What if your sulfur metabolism issues aren’t due to sulfite oxidase or molybdenum cofactor deficiency? Read on to learn about how there may be a different cause to your sulfur intolerance!
***This is not medical advice but written for informational purposes only. Please consult with your personal healthcare provider prior to making any changes to your diet, supplements, medications, or lifestyle.***
SUOX/MoCo deficiency. Some of us in the MoCo Steal: recovering from sulfite toxicity group on Facebook (https://www.facebook.com/share/g/17NqPUMKZj/) are struggling with sulfite due to burnout or inadequate SUOX function (a MoCo-dependent enzyme). Meaning that the amount of sulfite being produced by the transsulfuration pathway is exceeding our ability to convert it to sulfate. This causes high mitochondrial sulfite levels, which then spill out into the cytosol. This can lead to very high levels of s-sulfocysteine, SSC. We react to sulfur foods, garlic, NAC, and glutathione supplements.
Neutrophilic Sulfite Toxicity. Some of us in this group have lost our adaptive immune system (many have done the low vitamin A diet, which was a major contributing factor to loss of secretory IgA production and adaptive immune function). This causes the innate immune system (neutrophils and macrophages) to become dominant. In addition, many in this group struggle with SIBO, which provides additional H2S for neutrophils to use for sulfite production. In the portal vein, this excess sulfite can destroy B1 and B6 before they reach the liver and general circulation. We don’t have high levels of SSC because we don’t have SUOX/Sulfite toxicity. The sulfite and oxidative stress produced by the neutrophils does cause glutathione deficiency when these pro-oxidants diffuse across cell membranes in the liver cells, but our mitochondria are still protected by SUOX. We react to sulfur foods, garlic, NAC, and glutathione supplements.
Below is a diagram showing the neutrophilic contribution of sulfite during the immune response.
Neutrophils produce sulfite in response to LPS or when dealing with bacteria.
https://pubmed.ncbi.nlm.nih.gov/9823763
https://pubmed.ncbi.nlm.nih.gov/12512997
https://pubmed.ncbi.nlm.nih.gov/16317383
The overachiever. Some of us are doing both! This person is someone who overall has malnutrition and is unable to tolerate the supportive nutrients needed to maintain and restore SUOX function
(need to be able to make heme and MoCo to make SUOX). They have lost their adaptive immune system due to malnutrition as well, and now rely on neutrophils and macrophages to deal with viruses and bacteria.
Why is it important to find out which group you are in?
If you are not high in SSC, then whatever diet you are currently on is specifically adequate in molybdenum. It means you are likely converting excess sulfite to sulfate. It means that your cysteine salvage pathway, where you can salvage cysteine from SSC and then metabolize sulfite to sulfate is working as well.
If you have normal SSC, you likely don’t need to supplement with molybdenum beyond what you are currently doing, and, for some, you may be able to back off on high doses (TALK WITH YOUR PRACTITIONER) as long-term high exposure to molybdenum is found to cause chronic kidney disease.
SSC can be tested via OMX from Diagnostic Solutions Laboratory.
https://www.diagnosticsolutionslab.com/tests/omx
How does excess molybdenum cause damage to the kidneys?
Molybdenum induces oxidative stress in renal tubular cells. The oxidative stress upregulates pro-apoptotic genes (cell death genes) and decreases anti-apoptotic genes (cell saving genes).
https://pubmed.ncbi.nlm.nih.gov/33348253
https://pubmed.ncbi.nlm.nih.gov/31811574
https://pubmed.ncbi.nlm.nih.gov/31518807
https://pubmed.ncbi.nlm.nih.gov/25627418
Molybdenum also promotes inflammatory responses in the kidney through the JAK/STAT axis and pyroptosis (swelling, explosion, and release of inflammatory contents) via the NLRP3/caspase-1 pathway.
https://pubmed.ncbi.nlm.nih.gov/33157513
https://pubmed.ncbi.nlm.nih.gov/38104808
https://pubmed.ncbi.nlm.nih.gov/34479002
Below is a slide of a summary slide of “Making MoCo” which is the cofactor needed for sulfite oxidase (SUOX). I made the “ingredients” in green. Promise I am making the video to explain how making MoCo can go wrong, but definitely working on the nutrients needed is very helpful. The goal is to absorb MoCo (see this video…. https://youtu.be/tA5ImU2vJKw) and then incorporated into MoCo where it should be!
Something I have found helpful to prevent excess H2S from bacteria binding to my molybdenum (makes tetrathiomolybdate) is to either take it on an empty stomach away from meals or take it with an apple which should in theory decrease H2S production (Chris Masterjohn talks about this in his sulfur protocol).
Ingredients for MoCo (listed in case English isn’t your native language and the slide is hard to read or if you have low vision and needed your phone to read the post):
- molybdenum (molybdate)
- radical SAMe (iron-sulfur cluster dependent)
- iron-sulfurs clusters (need B6 for formation)
- iron (need for heme component of SUOX, needed for iron sulfur cluster formation)
- B12, folate, and betaine (needed for methionine salvage pathway OR just adequate methionine intake)
- Magnesium (MPT synthase, and adding molybdenum via gephyrin)
- Zinc (stabilizes MPT synthase)
- Copper (tiny bit for Cnx1E)
SUOX is complete when MoCo and Heme are part of the enzyme. Heme synthesis requires:
- P5P (vitamin B6)
- Iron
- Zinc
- Radical SAM (Fe-S cluster dependent. SAM is made from methionine. Methionine salvage is dependent on B12, folate, and/or betaine. The enzyme that makes SAM, MAT, is inhibited by hydroxyl radicals that occur during oxidative stress – look into Bob Miller and Dr. Jill’s remedy using molecular hydrogen if you have high methionine levels of plasma amino acid indicating a block at MAT.)
- Riboflavin (vitamin B2) for FAD
Additional references….
kidney disease and sulfite retention…
https://pubmed.ncbi.nlm.nih.gov/10770971/
https://pubmed.ncbi.nlm.nih.gov/40058144/
https://pubmed.ncbi.nlm.nih.gov/14717909/
Adapted diagram for sulfite oxidase deficiency is from….
https://pmc.ncbi.nlm.nih.gov/articles/PMC9607355/
The cysteine and methionine restriction on the diagram are specifically for those with SUOX/MoCo deficiency. They are life saving measures, but unless you have this genetic disease, prolonged restriction of methionine or cysteine will only lead to worsening of your health (in my opinion, consult with your own provider). A methionine and cysteine restriction to the level needed for the genetic diseases of SUOX is not life sustaining.
Article on molybdenum exposure and chronic kidney disease https://www.sciencedirect.com/…/pii/S0147651324004767
Neutrophilic Contribution to Sulfite Toxicity © 2025 by Meredith Arthur, MS, RD, LD and Jenny Jones, PhD is licensed under CC BY-NC-ND 4.0
