Gastrointestinal
infections, Hydrogen Sulfide, and Sulfite
A typical part of a viral gastroenteritis infection is
damage to the mucosa (lining) of the proximal small intestine (the part of the
small intestine closest to the stomach).[1]
Our bodies make and use hydrogen sulfide (H2S) while working to protect the
gastric[2]
[3]
and intestinal mucosa.[4]
It is still being investigated exactly how H2S is afterward
transformed in the body, but one of its catabolic products is known to be sulfite.
Moreover, it was recently discovered that there appears to be a previously-unknown
H2S oxidation pathway using neuroglobin.[5]
Neuroglobin has been discovered to be expressed in the cells of the stomach
fundus and the small intestine after hypoxia.[6]
I suspect that neuroglobin-assisted H2S catabolism results in more net sulfite
than the better known sulfide:quinone oxidoreductase catabolic pathway and that
it could be a major contributor to the presence of sulfite in the stomach and
small intestine at levels high enough to trigger vomiting.
In most people, sulfite oxidase typically seems able to
handle the amount of sulfite resulting from endogenous hydrogen sulfide
metabolism. However, in the absence of sufficient molybdenum, magnesium,[7]
or P5P (active vitamin B6 is involved in making heme, which is part of sulfite
oxidase),[8]
sulfite oxidase might not reach necessary levels of activity, for those three
nutrients are needed to form sulfite oxidase and the molybdenum cofactor. The
main result of insufficient sulfite oxidase activity is a buildup of
nausea-inducing sulfite. It thus follows that supplemental molybdenum can
reduce nausea.
mARC 1 and mARC 2
Two relatively recently discovered molybdenum-utilizing
enzymes are the mARC 1 and mARC 2 enzymes. They appear to be involved with
nitric oxide (NO) production,[9]
and NO and H2S cooperatively interact in many ways.[10]
[11]
Thus mARC1 and mARC2 might also be involved in the pathophysiology of nausea
and vomiting.
Conclusion
I have written this because I have seen molybdenum
dramatically prevent nausea and vomiting from gastrointestinal viruses, as well
as shorten the duration of gastrointestinal virus symptoms even after vomiting
has already begun. I think current research supports a hypothesis that
molybdenum does so by supporting optimal activity of the molybdenum-utilizing
enzymes sulfite oxidase and possibly mARC1 and mARC2.
Because this discovery has great potential for improvement
of public health, I think it urgent for professional researchers to explore
molybdenum’s effect in alleviating gastrointestinal virus-caused nausea and
vomiting and establish appropriate dosage guidelines for its use.
- CT
References
References
[1] Widerlite
L, Trier JS, Blacklow NR, Schreiber DS. Structure of the gastric mucosa in
acute infectious bacterial gastroenteritis. Gastroenterology 1975;68(3):425-430.
[2] Bronowicka-Adamska
P, Wróbel M, Magierowski M, Magierowska K, Kwiecień S, Brzozowski T. Hydrogen
sulphide production in healthy and ulcerated gastric mucosa of rats. Molecules
2017;22(4). pii: E530.
[3]
Souza LK, Araújo TS, Sousa NA, Sousa FB, Nogueira KM, Nicolau LA, Medeiros JV.
Evidence that d-cysteine protects mice from gastric damage via hydrogen sulfide
produced by d-amino acid oxidase. Nitric Oxide 2017;64:1-6.
[4] Wallace
JL, Caliendo G, Santagada V, Cirino G, Fiorucci S. Gastrointestinal safety and
anti-inflammatory effects of a hydrogen sulfide-releasing diclofenac derivative
in the rat. Gastroenterology 2007;132(1):261-271.
[5] Bilska-Wilkosz
A, Iciek M, Górny M, Kowalczyk-Pachel D. The Role of Hemoproteins: Hemoglobin,
Myoglobin and Neuroglobin in Endogenous Thiosulfate Production Processes. Int
J Mol Sci 2017;18(6). pii: E1315. doi: 10.3390/ijms18061315.
[6]
Emara M, Turner AR, Allalunis-Turner J. Hypoxic regulation of cytoglobin and
neuroglobin expression in human normal and tumor tissues. Cancer Cell Int
2010;10:33.
[7] Mendel
RR. The Molybdenum Cofactor. J Bio Chem
2013;288:13165-13172.
[8] Heinemann
IU, Jahn M, Jahn D. Arch. The biochemistry of heme biosynthesis. Biochem Biophys 2008;474(2):238-251.
[9] Sparacino-Watkins
CE, Tejero J, Sun B, Gauthier MC, Thomas J, Ragireddy V, Merchant BA, Wang J,
Azarov I, Basu P, Gladwin MT. Nitrite reductase and nitric-oxide synthase
activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. J Biol
Chem 2014; 289(15):10345-10358.
[10] Farrugia
G, Szurszewski JH. Carbon Monoxide, Hydrogen Sulfide, and Nitric Oxide as
Signaling Molecules in the Gastrointestinal Tract. Gastroenterology
2014;147(2): 303–313.
[11] Szabo
C. Hydrogen sulfide, an enhancer of vascular nitric oxide signaling: mechanisms
and implications. Am J Physiol Cell Physiol 2017 Jan 1;312(1):C3-C15.
(Disclaimer: I do not prescribe the use of pharmaceutical drugs in any way. I am not a physician, and I reject out of hand any attempt to hold me liable for what boils down to a discussion of food. Any use of a molybdenum supplement should be prudent and guided by the tested tolerable upper intake levels for its usage (see http://lpi.oregonstate.edu/mic/minerals/molybdenum for those limits). Any use of an isolated molybdenum supplement during pregnancy should be under the direction of a medical professional as such supplements have apparently not been tested during pregnancy.)
(Disclaimer: I do not prescribe the use of pharmaceutical drugs in any way. I am not a physician, and I reject out of hand any attempt to hold me liable for what boils down to a discussion of food. Any use of a molybdenum supplement should be prudent and guided by the tested tolerable upper intake levels for its usage (see http://lpi.oregonstate.edu/mic/minerals/molybdenum for those limits). Any use of an isolated molybdenum supplement during pregnancy should be under the direction of a medical professional as such supplements have apparently not been tested during pregnancy.)
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