It seems the iron overload in thalassemia is being targeted with ..
natural iron chelators like milk thistle .. and getting much better
results by adding a little .. lecithin / phosphatidylcholine.

<<snip>>
Thalassemia major is characterized by anemia, iron overload, and
oxidant damage to major organs, especially the cardiovascular system.

Although silymarin is a complex of 7 flavonolignans and polyphenols,
silibinin is usually regarded as the most active component.

GSH restoration and improvement of PBMC growth by silymarin is a
possible explanation for its recently reported antioxidant and
immunostimulatory activities.

Silybin administration significantly reduced bothfunctional anomalies
and the fibrotic process by chelating desferrioxamine chelatable iron.
<<snip>>

Pediatr Cardiol. 2007 Sep 22; [Epub ahead of print]
Endothelial Dysfunction and Oxidant Status in Pediatric Patients with
Hemoglobin E-beta Thalassemia.
Kukongviriyapan V, Somparn N, Senggunprai L, Prawan A, Kukongviriyapan
U, Jetsrisuparb A.
Department of Pharmacology, Faculty of Medicine, Khon Kaen University,
Khon Kaen, Thailand, 40002, veerapol@kku.ac.th.

Thalassemia major is characterized by anemia, iron overload, and
oxidant damage to major organs, especially the cardiovascular system.
Oxidative stress is ultimately involved in endothelial dysfunction, a
condition which is evident in adults suffering from various
cardiovascular diseases including thalassemia. We investigated
endothelial function in pediatric patients with hemoglobin E-beta
thalassemia (HbE-beta thalassemia), who have been exposed to excessive
iron and oxidative stress for much shorter period than adults with
thalassemia. We recruited 22 blood transfusion-dependent HbE-beta
thalassemia patients aged 11.8 +/- 2.9 years and 20 healthy controls
aged 12.1 +/- 1.7 years. Oxidant status was determined, and
endothelial function was assessed by a forearm blood flow technique.
Oxidative stress was increased in the thalassemic patients, as blood
glutathione (GSH) and ratios of reduced GSH to GSH disulfide were
markedly reduced, and superoxide anion released from blood cells was
highly elevated. Oxidative stress response, assessed by gamma-
glutamylcysteine ligase activity, was increased approximately twofold
in thalassemia patients. Basal forearm blood flow was significantly
increased in patients compared with controls (7.3 +/- 1.8 vs 6.0 +/-
1.8 ml/100 ml tissue/min, respectively), whereas forearm vasodilatory
response to reactive hyperemia was depressed by 50% in patients
compared with controls. Endothelial function is impaired in young
thalassemia patients, and impaired endothelial function is associated
with oxidant stress.

PMID: 17891513 [PubMed - as supplied by publisher]

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Int Immunopharmacol. 2006 Aug;6(8):1305-10. Epub 2006 May 2. Links
Effects of silymarin on the proliferation and glutathione levels of
peripheral blood mononuclear cells from beta-thalassemia major
patients.
Alidoost F, Gharagozloo M, Bagherpour B, Jafarian A, Sajjadi SE,
Hourfar H, Moayedi B.
Department of Immunology, School of Medicine, Hezar Jerib Avenue,
Isfahan University of Medical Sciences, Isfahan, Iran.

Iron toxicity in beta-thalassemia major is the main cause of oxidative
stress and cell mediated immune deficiencies. Despite indicative signs
of severe oxidative deficiencies associated with beta-thalassemia
major, such as decreased level of plasma antioxidants and depletion of
erythrocyte glutathione, little is known about intracellular redox
status of immune cells. Since glutathione is a primary intracellular
antioxidant and plays an essential role in several functions in T
cells, in this study intracellular glutathione (GSH) levels as well as
proliferation of PHA-activated peripheral blood mononuclear cells
(PBMC) were investigated in 28 beta-thalassemia major patients and 28
healthy age-matched individuals. Considering the potential benefits of
flavonoids in the therapy of oxidative stress, the effects of
silymarin on the GSH levels and proliferation of PBMC from normal and
thalassemia individuals were further examined. Quantitative
determination of intracellular GSH and proliferative response of PBMC
to PHA were performed before and after 72 h incubation of PBMC with
various concentrations of silymarin (0, 5, 10, or 20 mug/ml). Results
demonstrated a significant reduction of GSH and proliferation in beta-
thalassemia major cells; however treatment with silymarin led to
restoration of both GSH levels and PBMC proliferation in thalassemia
patients. Considerably low levels of GSH and depressed proliferative
response of PBMC in beta-thalassemia major may be responsible for the
cell mediated immune abnormalities in iron overload conditions.
Moreover, the GSH restoration and improvement of PBMC growth by
silymarin is a possible explanation for its recently reported
antioxidant and immunostimulatory activities. These data suggest the
benefit of using flavonoids to normalize immune dysfunction in beta-
thalassemia major. The immunomodulatory effects of silymarin in beta-
thalassemia major are currently under further investigation in a
double blind clinical trial.

PMID: 16782543 [PubMed - indexed for MEDLINE]
------------------------------------------------------------------------------

J Vet Pharmacol Ther. 2007 Apr;30(2):132-8. Links
Bioavailability of a silybin-phosphatidylcholine complex in dogs.
Filburn CR, Kettenacker R, Griffin DW.
Veterinary Science Division, Nutramax Laboratories, Inc., Edgewood, MD
21040, USA.

Liver dysfunction often is associated with an imbalance in the
production and removal of free radicals derived from oxygen and
nitrogen and has been managed clinically with antioxidant supplements,
including silymarin extract derived from milk thistle. The potential
for enhanced bioavailability of a phytosome complex containing
phosphatidylcholine and silybin, the primary active flavonolignan in
silymarin extract, was tested in dogs. A group of eight beagles (four
males, four females) were dosed orally with a silybin-
phosphatidylcholine complex (SPC) and a commercially available
standardized silymarin extract containing equivalent levels of
silybin. Dosing with the SPC resulted in Cmax, Tmax, and AUC0-24 h
values (mean+/-SD) for total silybin of 1310+/-880 ng/mL, 2.87+/-2.23
h, and 11,200+/-6520 ng.h/mL, respectively; corresponding values for a
standardized silymarin extract were 472+/-383 ng/mL, 4.75+/-2.82 h,
and 3720+/-4970 ng.h/mL. A second, separate group of beagles were also
dosed with the extract alone, yielding values of 449+/-402 ng/mL,
6.87+/-7.43 h, and 2520+/-2976 ng.h/mL. These data show that a
phytosome complex of phosphatidylcholine and silybin markedly enhances
bioavailability in dogs.

PMID: 17348898 [PubMed - indexed for MEDLINE]

----------------------------------------------------------------------------

<<snip>>
Silybin administration significantly reduced bothfunctional anomalies
and the fibrotic process by chelating desferrioxamine chelatable iron.
<<snip>>

Alberto Masini1 , Daniela Ceccarelli2, Fabiola Giovannini2, Giuliana
Montosi2, Cinzia Garuti2 and Antonello Pietrangelo2

(1)  Sezione di Patologia Generale, Dipartimento di Scienze
Biomediche, Universita di Modena, Modena, Italy
(2)  Dipartimento di Medicina Interna, Università di Modena, Modena,
Italy

Abstract  Hepatic iron toxicity because of iron overload seems to be
mediated by lipid peroxidation ofbiological membranes and the
associated organelle dysfunctions. However, the basicmechanisms
underlying this process in vivo are still little understood. Gerbils
were dosed with weeklyinjections of iron-dextran alone or in
combination with sylibin, a well-known antioxidant,by gavage for 8
weeks. A strict correlation was found between lipid peroxidation and
the levelof desferrioxamine chelatable iron pool. A consequent
derangement in the mitochondrialenergy-transducing capability,
resulting from a reduction in the respiratory chain enzymeactivities,
occurred. These irreversible oxidative anomalies brought about a
dramatic drop intissue ATP level. The mitochondrial oxidative
derangement was associated with thedevelopment of fibrosis in the
hepatic tissue. Silybin administration significantly reduced
bothfunctional anomalies and the fibrotic process by chelating
desferrioxamine chelatable iron.
Iron - oxidant stress - liver mitochondria (gerbil)

--------------------------------------------------------------------------------

Alberto Masini
Email: masini@unimo.it

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