Hi, Freddd.
I'm afraid I have to take issue with your statement quoted below:
Research has shown that mercuric mercury can accept methyl groups only from methylcobalamin and related corrinoid molecules. The reason is that mercuric ion has two positive charges, and it can accept only a negatively charged methyl group (that is, a carbanion). Methylcobalamin and related corrinoid molecules are the only methyl donors that can supply carbaniions.
This was shown by Wood et al. back in the 70s.
The bacteria in the aquatic environment that methylate mercury use these molecules to do it, and this is apparently a protective mechanism to move mercury out of the bacterial cells. The mercury in the environment comes primarily from coal-fired power plants, and rains out of the atmosphere to enter the waterways, where certain bacteria methylate it. It has been shown that the sulfate-reducing bacteria are the ones that produce most of the methylmercury in the aquatic environment. The methylmercury then moves up the food chain, and that's how the larger fish, such as tuna, end up containing enough methylmercury that the EPA has put limits on its consumption.
With the recent attention given to sulfate-reducing bacteria in the gut of PWCs (as evidenced by positive responses on the urine H2S test), I'm wondering how much methylation of mercury is also going on in the gut in these people. If this is a significant process, it really points to the importance of giving a high priority to fixing the gut problems in CFS.
Best regards,
Rich
I'm afraid I have to take issue with your statement quoted below:
Research has shown that mercuric mercury can accept methyl groups only from methylcobalamin and related corrinoid molecules. The reason is that mercuric ion has two positive charges, and it can accept only a negatively charged methyl group (that is, a carbanion). Methylcobalamin and related corrinoid molecules are the only methyl donors that can supply carbaniions.
This was shown by Wood et al. back in the 70s.
The bacteria in the aquatic environment that methylate mercury use these molecules to do it, and this is apparently a protective mechanism to move mercury out of the bacterial cells. The mercury in the environment comes primarily from coal-fired power plants, and rains out of the atmosphere to enter the waterways, where certain bacteria methylate it. It has been shown that the sulfate-reducing bacteria are the ones that produce most of the methylmercury in the aquatic environment. The methylmercury then moves up the food chain, and that's how the larger fish, such as tuna, end up containing enough methylmercury that the EPA has put limits on its consumption.
With the recent attention given to sulfate-reducing bacteria in the gut of PWCs (as evidenced by positive responses on the urine H2S test), I'm wondering how much methylation of mercury is also going on in the gut in these people. If this is a significant process, it really points to the importance of giving a high priority to fixing the gut problems in CFS.
Best regards,
Rich
Hi Rich,
So how the cycle works then is that mercury takes the methyl from the methylb12, the former methylb12 becomes remethylated in the usual scheme of things from SAM-e and methylfolate, if available, or is just disabled, and then has that methy group taken my mercury again, acting as the intermediate carrier? Or is it immediately latched onto by TCIII and escorted to the liver for recycling? In any case hydroxyb12 is converted to methylb12 to be active, just a trickle of it.
A side note, there are mercury alerts even for bluegills in some Utah waters the situation has gotten so bad. I don't eat fish from Utah waters because even the ones that are not alerted have substantial mercury.