Age-related Macular Iron Accumulation

Discussion in 'Optometry Archives' started by ironjustice, Sep 1, 2009.

  1. ironjustice

    ironjustice Guest

    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
     
    ironjustice, Sep 1, 2009
    #1
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  2. ironjustice

    ken Guest

    Spamming Canuck Cocksucker
     
    ken, Sep 1, 2009
    #2
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  3. ironjustice

    ironjustice Guest

    Giiiiiit .. like you've been TOLD ..

    Giiiiiit ..

    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
     
    ironjustice, Sep 1, 2009
    #3
  4. ironjustice

    ken Guest

    Spamming Canuck Dickwadd
     
    ken, Sep 1, 2009
    #4
  5. ironjustice

    ironjustice Guest

    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
     
    ironjustice, Sep 1, 2009
    #5
  6. BeechSundowner, Sep 1, 2009
    #6
  7. BeechSundowner, Sep 2, 2009
    #7
  8. ironjustice

    ironjustice Guest

    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
     
    ironjustice, Sep 2, 2009
    #8
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