Posted by tealady on November 16, 2003, at 21:59:28
In reply to Re: Confused about methylation...Larry H., DSCH, help? » McPac, posted by DSCH on November 10, 2003, at 20:38:47
> > "A small percentage of persons with sufficient dietary methionine cannot efficiently produce SAMe --- These persons need supplemental SAMe, and not methionine or TMG and are the exception to the rule."
> >
> > >>>>>>>>>> I wonder if I am in this small percentage? Pfeiffer recently increased my methionine to 2,500 mg/day, as 1,500 mg/day for MANY months wasn't doing anything....in this small % of folks, WHY is their methionine not converted to SAMe?
>
> Not enough ATP or magnesium to spare from other duties?A deficency in the enzymes that accomplish this task?
Perhaps too much selenium or too little?
RTF] MECHANISMS OF SELENIUM METHYLATION AND TOXICITY IN MICE TREATED ...
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... These results suggest that the depression of selenium methylation ability resulting
from inactivation of SAM synthetase and selenium methylating enzyme(s) was ...http://www.google.com.au/search?q=cache:o62M9jkpWOsJ:www-tiresias.bio.unipd.it/HomeSele/poster/9(Miscellanea)/Hasegawa.rtf+sam+selenium&hl=en&ie=UTF-8
ENHANCEMENT OF SELENOCYSTINE TOXICITY CAUSED BY THE INHIBITION OF SELENIUM METHYLATION
T. Hasegawa1, T. Okuno2, K. Nakamuro2 and Y. Seko1
1Yamanashi Institute of Environmental Sciences, Fujiyoshida, Yamanashi, Japan2Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka, Japan.
We have already reported that the liver was damaged in mice treated orally with selenocystine (SeCys). The present study was carried out to elucidate the relationship between hepatic toxicity and selenium methylation in mice after repeated oral administration of SeCys (10 or 20 mg/kg) for 10 days. The animals exposed to the high dose showed a significant rise of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in plasma. Urinary total selenium increased with SeCys dose. Although content of trimethylselenonium ion (TMSe) as the end-product of selenium methylation in urine amounted to 85 % of total selenium at the low dose, it was only 25 % at the high dose. In the liver, the high dose resulted in inactivation of selenium methylating enzyme(s) and decrease in S-adenosylmethionine (SAM) level due to the inhibition of SAM synthetase activity. To determine whether hepatic toxicity was enhanced by the depression of selenium methylation, mice were injected with periodate-oxidized adenosine (PAD; 100 mol/kg, i.p.), a known potent inhibitor of the SAM-dependent methyltransferase, 30 min before oral treatment of SeCys (10, 20 or 50 mg/kg). Hepatic toxicity induced by SeCys was significantly enhanced by the PAD-pretreatment. In vitro experiment was carried out to determined a chemical species of SeCys metabolite which inactivated the SAM synthetase. The enzyme was strongly inhibited by selenide, which is a precursor of methylated selenium compounds. These results suggest that the depression of selenium methylation ability resulting from inactivation of SAM synthetase and selenium methylating enzyme(s) was caused by selenide in mice following repeated oral administration of a toxic dose of SeCys. The excess selenide accumulated by depression of selenium methylation may be involved in the liver toxicity caused by SeCys.
----------http://www.genome.ad.jp/dbget-bin/show_pathway?hsa00450+27430
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Looks like selenium is in there somewhere?Jan
poster:tealady
thread:278139
URL: http://www.dr-bob.org/babble/alter/20031104/msgs/280365.html