Cause and effect in iron accumulation

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From time to time the subject of iron being found in higher levels

in the

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cells of disorders/diseases has arisen. Often some research will

note the

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relationship as an observation with no way to know if the iron is a

cause

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or effect of the problem. Here we have one example where high iron

is an

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effect not the cause of cell life:

"Thus, iron accumulation is not a cause, but a consequence of normal
cellular senescence in vitro."

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstr

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Ann N Y Acad Sci. 2004 Jun;1019:365-367.

Iron Accumulation during Cellular Senescence.

Killilea DW, Wong SL, Cahaya HS, Atamna H, Ames BN.

Nutritional Genomics Center, Children's Hospital Oakland Research
Institute, 5700 Martin Luther King, Jr. Way, Oakland, CA 94609.
bames[remove]@chori.org

Iron accumulates as a function of age and is associated with the
pathology of numerous age-related diseases. These changes may

becaused by

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altered iron homeostasis at the cellular level, yet this is
poorly understood. Therefore, changes in iron content in primary

human

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fibroblasts were studied in culture models of cellular senescence.
Total iron content increased exponentially during cellular

senescence,

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reaching approximately 10-fold higher levels than young cells.
Increasing intracellular iron levels through iron-citrate
supplementation or decreasing intracellular iron levels using
iron-selective chelators had little effect on cellular life span and
markers of cellular senescence when used at subtoxic doses. However,
accelerating cellular senescence with low-dose H(2)O(2) also
accelerated senescence-associated iron accumulation. Delaying
cellularsenescence with N-tert-butyl-hydroxylamine (NtBHA)

attenuated

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senescence-associated iron accumulation. Furthermore, H(2)O(2) or
NtBHA had no effect on iron intracellular levels in immortalized
fibroblasts. Thus, iron accumulation is not a cause, but a

consequence

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of normal cellular senescence in vitro. Senescence-associated iron
accumulation may contribute to the increased oxidative stress and
cellular dysfunction seen in senescent cells.

Just can't let go of it?

"In healthy individuals there is little if any unbound iron
circulating in the blood. In all disease states, however, unbound iron
(also called free iron) is released at sites of inflammation and can
spark uncontrolled oxidation."

Griffiths, E. Iron and Infection: Molecular, Physiological and
Clinical Aspects, Second Edition. New York: John Wiley & Sons.

http://www.wiley.com/WileyCDA/WileyTitle/productCd-0471939404.html