Age-related Macular Iron Accumulation

Apr 21, 2009
Iron accumulation within the retina increases with age

Age-related iron accumulation within the retinal pigment epithelium
(RPE) may increase oxidative stress and contribute to the development
of age-related macular degeneration (AMD), according to a newly
published study.

Increasing evidence shows oxidative stress and free radical damage in
the RPE may underlie the pathogenesis of AMD. The RPE generates
reactive oxygen species through the phagocytosis of photoreceptor
outer segment (POS), the digestion of phagocytosed POS, and exposure
to intense light. Retinal pigment epithelial cells in the macular
area, which has the highest oxygen consumption in the retina, carry an
additional oxidative stress burden. Although many studies suggest that
cumulative oxidative stress contributes to the pathogenesis of AMD,
the sources of free radicals with age are not completely known.


Recent studies show iron may contribute to the pathogenesis of AMD as
a source of free radicals that damage the tissues. Iron is an
essential element for many metabolic processes, but excess iron
generates highly reactive hydroxyl radicals that damage lipid
membranes and proteins. Changes of iron homeostasis have been
associated with photoreceptor degeneration. Excess iron has been
observed in the macular region of the retina, in the RPE, and in the
drusen of AMD-affected eyes. Several studies show iron levels increase
normally with age in the neural retina. However, there are few studies
on iron levels in the RPE, the effects of aging, the physiological
effects of excess iron on RPE function, and the way iron homeostasis
in the RPE changes with age.

In the current study, young and old rodent RPE/choroid were compared
to assess iron homeostasis during normal aging and the effects of
increased iron on the functions of retinal pigment epithelial cells.
The iron level, mRNA expression, and protein level of iron-regulatory
molecules in RPE/choroid were quantitatively compared between young
and old animals. To test the effects of increased intracellular iron
on the functions of retinal pigment epithelial cells, in vitro ARPE-19
cells were treated with high levels of iron and assessed for
phagocytosis activity and lysosomal activity.

Iron level was significantly increased in the aged RPE/choroid.
Ferritin and ceruloplasmin mRNAs were significantly increased in the
aged RPE/choroid, whereas transferrin, transferrin receptor, and
ferroportin mRNAs did not change with age. At the protein level,
decreased transferrin and transferrin receptor, increased ferritin and
ceruloplasmin, and unchanged ferroportin were observed in the aged RPE/
choroid. Exposure of ARPE-19 cells to increased iron markedly
decreased phagocytosis activity, interrupted cathepsin D processing,
and reduced cathepsin D activity in retinal pigment epithelial cells.

The investigators conclude that the RPE/choroid of aged animals
demonstrates iron accumulation and associated alterations in iron
homeostasis. Iron accumulation with age may impair the phagocytosis
and lysosomal functions of retinal pigment epithelial cells in the
aged RPE/choroid. Therefore, age-related changes of iron homeostasis
in the RPE could increase the susceptibility of the tissue to genetic
mutations associated with AMD.

The researchers state that elevated intracellular iron is probably not
the primary cause of AMD, but age-related accumulation of iron may
compromise the RPE in older animals. To the extent that increased iron
occurs in human RPE with age, iron overload may be an age-related
susceptibility factor or risk factor that exacerbates the development
of AMD. Therapeutic strategies to ameliorate age-related iron
accumulation in retinal pigment epithelial cells may provide new
treatments for age-related retinal diseases such as AMD.

WHAT IT MEANS TO YOU: This study confirms earlier research that has
identified high iron levels within the retina as a contributor to the
development of AMD. Iron is essential for normal retinal function, but
iron, even at normal levels, is a potent generator of oxidative
stress. Retinal iron levels increase as part of the normal aging of
the eye, and it is suspected that the increased oxidative stress of
iron overload contributes to the development of AMD. Recently, a study
found that a diet very high in red meat increased the risk of AMD.
This would be consistent with the hypothesis that excess iron
consumption contributes to high iron levels, and ultimately to AMD.
There are few studies examining retinal iron metabolism in humans, and
currently no treatments designed to curb excess retinal iron. However,
based on our current understanding of the role of iron in retinal
degeneration, it is recommended that persons at risk for AMD should
avoid taking oral iron supplements or eating a diet high in red meat
unless there is medical indication for the supplements, such as iron
deficiency anemia.

Read more...
Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1895-902

Tags: animal study, retinal degeneration, iron


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Apr 21, 2009
Iron accumulation within the retina increases with age

Age-related iron accumulation within the retinal pigment epithelium
(RPE) may increase oxidative stress and contribute to the development
of age-related macular degeneration (AMD), according to a newly
published study.


Increasing evidence shows oxidative stress and free radical damage in
the RPE may underlie the pathogenesis of AMD. The RPE generates
reactive oxygen species through the phagocytosis of photoreceptor
outer segment (POS), the digestion of phagocytosed POS, and exposure
to intense light. Retinal pigment epithelial cells in the macular
area, which has the highest oxygen consumption in the retina, carry
an
additional oxidative stress burden. Although many studies suggest
that
cumulative oxidative stress contributes to the pathogenesis of AMD,
the sources of free radicals with age are not completely known.


Recent studies show iron may contribute to the pathogenesis of AMD as
a source of free radicals that damage the tissues. Iron is an
essential element for many metabolic processes, but excess iron
generates highly reactive hydroxyl radicals that damage lipid
membranes and proteins. Changes of iron homeostasis have been
associated with photoreceptor degeneration. Excess iron has been
observed in the macular region of the retina, in the RPE, and in the
drusen of AMD-affected eyes. Several studies show iron levels
increase
normally with age in the neural retina. However, there are few
studies
on iron levels in the RPE, the effects of aging, the physiological
effects of excess iron on RPE function, and the way iron homeostasis
in the RPE changes with age.


In the current study, young and old rodent RPE/choroid were compared
to assess iron homeostasis during normal aging and the effects of
increased iron on the functions of retinal pigment epithelial cells.
The iron level, mRNA expression, and protein level of iron-regulatory
molecules in RPE/choroid were quantitatively compared between young
and old animals. To test the effects of increased intracellular iron
on the functions of retinal pigment epithelial cells, in vitro
ARPE-19
cells were treated with high levels of iron and assessed for
phagocytosis activity and lysosomal activity.


Iron level was significantly increased in the aged RPE/choroid.
Ferritin and ceruloplasmin mRNAs were significantly increased in the
aged RPE/choroid, whereas transferrin, transferrin receptor, and
ferroportin mRNAs did not change with age. At the protein level,
decreased transferrin and transferrin receptor, increased ferritin
and
ceruloplasmin, and unchanged ferroportin were observed in the aged
RPE/
choroid. Exposure of ARPE-19 cells to increased iron markedly
decreased phagocytosis activity, interrupted cathepsin D processing,
and reduced cathepsin D activity in retinal pigment epithelial cells.


The investigators conclude that the RPE/choroid of aged animals
demonstrates iron accumulation and associated alterations in iron
homeostasis. Iron accumulation with age may impair the phagocytosis
and lysosomal functions of retinal pigment epithelial cells in the
aged RPE/choroid. Therefore, age-related changes of iron homeostasis
in the RPE could increase the susceptibility of the tissue to genetic
mutations associated with AMD.


The researchers state that elevated intracellular iron is probably
not
the primary cause of AMD, but age-related accumulation of iron may
compromise the RPE in older animals. To the extent that increased
iron
occurs in human RPE with age, iron overload may be an age-related
susceptibility factor or risk factor that exacerbates the development
of AMD. Therapeutic strategies to ameliorate age-related iron
accumulation in retinal pigment epithelial cells may provide new
treatments for age-related retinal diseases such as AMD.


WHAT IT MEANS TO YOU: This study confirms earlier research that has
identified high iron levels within the retina as a contributor to the
development of AMD. Iron is essential for normal retinal function,
but
iron, even at normal levels, is a potent generator of oxidative
stress. Retinal iron levels increase as part of the normal aging of
the eye, and it is suspected that the increased oxidative stress of
iron overload contributes to the development of AMD. Recently, a
study
found that a diet very high in red meat increased the risk of AMD.
This would be consistent with the hypothesis that excess iron
consumption contributes to high iron levels, and ultimately to AMD.
There are few studies examining retinal iron metabolism in humans,
and
currently no treatments designed to curb excess retinal iron.
However,
based on our current understanding of the role of iron in retinal
degeneration, it is recommended that persons at risk for AMD should
avoid taking oral iron supplements or eating a diet high in red meat
unless there is medical indication for the supplements, such as iron
deficiency anemia.


Read more...
Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1895-902


Tags: animal study, retinal degeneration, iron


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

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Giiiiiit ..

Giiiiiit .. like you've been TOLD ..

Useless shteating lmpdck atheist dweeeeeeeeeb btch ..


Apr 21, 2009
Iron accumulation within the retina increases with age


Age-related iron accumulation within the retinal pigment epithelium
(RPE) may increase oxidative stress and contribute to the development
of age-related macular degeneration (AMD), according to a newly
published study.


Increasing evidence shows oxidative stress and free radical damage in
the RPE may underlie the pathogenesis of AMD. The RPE generates
reactive oxygen species through the phagocytosis of photoreceptor
outer segment (POS), the digestion of phagocytosed POS, and exposure
to intense light. Retinal pigment epithelial cells in the macular
area, which has the highest oxygen consumption in the retina, carry
an
additional oxidative stress burden. Although many studies suggest
that
cumulative oxidative stress contributes to the pathogenesis of AMD,
the sources of free radicals with age are not completely known.


Recent studies show iron may contribute to the pathogenesis of AMD as
a source of free radicals that damage the tissues. Iron is an
essential element for many metabolic processes, but excess iron
generates highly reactive hydroxyl radicals that damage lipid
membranes and proteins. Changes of iron homeostasis have been
associated with photoreceptor degeneration. Excess iron has been
observed in the macular region of the retina, in the RPE, and in the
drusen of AMD-affected eyes. Several studies show iron levels
increase
normally with age in the neural retina. However, there are few
studies
on iron levels in the RPE, the effects of aging, the physiological
effects of excess iron on RPE function, and the way iron homeostasis
in the RPE changes with age.


In the current study, young and old rodent RPE/choroid were compared
to assess iron homeostasis during normal aging and the effects of
increased iron on the functions of retinal pigment epithelial cells.
The iron level, mRNA expression, and protein level of iron-regulatory
molecules in RPE/choroid were quantitatively compared between young
and old animals. To test the effects of increased intracellular iron
on the functions of retinal pigment epithelial cells, in vitro
ARPE-19
cells were treated with high levels of iron and assessed for
phagocytosis activity and lysosomal activity.


Iron level was significantly increased in the aged RPE/choroid.
Ferritin and ceruloplasmin mRNAs were significantly increased in the
aged RPE/choroid, whereas transferrin, transferrin receptor, and
ferroportin mRNAs did not change with age. At the protein level,
decreased transferrin and transferrin receptor, increased ferritin
and
ceruloplasmin, and unchanged ferroportin were observed in the aged
RPE/
choroid. Exposure of ARPE-19 cells to increased iron markedly
decreased phagocytosis activity, interrupted cathepsin D processing,
and reduced cathepsin D activity in retinal pigment epithelial cells.


The investigators conclude that the RPE/choroid of aged animals
demonstrates iron accumulation and associated alterations in iron
homeostasis. Iron accumulation with age may impair the phagocytosis
and lysosomal functions of retinal pigment epithelial cells in the
aged RPE/choroid. Therefore, age-related changes of iron homeostasis
in the RPE could increase the susceptibility of the tissue to genetic
mutations associated with AMD.


The researchers state that elevated intracellular iron is probably
not
the primary cause of AMD, but age-related accumulation of iron may
compromise the RPE in older animals. To the extent that increased
iron
occurs in human RPE with age, iron overload may be an age-related
susceptibility factor or risk factor that exacerbates the development
of AMD. Therapeutic strategies to ameliorate age-related iron
accumulation in retinal pigment epithelial cells may provide new
treatments for age-related retinal diseases such as AMD.


WHAT IT MEANS TO YOU: This study confirms earlier research that has
identified high iron levels within the retina as a contributor to the
development of AMD. Iron is essential for normal retinal function,
but
iron, even at normal levels, is a potent generator of oxidative
stress. Retinal iron levels increase as part of the normal aging of
the eye, and it is suspected that the increased oxidative stress of
iron overload contributes to the development of AMD. Recently, a
study
found that a diet very high in red meat increased the risk of AMD.
This would be consistent with the hypothesis that excess iron
consumption contributes to high iron levels, and ultimately to AMD.
There are few studies examining retinal iron metabolism in humans,
and
currently no treatments designed to curb excess retinal iron.
However,
based on our current understanding of the role of iron in retinal
degeneration, it is recommended that persons at risk for AMD should
avoid taking oral iron supplements or eating a diet high in red meat
unless there is medical indication for the supplements, such as iron
deficiency anemia.


Read more...
Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1895-902


Tags: animal study, retinal degeneration, iron


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

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On Sep 1, 5:49*pm, BeechSundowner <atl...@gmail.com> wrote:
> On Sep 1, 5:25*pm, ironjustice <ironjust...@cool.zzn.com> wrote:
>
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Apr 21, 2009
Iron accumulation within the retina increases with age


Age-related iron accumulation within the retinal pigment epithelium
(RPE) may increase oxidative stress and contribute to the development
of age-related macular degeneration (AMD), according to a newly
published study.


Increasing evidence shows oxidative stress and free radical damage in
the RPE may underlie the pathogenesis of AMD. The RPE generates
reactive oxygen species through the phagocytosis of photoreceptor
outer segment (POS), the digestion of phagocytosed POS, and exposure
to intense light. Retinal pigment epithelial cells in the macular
area, which has the highest oxygen consumption in the retina, carry
an
additional oxidative stress burden. Although many studies suggest
that
cumulative oxidative stress contributes to the pathogenesis of AMD,
the sources of free radicals with age are not completely known.


Recent studies show iron may contribute to the pathogenesis of AMD as
a source of free radicals that damage the tissues. Iron is an
essential element for many metabolic processes, but excess iron
generates highly reactive hydroxyl radicals that damage lipid
membranes and proteins. Changes of iron homeostasis have been
associated with photoreceptor degeneration. Excess iron has been
observed in the macular region of the retina, in the RPE, and in the
drusen of AMD-affected eyes. Several studies show iron levels
increase
normally with age in the neural retina. However, there are few
studies
on iron levels in the RPE, the effects of aging, the physiological
effects of excess iron on RPE function, and the way iron homeostasis
in the RPE changes with age.


In the current study, young and old rodent RPE/choroid were compared
to assess iron homeostasis during normal aging and the effects of
increased iron on the functions of retinal pigment epithelial cells.
The iron level, mRNA expression, and protein level of iron-regulatory
molecules in RPE/choroid were quantitatively compared between young
and old animals. To test the effects of increased intracellular iron
on the functions of retinal pigment epithelial cells, in vitro
ARPE-19
cells were treated with high levels of iron and assessed for
phagocytosis activity and lysosomal activity.


Iron level was significantly increased in the aged RPE/choroid.
Ferritin and ceruloplasmin mRNAs were significantly increased in the
aged RPE/choroid, whereas transferrin, transferrin receptor, and
ferroportin mRNAs did not change with age. At the protein level,
decreased transferrin and transferrin receptor, increased ferritin
and
ceruloplasmin, and unchanged ferroportin were observed in the aged
RPE/
choroid. Exposure of ARPE-19 cells to increased iron markedly
decreased phagocytosis activity, interrupted cathepsin D processing,
and reduced cathepsin D activity in retinal pigment epithelial cells.


The investigators conclude that the RPE/choroid of aged animals
demonstrates iron accumulation and associated alterations in iron
homeostasis. Iron accumulation with age may impair the phagocytosis
and lysosomal functions of retinal pigment epithelial cells in the
aged RPE/choroid. Therefore, age-related changes of iron homeostasis
in the RPE could increase the susceptibility of the tissue to genetic
mutations associated with AMD.


The researchers state that elevated intracellular iron is probably
not
the primary cause of AMD, but age-related accumulation of iron may
compromise the RPE in older animals. To the extent that increased
iron
occurs in human RPE with age, iron overload may be an age-related
susceptibility factor or risk factor that exacerbates the development
of AMD. Therapeutic strategies to ameliorate age-related iron
accumulation in retinal pigment epithelial cells may provide new
treatments for age-related retinal diseases such as AMD.


WHAT IT MEANS TO YOU: This study confirms earlier research that has
identified high iron levels within the retina as a contributor to the
development of AMD. Iron is essential for normal retinal function,
but
iron, even at normal levels, is a potent generator of oxidative
stress. Retinal iron levels increase as part of the normal aging of
the eye, and it is suspected that the increased oxidative stress of
iron overload contributes to the development of AMD. Recently, a
study
found that a diet very high in red meat increased the risk of AMD.
This would be consistent with the hypothesis that excess iron
consumption contributes to high iron levels, and ultimately to AMD.
There are few studies examining retinal iron metabolism in humans,
and
currently no treatments designed to curb excess retinal iron.
However,
based on our current understanding of the role of iron in retinal
degeneration, it is recommended that persons at risk for AMD should
avoid taking oral iron supplements or eating a diet high in red meat
unless there is medical indication for the supplements, such as iron
deficiency anemia.


Read more...
Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1895-902


Tags: animal study, retinal degeneration, iron


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