jimmylegs wrote:wow i have rarely seen 25 mg of zinc in a multi. i think testing levels is the key. low zinc is often seen in ms and other diseases. zinc deficiency or low zinc status is far more common than toxicity.
zinc deficiency is also correlated with iron dysregulation and abnormal deposition in tissue, as i have posted elsewhere, specifically the earlier days of the original ccsvi thread.
i find those zinc/selenium/cancer abstracts quite informative. particularly where zinc status was shown to be progressively worse through breast cancer stages.
lyndacarol wrote:Depue, Illinois is not the only Illinois town with a cluster of MS cases.
An article from the Chicago Tribune, January 5, 2003, tells about an epidemiological study planned for PawPaw, Illinois (tiny agricultural town of 850 near Rockford) where Harold Ikeler's family has been targeted by MS--his wife died of it, all three of his daughters have it, and five grandchildren have it!
At the time of the article and for the study, a resident had tracked down 14 current and former residents with the disease. (Kind of shoots the usual estimates of one case for every 1,000 people, doesn't it?)
jackD wrote:I think you are presenting a followup study to the one I just posted which listed the location as "DePue, Illinois--a small, north-central Illinois community". These communities are very close to each other and may be the same community just known by different names.
J Surg Res. 2012 Apr 29. [Epub ahead of print]
Pterostilbene induces mitochondrially derived apoptosis in breast cancer cells in vitro.
Moon D, McCormack D, McDonald D, McFadden D.
Division of Surgical Research, University of Vermont, 111 Colchester Avenue, Fletcher House 311, MCHV Campus, Burlington, Vermont.
The ability of a breast cancer cell to evade apoptosis has a key role in tumor progression and sensitivity to treatment. High levels of Bcl-2-associated X protein (Bax) in tumor cells have been found to promote apoptosis and sensitize cells to anti-cancer therapies. Bcl-2-associated X protein redistribution to the mitochondrial membrane results in the release of proapoptotic factors including cytochrome C, second-mitochondrial-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low PI (Smac/DIABLO), and Ca(2+). We aimed to explore this pathway in cancerous breast cell lines treated with the naturally occurring antioxidant 3,5-dimethoxy-4-hydroxystilbene (pterostilbene).
We used whole cell lysates +/- Bax SiRNA from the cell lines MCF-7 and MDA-MB-231 in an enzyme-linked immunosorbent assay to quantify Bax, cytochrome C, Smac/DIABLO expression, and manganese superoxide dismutase (MnSOD) activity after treatment with pterostilbene. We quantified cell death using histone-related DNA complexes from cytosolic and mitochondrial fractions and used methylthiazol tetrazolium assay to analyze cell proliferation, in the presence of Bax-silencing or scrambled RNA. We measured changes in cytosolic calcium using the ratiometric calcium-sensitive dye fura-2-AM using an inverted ratiometric monochromator microscope.
Treatment of MCF-7 and MDA-MB-231 (MDA) cells with pterostilbene caused concentration-dependent increases in intracellular Bax at all doses tested. RNA silencing of Bax resulted in reduced rates of apoptosis in both cells types and increased cell survival when treated with pterostilbene. We observed an increase in cytochrome C in MDA cells after treatment with pterostilbene. The MCF-7 cells showed a net increase in cytosolic cytochrome C, with a corresponding reduction in mitochondrial cytochrome C after treatment with 50 and 75 μmol/L pterostilbene. We observed this again in Smac/DIABLO expression in both cell types. In MCF-7 cells, pterostilbene treatment caused an increase in cytosolic but a decrease in mitochondrial Smac/DIABLO protein concentrations. Pterostilbene significantly increase MnSOD activity in MDA-MB-231 cells. Finally, pterostilbene resulted in significant increases in cytosolic calcium concentrations.
The natural dietary compound pterostilbene has an anti-proliferative effect and induces apoptosis in breast cancer cells in vitro via Bax activation and overexpression, resulting in increased MnSOD, Smac/DIABLO, and cytochrome C activity and cytosolic Ca(2+) overload.
]Copyright © 2012 Elsevier Inc. All rights reserved.
PMID: 22572619 [PubMed - as supplied by publisher]
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