Ironjustic
Sun, May-25-08, 17:15
"Oxidized LDL associated with metabolic syndrome"
"Iron might be toxic through the generation of oxidized forms
of low- density lipoprotein (LDL)."
--------------------------------------------
http://www.medscape.com/viewarticle/574827
Oxidized LDL Associated With Metabolic Syndrome CME News
Author: Sue Hughes CME Author: Charles Vega, MD Release
Date: May 21, 2008; Valid for credit through May 21, 2009
Credits Available
=46rom Heartwire =97 a professional news service of WebMD
May 21, 2008 =97 A higher concentration of oxidized
low-density lipoprotein (LDL)-cholesterol was associated with
increased incidence of metabolic syndrome overall, as well as
its components of abdominal obesity, hyperglycemia, and
hypertriglyceridemia in a new population- based study [1].
--------------------------------------
Blood 2002 Aug 1;100(3):879-87
Pro-oxidant and cytotoxic effects of circulating heme.
Jeney V, Balla J, Yachie A, Varga Z, Vercellotti GM, Eaton
JW, Balla G Department of Medicine, University of
Debrecen, Hungary.
Numerous pathologies may involve toxic side effects of free
heme and heme-derived iron. Deficiency of the
heme-catabolizing enzyme, heme oxygenase-1 (HO-1), in both a
human patient and transgenic knockout mice leads to an
abundance of circulating heme and damage to vascular
endothelium. Although heme can be directly cytotoxic, the
present investigations examine the possibility that
hemoglobin-derived heme and iron might be indirectly toxic
through the generation of oxidized forms of low-density
lipoprotein (LDL). In support, hemoglobin in plasma, when
oxidized to methemoglobin by oxidants such as
leukocyte-derived reactive oxygen, causes oxidative
modification of LDL. Heme, released from methemoglobin,
catalyzes the oxidation of LDL, which in turn induces
endothelial cytolysis primarily caused by lipid
hydroperoxides. Exposure of endothelium to sublethal
concentrations of this oxidized LDL leads to induction of both
HO-1 and ferritin. Similar endothelial cytotoxicity was caused
by LDL isolated from plasma of an HO-1-deficient child.
Spectral analysis of the child's plasma revealed a substantial
oxidation of plasma hemoglobin to methemoglobin. Iron
accumulated in the HO-1-deficient child's LDL and several
independent assays revealed oxidative modification of the
LDL.We conclude that hemoglobin, when oxidized in plasma, can
be indirectly cytotoxic through the generation of oxidized
LDL by released heme and that, in response, the
intracellular defense-HO-1 and ferritin-is induced. These
results may be relevant to a variety of disorders-such as
renal failure associated with intravascular hemolysis,
hemorrhagic injury to the central nervous system, and,
perhaps, atherogenesis-in which hemoglobin-derived heme
may promote the formation of fatty acid hydroperoxides.
PMID: 12130498, UI: 22122442
-------------------------------------
"Iron chelators may be effective in preventing vascular
damage"
Hemoglobin. 2008;32(1-2):123-34 Can iron chelators influence
the progression of atherosclerosis? Marx JJ, Kartikasari AE,
Georgiou NA. Eijkman Winkler Institute, University Medical
Centre Utrecht, Utrecht, The Netherlands. m...@planet.nl
Epidemiological studies and experimental data suggest iron
involvement in atherosclerosis. The relation between iron and
atherosclerosis is complex and remains contradictory. In
thalassemia patients, non transferrin bound iron (NTBI) and
free hemoglobin (Hb) are present in plasma and may accelerate
atherogenesis, but its progression may be inhibited by iron
chelators. The mechanism whereby iron may stimulate
atherogenesis has been intensively investigated. Non
transferrin bound iron and sera from subjects with
hemochromatosis induced endothelial activation with expression
of vascular adhesion molecules and endothelial inflammatory
chemokines. Such events could be inhibited by iron chelators
and oxygen radical scavengers with intracellular activity.
Iron chelators may be effective in preventing vascular damage
in patients with high concentrations of NTBI as found in
thalassemia.
Publication Types: Review
PMID: 18274990 [PubMed - indexed for MEDLINE]
Who loves ya. Tom
Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
"Iron might be toxic through the generation of oxidized forms
of low- density lipoprotein (LDL)."
--------------------------------------------
http://www.medscape.com/viewarticle/574827
Oxidized LDL Associated With Metabolic Syndrome CME News
Author: Sue Hughes CME Author: Charles Vega, MD Release
Date: May 21, 2008; Valid for credit through May 21, 2009
Credits Available
=46rom Heartwire =97 a professional news service of WebMD
May 21, 2008 =97 A higher concentration of oxidized
low-density lipoprotein (LDL)-cholesterol was associated with
increased incidence of metabolic syndrome overall, as well as
its components of abdominal obesity, hyperglycemia, and
hypertriglyceridemia in a new population- based study [1].
--------------------------------------
Blood 2002 Aug 1;100(3):879-87
Pro-oxidant and cytotoxic effects of circulating heme.
Jeney V, Balla J, Yachie A, Varga Z, Vercellotti GM, Eaton
JW, Balla G Department of Medicine, University of
Debrecen, Hungary.
Numerous pathologies may involve toxic side effects of free
heme and heme-derived iron. Deficiency of the
heme-catabolizing enzyme, heme oxygenase-1 (HO-1), in both a
human patient and transgenic knockout mice leads to an
abundance of circulating heme and damage to vascular
endothelium. Although heme can be directly cytotoxic, the
present investigations examine the possibility that
hemoglobin-derived heme and iron might be indirectly toxic
through the generation of oxidized forms of low-density
lipoprotein (LDL). In support, hemoglobin in plasma, when
oxidized to methemoglobin by oxidants such as
leukocyte-derived reactive oxygen, causes oxidative
modification of LDL. Heme, released from methemoglobin,
catalyzes the oxidation of LDL, which in turn induces
endothelial cytolysis primarily caused by lipid
hydroperoxides. Exposure of endothelium to sublethal
concentrations of this oxidized LDL leads to induction of both
HO-1 and ferritin. Similar endothelial cytotoxicity was caused
by LDL isolated from plasma of an HO-1-deficient child.
Spectral analysis of the child's plasma revealed a substantial
oxidation of plasma hemoglobin to methemoglobin. Iron
accumulated in the HO-1-deficient child's LDL and several
independent assays revealed oxidative modification of the
LDL.We conclude that hemoglobin, when oxidized in plasma, can
be indirectly cytotoxic through the generation of oxidized
LDL by released heme and that, in response, the
intracellular defense-HO-1 and ferritin-is induced. These
results may be relevant to a variety of disorders-such as
renal failure associated with intravascular hemolysis,
hemorrhagic injury to the central nervous system, and,
perhaps, atherogenesis-in which hemoglobin-derived heme
may promote the formation of fatty acid hydroperoxides.
PMID: 12130498, UI: 22122442
-------------------------------------
"Iron chelators may be effective in preventing vascular
damage"
Hemoglobin. 2008;32(1-2):123-34 Can iron chelators influence
the progression of atherosclerosis? Marx JJ, Kartikasari AE,
Georgiou NA. Eijkman Winkler Institute, University Medical
Centre Utrecht, Utrecht, The Netherlands. m...@planet.nl
Epidemiological studies and experimental data suggest iron
involvement in atherosclerosis. The relation between iron and
atherosclerosis is complex and remains contradictory. In
thalassemia patients, non transferrin bound iron (NTBI) and
free hemoglobin (Hb) are present in plasma and may accelerate
atherogenesis, but its progression may be inhibited by iron
chelators. The mechanism whereby iron may stimulate
atherogenesis has been intensively investigated. Non
transferrin bound iron and sera from subjects with
hemochromatosis induced endothelial activation with expression
of vascular adhesion molecules and endothelial inflammatory
chemokines. Such events could be inhibited by iron chelators
and oxygen radical scavengers with intracellular activity.
Iron chelators may be effective in preventing vascular damage
in patients with high concentrations of NTBI as found in
thalassemia.
Publication Types: Review
PMID: 18274990 [PubMed - indexed for MEDLINE]
Who loves ya. Tom
Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk