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Medical Forum / General / Nutrition / July 2004Iron accumulation, cause or effect in cell life
From time to time the subject of iron being found in higher levels in the cells of disorders/diseases has arisen. Often some research will note the relationship as an observation with no way to know if the iron is a cause or effect of the problem. Here we have one example where high iron is an 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 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 altered iron homeostasis at the cellular level, yet this is poorly understood. Therefore, changes in iron content in primary human fibroblasts were studied in culture models of cellular senescence. Total iron content increased exponentially during cellular senescence, 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 cellular senescence with N-tert-butyl-hydroxylamine (NtBHA) attenuated 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 of normal cellular senescence in vitro. Senescence-associated iron accumulation may contribute to the increased oxidative stress and cellular dysfunction seen in senescent cells. PMID: 15247045 [PubMed - as supplied by publisher] Perhaps a human body in iron overload is just finding a place to dump the excess iron? GT > From time to time the subject of iron being found in higher levels in the > cells of disorders/diseases has arisen. Often some research will note the [quoted text clipped - 4 lines] > "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 > Ann N Y Acad Sci. 2004 Jun;1019:365-367. > [quoted text clipped - 28 lines] > > PMID: 15247045 [PubMed - as supplied by publisher] "Perhaps a human body in iron overload is just finding a place to dump the excess iron?" Perhaps, but no sign of it in the study, it has to do with the sequence of events and no cause in terms of overal process was offered. Your notion, Tom, finds no support in the results, one might as well speculate that iron deposit is the bodies attempt to control the situation because it has some healing effect. In the absence of any other info that is as good an idea as any,ie. why does iron show up in distressed areas of the body? > "Perhaps a human body in iron overload is just finding a place to dump > the excess iron?" [quoted text clipped - 5 lines] > has some healing effect. In the absence of any other info that is as good > an idea as any,ie. why does iron show up in distressed areas of the body? Hogwash Perhaps you would like to give a dissertation on where the body stores excess iron when in overload? I am not Tom. Never have been. Never will be. Don't even want to be. Appalled at the idea. > > "Perhaps a human body in iron overload is just finding a place to > dump [quoted text clipped - 20 lines] > I am not Tom. Never have been. Never will be. Don't even want to be. > Appalled at the idea. Life must be a continuing horror for Mark. Can you imagine what it must be like? A Tom in every closet. A Tom under every bed, in every commode. Has anyone ever researched an association between iron overload (or underload) and delerium tremens? MikeV > > > "Perhaps a human body in iron overload is just finding a place to > > dump [quoted text clipped - 27 lines] > > MikeV I can't imagine a Tom in every closet or commode. The latter would be frightening - good horror movie material. Could be a connection to delerium tremens! :-) Perhaps excess iron reduces cognitive function... GT > "Perhaps a human body in iron overload is just finding a place to dump > the excess iron?" [quoted text clipped - 5 lines] > has some healing effect. In the absence of any other info that is as good > an idea as any,ie. why does iron show up in distressed areas of the body? Mark - For what it's worth, "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 This book is expensive - costs around $300 for the revised edition. But the author is quite knowledgable. Any comments? .... GT ""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."" Yes, I posted an abstract to the exact same effect here previously, in response to "rust" causing problems when most iron is already bound. The oxidation question is complex. There are instances where so called antiox substances can promote oxidation to the benefit of the body. In some situations the same substance can retard or promote oxidation. It is possible that free iron because of injury can promote some healthy benefit, consider: Toxicol In Vitro. 2004 Oct;18(5):555-61. Prooxidant property of green tea polyphenols epicatechin and epigallocatechin-3-gallate: implications for anticancer properties. Azam S, Hadi N, Khan NU, Hadi SM. Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh 202002, U.P., India. It is believed that anticancer and apoptosis inducing properties of green tea are mediated by it's polyphenolic constituents particularly catechins. A number of reports have shown that green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) is among the most effective chemopreventive and apoptosis-inducing agents present in the beverage. Plant polyphenols are naturally occurring antioxidants but they also exhibit prooxidant properties. Over the last several years we have shown that various classes of plant polyphenols including flavonoids, curcuminoids and tannins are capable of catalyzing oxidative DNAcleavage particularly in the presence of transition metal ions such as copper and iron. With a view to understand the chemical basis of various pharmacological properties of green tea, in this paper we have compared the prooxidant properties of green tea polyphenols--EGCG and EC ((-)-epicatechin). The rate of oxidative DNA degradation as well as hydroxyl radical and superoxide anion formation was found to be greater in the case of EGCG as compared with EC. It was also shown that copper mediated oxidation of EC and EGCG possibly leads to the formation of polymerized polyphenols. Further, it was indicated that copper oxidized catechins were more efficient prooxidants as compared with their unoxidized forms. These results correlate with the observation by others that EGCG is the most effective apoptosis inducing polyphenol present in green tea. They are also in support of our hypothesis that prooxidant action of plant polyphenols may be an important mechanism of their anticancer properties. A model for binding of Cu(II) to EC has been presented where the formation of quinone and a quinone methide has been proposed. PMID: 15251172 [PubMed - in process] > ""In healthy individuals there is little if any unbound iron > circulating in the blood. In all disease states, however, unbound iron [quoted text clipped - 47 lines] > > PMID: 15251172 [PubMed - in process] Blabber!! This is an attempt to pull OFF TOPIC! We were not talking about antioxidants and green tea. The real topic is that the body releases free iron at the site of inflammation. Free iron comes from iron in the body that is not bound to proteins, e.g.: a result of iron overload. The logical conclusion is that without iron overload, no free iron is available, and no iron is released. Any released iron will cause irritation and oxidation at the inflammation site, accelerating disease processes. The logical solution is to remove the iron. Hence, in my opinion, it is better to be closer to iron deficiency anemia than it is to be in iron overload. Go take your beloved iron supplements if you wish, I think any iron supplementation is very dangerous in male adults and women past menopause. It's also a good idea to give blood regularly. GT P.S.: I'm not Tom. |
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