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Sunday, October 25, 2009

Methyl Succinic Acid - does anyone know anything about it from a medical standpoint?

Someone recently told me that they have high levels of Methyl Succinic Acid. The only thing I can find is that it is a poison. Would there be any medical reason that it may occur in the body or should they be concerned that they are being poisoned somehow?
Answer:
Dear BPD Wife (who henceforth shall be honorary called Dr. HOUSE MD) http://www.fox.com/house/ because of this tough question.

A person that has elevated methyl succinic acid? Very rare case in deed. The closes found in the medical literature and references is this excerpt from Acta Paediatr Jpn. [ACTA Paediatrica Japonica (Tokyo)] Feb 1990
http://www.jpeds.or.jp/english/welcome.h...

Organic acid and acylcarnitine profiles of glutaric aciduria type I.
Matsumoto M, Matsumoto I, Shinka T, Kuhara T, Imamura H, Shimao S, Okada T.
Division of Human Genetics, Kanazawa Medical University, Ishikawa, Japan.

Urinary organic acid and acylcarnitine profiles from a 2-month-old boy were studied by gas chromatography-mass spectrometry and fast atom bombardment mass spectrometry. The patient excreted large amounts of glutaric acid and significant amounts of 3-hydroxyglutaric acid, glutaconic acid and glutarylcarnitine, and his serum glutaric acid level was markedly elevated. Thus he was chemically diagnosed as having glutaric aciduria type I (GAI).

In addition to the above metabolites previously described in GAI, SIGNIFICANTLY INCREASED EXCRETION of 2-ketoglutaric acid, SUCCINIC ACID, adipic acid, adipylcarnitine, suberic acid and azelaic acid was found. 2-Ketoadipic acid methylsuccinic acid and ethylmalonic acid were also detectable, suberylcarnitine was not increased, and dehydroadipylcarnitine was decreased in his urine.

These results suggest that excess glutaryl-CoA causes the competitive inhibition of the dehydrogenation of adipyl-CoA to dehydroadipyl-CoA and results in an increase of adipic acid and adipylcarnitine and a decrease of dehydroadipylcarnitine.

It is also suggested that oxidative decarboxylation of 2-ketoglutaric acid to succinyl-CoA is inhibited by high levels of glutaryl-CoA, and that the dehydrogenation of succinic acid to fumaric acid is inhibited owing to the increased glutaric acid derived from excess glutaryl-CoA. These results indicate that gas chromatography-mass spectrometry is the most appropriate and accurate method for the differential chemical diagnosis of GAI and glutaric aciduria type II.

You can read more about Glutaric aciduria type I %26 II from this website: http://www.savebabies.org/diseasedescrip...
Isn't that part of malathion?
If so they may be getting poisoned inadvertently from insecticide.
Hi. I cant go right ahead at accusing someone of poisoning your friend, but as far as I can find, we do not produce it naturally. All the websites I found said it is produced synthetically, and that it is indeed a poison. It stops the production of D-glucose (a type of enantiomer of glucose, the other type is L). So, I would not think we had it in us naturally: we need to produce glucose!

Well, hope that helped,

Ashley

1 comment:

  1. "Here is an additional resource about the genetics of Glutaric Acidemia Type II: http://www.accessdna.com/condition/Glutaric_Acidemia_Type_II/167. I hope it helps. Thanks, AccessDNA"

    ReplyDelete

 
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