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selenium and P53
 

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Zosimos Views: 1,522
Published: 13 years ago
 
This is a reply to # 1,476,753

selenium and P53


I recently have come across a lot of interesting information about selenium, P53, and cancer.

P53 is the gene that protects your cells from becoming cancerous. It either tells your cell to repair itself so it won't become carcinogenic, or it initiates apoptosis, which is cell suicide, which doesn't sound good but it's better than the cell becoming carcinogenic

Anyway p53 absolutely selenium to work properly. If it doesn't have selenium it can mutate and once that happens you no longer have a defense against cancer

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http://lpi.oregonstate.edu/ss04/selenium.html


Since non-vascularized tumors containing a normal p53 gene rarely grow larger than the size of a grain of rice, p53 may be activated by the abnormally low oxygen levels in the interior of these tumors. P53 activation then limits tumor growth by triggering cell cycle arrest or cell suicide. Conversely, once blood vessels develop within a tumor, the resulting increase in oxygen levels may lead to oxidative inactivation of p53 and resumption of tumor growth. In this scenario, induction of selenoenzymes like thioredoxin reductase by dietary selenium may help keep p53 in its reduced and active state. To test the link between selenium, thioredoxin, p53, and tumor suppression, we are now conducting studies in mice, thanks to support from a Linus Pauling Institute pilot project grant.

http://www.springerlink.com/content/h52knr2540517h7j/


Following the DNA damage, selenite activated p53-dependent pathway as evidenced by the appearance of phosphorylated p53 and accumulation of p21 in the treated cells. Concomitantly, selenite activated p38 pathway but its effect on JNK was very weak. p53- and p38-dependent signaling led to the accumulation of Bax protein, which was preventable by specific inhibitors of p38 (SB 203580) and p53 (Pifithrin-a). Mitochondria in selenite-treated cells changed their dynamics (shape and localization) and released AIF and Smac/Diablo, which initiated caspase-independent apoptosis as confirmed by the caspase-3 activity assay and the low effect of caspase inhibitors z-DEVD-fmk and z-VAD-fmk on cell death. We conclude that selenite induces caspase-independent apoptosis in cervical carcinoma cells mostly by oxidative stress-mediated activation of p53 and p38 pathways, but other selenite-mediated effects, in particular mitochondria-specific ones, are also involved.
 

 
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