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Home > Archive > Alzheimers support > October 2005 > Pathological iron deposition / (AD), (PD), (MS)
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Pathological iron deposition / (AD), (PD), (MS)
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| ironjustice@aol.com 2005-10-14, 11:06 am |
| <<snip>>
pathological iron deposition
<<snip>>
Over-expression of heme oxygenase-1 promotes oxidative mitochondrial
damage in rat astroglia.
Song W, Su H, Song S, Paudel HK, Schipper HM
J Cell Physiol. 2005 Oct 12;
Glial heme oxygenase-1 is over-expressed in the CNS of subjects with
Alzheimer disease (AD), Parkinson disease (PD) and multiple sclerosis
(MS). Up-regulation of HO-1 in rat astroglia has been shown to
facilitate iron sequestration by the mitochondrial compartment. To
determine whether HO-1 induction promotes mitochondrial oxidative
stress, assays for 8-epiPGF(2alpha) (ELISA), protein carbonyls (ELISA)
and 8-OHdG (HPLC-EC) were used to quantify oxidative damage to lipids,
proteins, and nucleic acids, respectively, in mitochondrial fractions
and whole-cell compartments derived from cultured rat astroglia
engineered to over-express human (h) HO-1 by transient transfection.
Cell viability was assessed by trypan blue exclusion and the MTT assay,
and cell proliferation was determined by [(3)H] thymidine incorporation
and total cell counts. In rat astrocytes, hHO-1 over-expression (x3
days) resulted in significant oxidative damage to mitochondrial lipids,
proteins, and nucleic acids, partial growth arrest, and increased cell
death. These effects were attenuated by incubation with 1 microM tin
mesoporphyrin, a competitive HO inhibitor, or the iron chelator,
deferoxamine. Up-regulation of HO-1 engenders oxidative mitochondrial
injury in cultured rat astroglia. Heme-derived ferrous iron and carbon
monoxide (CO) may mediate the oxidative modification of mitochondrial
lipids, proteins and nucleic acids in these cells. Glial HO-1
hyperactivity may contribute to cellular oxidative stress, pathological
iron deposition, and bioenergetic failure characteristic of
degenerating and inflamed neural tissues and may constitute a rational
target for therapeutic intervention in these conditions. (c) 2005
Wiley-Liss, Inc.
Abstract =B7 PubMed =B7 FullText =B7 SFX =B7 GS =B7 Order =B7 Clip =B7
Citation =B7 BibTeX =B7 Related =B7 TouchGraph =B7 Scopus =B7 References =
=B7
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