Peroxide-induced necrosis (old post)

unearthed from Google's "cache"

The most understandable source I have been able to find on this. Our bodies are truly amazing...H202, "both required and potentially harmful." The good news? "The thyroid gland, by unknown mechanisms, retains its selenium content even in moderate to severe selenium deficiency." So, selenium deficiency is RARE.

But still...take your selenium, folks!

Lots of good info at the link:


http://lists.calorierestriction.org/pipermail/crcomm_lists.calorierestriction...



"BEYOND THE REDOX BALANCE: SELENIUM AND THE THYROID GLAND The synthesis of thyroid hormones is achieved by iodination of thyronine residues at thyroglobulin by means of an H2O2- dependent heme peroxidase. No wonder the thyroid gland is also equipped with cGPx and PHGPx to regulate the amount of H2O2 (Hydrogen-Peroxid) present, which is both required and potentially harmful (97). Moreover, the processing of the prohormone, tetraiodothyronine (thyroxin, T4), to the active form, triiodothyronine (T3), is catalysed by selenoproteins, 50 deiodinase I (56, 57) and 50 -deiodinase II (58), two complementarily distributed enzymes that regulate T3 supply in target tissues (98). Moreover, the degradation or inactivation of T4 and T3, respectively, is also achieved by a selenoprotein, type III 5-deiodinase (59). Nevertheless, our knowledge on the relevance of selenium de- ficiency to thyroid function is scarce, because the thyroid gland, by unknown mechanisms, retains its selenium content even in moderate to severe selenium deficiency. The deiodinases, too, are only marginally affected by selenium deprivation (97). However, new insights and epidemiological data might challenge the seemingly established knowledge on related diseases. The myxedematous form of cretinism, for instance, appears to result from a combined deficiency of Iodine and selenium (99)."
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