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Increase MetabolismSubject: Oxidative Stress Confirmed In Arthritis
Author: ironjustice@aol.comDate: 20 Jul
"Taking away iron should be considered"
Lipid, protein, DNA oxidation and antioxidant status in rheumatoid
arthritis.
Clin Biochem. 2008 May;41(7-8):538-43. Epub 2008 Feb 15. Links
Seven A, Güzel S, Aslan M, Hamuryudan V.
Department of Biochemistry, Cerrahpaşa Medical Faculty, Istanbul
University, Istanbul, Turkey. arzu_seven@hotmail.com
OBJECTIVES:
To investigate lipid, protein, DNA oxidation and antioxidant status in
blood and synovial fluid of rheumatoid arthritis (RA) patients and to
determine the importance of oxidative stress parameters in reflecting
disease activity.
DESIGN AND METHODS:
20 RA patients and 15 healthy controls were included. Lipid
peroxidation (thiobarbituric acid reactive substances (TBARS), lipid
hydroperoxide, and conjugated diene), protein oxidation (carbonyl and
thiol), DNA oxidation (8-OHdG) and antioxidant status markers
(glutathione (GSH), glutathione peroxidase (GSH Px), superoxide
dismutase (CuZn SOD), and catalase) were determined in blood and
synovial fluid.
RESULTS:
TBARS (p<0.001), lipid hydroperoxide (p<0.001), conjugated diene
(p<0.001), carbonyl (p<0.001) and 8-OHdG (p<0.01) levels were
significantly higher; thiol (p<0.01) and GSH levels (p<0.01) and GSH
Px (p<0.001) and CuZn SOD (p<0.01) activities were significantly lower
in blood of RA patients. TBARS (p<0.001), lipid hydroperoxide
(p<0.001), conjugated diene (p<0.01), carbonyl (p<0.001) and 8-OHdG
(p<0.05) levels were significantly higher, catalase activity (p<0.001)
significantly lower in synovial fluid of RA patients.
CONCLUSIONS:
Increased lipid, protein and DNA oxidation markers and impaired
antioxidant status confirm the role of oxidative stress in the
pathogenesis of RA. Lipid peroxidation markers can serve as surrogate
markers for disease activity.
PMID: 18313405
--------------------------------------------------------------------------------
Biochem Pharmacol 1999 Jun 15;57(12):1345-9
Therapy by taking away: the case of iron.
Polla BS
Laboratoire de Physiologie Respiratoire, UFR Cochin Port-Royal,
Paris, France. Barbara.Po...@cochin.univ-paris5.fr
The recent finding of the beneficial effects of iron deprivation in
the outcome of muscle necrosis in an animal model of genetic myopathy
served as the basis of this commentary.
Here, "taking away" iron by controlled dietary deprivation is proposed
as a reasonable, feasible, cheap, and efficient clinical approach to
many diverse diseases, all of which have a free radical component.
Indeed, iron potentiates the generation of the highly reactive and
toxic hydroxyl radical, and, thus, of oxidative damage. Iron
deprivation may represent the first really efficient antioxidant,
preventing oxidative stress in all subcellular compartments, tissues,
and organs.
Iron/iron deprivation also modulates programmed cell death
(apoptosis), which should be the subject of further studies to better
define the mechanisms mediating these complex effects.
Finally, related to its antioxidant effects, iron deprivation may find
applications in the anti-aging field, whether programmed or premature
aging, and whether in cosmetics or in gerontology.
PMID: 10353254, UI: 99279694
--------------------------------
CONCLUSION
In conclusion, therapy by taking away (iron) has a great potential for
many different diseases, all of which share ROS-mediated mechanisms.
The development of new, non-toxic , easily administrable iron
chelators such as IRCO11 may shortly become the most efficient and
fashionable antioxidant, anti-aging, anti-infectious, and anti-
inflammatroy therapy.
In the meantime, although taking away by controlled dietary
deprivation is less attractive , it should be considered in all of the
above, as well as in the currently incurable, devastating genetic or
acquired myopathies such as DMD.
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