in β-thalassemia major patients: A double-blind randomized controlled clinical trial.
Mohammadi E1, Tamaddoni A2, Qujeq D3, Nasseri E4, Zayeri F5, Zand H6, Gholami M7, Mir SM7.
Author information
Abstract
This study investigated the effects of curcumin, the active polyphenol in turmeric, on iron overload, hepcidin level, and liver function in β-thalassemia major patients. This double-blind randomized controlled clinical trial was conducted on 68 β-thalassemia major patients. The subjects were randomly divided into 2 groups to receive either 500 mg curcumin capsules (total: 1,000 mg) twice daily or placebo for 12 weeks. Dietary intakes and biochemical variables including hemoglobin, transferrin saturation, total iron binding capacity, nontransferrin bound iron (NTBI), ferritin, hepcidin, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were assessed at the beginning and end of the trial. Curcumin significantly reduced serum levels of NTBI (2.83 ± 1.08 compared with 2.22 ± 0.97 μmol/L, p = .001), ALT (42.86 ± 11.15 compared with 40.60 ± 9.89 U/L, p = .018), and AST (49.45 ± 12.39 compared with 46.30 ± 10.85 U/L, p = .002) at the end of the study. Based on analysis of covariance, a significant decrease was also observed in levels of NTBI (2.22 ± 0.97 vs. 2.55 ± 0.94 μmol/L, p = .026), ALT (40.60 ± 9.89 vs. 45.01 ± 10.42 U/L, p = .004), and AST (46.30 ± 10.85 vs. 50.99 ± 9.36 U/L, p = .009) in curcumin group in comparison with placebo group. There were no significant changes in hepcidin and other variables in any of the 2 groups. Curcumin administration alleviated iron burden and liver dysfunction by reducing NTBI, ALT, and AST levels in patients with β-thalassemia major.

KEYWORDS:
curcumin; hepcidin; iron overload; randomized clinical trial; β-thalassemia major

PMID: 29806132 DOI: 10.1002/ptr.6118

This is very important evidence about the use of curcumin as a supplemental chelator and once again establishes the fact that natural chelators have a protective effect in the body, as demonstrated by the reduced liver dysfunction.