Schimmelpilze / Mykotoxine: the pathway in the body · Biomarker & Laboratory Analysis

Schimmelpilze / Mykotoxine is part of the pathway “Mycotoxins”. This page shows the whole pathway; the station of Schimmelpilze / Mykotoxine is highlighted.

Where this laboratory value sits: Moulds — Aspergillus, Penicillium. Some moulds growing on grain, nuts, coffee or dried fruit produce substances they do not need for their own growth. Such substances are called mycotoxins. How much they form depends on moisture and warmth. Source 1

In brief

Mycotoxins are substances that some moulds form on foods, such as aflatoxin B1 and ochratoxin A. In the body, liver enzymes convert them; the products are bound to glutathione and leave with urine and stool. Otherwise an intermediate binds to genetic material.

The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

1. Moulds → Aflatoxin B1 Fungal enzymes Aflatoxin B1 is made by a long chain of fungal enzymes. It largely withstands heat and is absorbed into the blood in the small intestine. Only the liver makes it reactive. Source 1, 2↑ supplies Aflatoxin B1 itself barely reacts; it supplies the starting material that the liver converts into the reactive epoxide. established physiology Source 2, 3
   ⚖ When the balance tips

   too much — If more aflatoxin B1 reaches the liver, more epoxide forms, and more glutathione is used up in capturing it.

   too little — If little arrives, little epoxide forms, and glutathione captures most of it.

   established physiology · Source 2, 3

2. Aflatoxin B1 → Aflatoxin epoxide CYP1A2, CYP3A4 · NADPH, oxygen In the liver, the enzymes CYP1A2 and CYP3A4 attach an oxygen atom as a ring. This form is highly reactive and readily combines with proteins and genetic material. Lasting adducts form on the genetic material. Source 2, 3↓ depletes The epoxide combines with genetic material and proteins; lasting adducts form on the genetic material unless the cell repairs them. established physiology Source 2, 3
   ⚖ When the balance tips

   too much — If more epoxide forms than glutathione S-transferases can capture, more adducts form on the genetic material and on albumin in the blood.

   too little — If little epoxide forms, it is almost completely bound to glutathione before it reaches the genetic material.

   observed in studies · Source 3

3. Aflatoxin epoxide → Glutathione conjugate Glutathione S-transf. · glutathione (GSH) Glutathione S-transferases attach glutathione to the epoxide. This neutralises its reactive site and makes it water-soluble. This uses up glutathione. Source 3, 2↓ depletes Glutathione S-transferases attach glutathione to the epoxide and so withdraw it from the genetic material; glutathione is used up in the process. established physiology Source 3, 2
   ⚖ When the balance tips

   too much — If a lot of epoxide is captured, the glutathione pool of the liver cell falls until it makes new glutathione.

   too little — If little glutathione or little transferase activity is present, for example owing to gene forms, more epoxide stays free and binds to the genetic material.

   observed in studies · Source 3, 2

4. Glutathione conjugate → Mercapturic acid γ-GT, N-acetyltransf. Further enzymes shorten the conjugate and add an acetyl group. The resulting mercapturic acid leaves the body in the urine. It no longer binds to genetic material. Source 3↓ depletes As mercapturic acid, the captured epoxide leaves the body via the urine; it no longer binds to proteins or genetic material. established physiology Source 3
   ⚖ When the balance tips

   too much — If a lot of epoxide is captured, more mercapturic acid appears in the urine.

   too little — If little epoxide is captured, correspondingly little mercapturic acid forms.

   established physiology · Source 3

5. Ochratoxin A → Bound to albumin · albumin In the blood, ochratoxin A is almost entirely bound to albumin. It is excreted in bile, reabsorbed in the gut and therefore stays in circulation for a long time. It thus escapes the kidney's filter. Source 4↓ depletes Albumin holds on to ochratoxin A and so withdraws it from the kidney's filter; via the bile and renewed absorption in the gut it also stays in circulation for a long time. established physiology Source 4
   ⚖ When the balance tips

   too much — If there is a lot of ochratoxin A in the blood, the free share grows only once the binding sites of albumin are occupied; more of it then reaches kidney and liver.

   too little — If there is little in the blood, it is likewise almost entirely bound to albumin, and only a very small free part reaches the tissues.

   observed in studies · Source 4

6. Bound to albumin → Ochratoxin α Carboxypeptidase A Carboxypeptidase A from the pancreas and enzymes of gut bacteria cleave off the phenylalanine. What remains is ochratoxin α. Ochratoxin α is markedly less active. Source 4, 5↓ depletes Cleaving off the phenylalanine uses up ochratoxin A; ochratoxin α is markedly less active and is excreted more easily. established physiology Source 4, 5
   ⚖ When the balance tips

   too much — If a lot of ochratoxin A is cleaved, more ochratoxin α forms, which appears in urine and stool.

   too little — If little is cleaved, for example because little of it reaches the gut, more unchanged ochratoxin A remains in circulation.

   established physiology · Source 4, 5

7. Ochratoxin α → Excretion Ochratoxin α and a smaller share of unchanged ochratoxin A leave the body in urine and stool. Both can be detected there. This proceeds slowly. Source 5↓ depletes Urine and stool remove ochratoxin α and unchanged ochratoxin A from the body; because of the binding to albumin this proceeds slowly. established physiology Source 5
   ⚖ When the balance tips

   too much — If a lot is absorbed, the amount in urine and stool rises slowly and stays raised for weeks.

   too little — If little is absorbed, only a little is detectable in the urine; earlier intakes remain detectable for longer because of the slow excretion.

   established physiology · Source 5

Further stations

• Moulds — Aspergillus, Penicillium Some moulds growing on grain, nuts, coffee or dried fruit produce substances they do not need for their own growth. Such substances are called mycotoxins. How much they form depends on moisture and warmth. Source 1↑ supplies Moulds supply the mycotoxins that enter the body with contaminated foods; how much they form depends on moisture, warmth and storage. established physiology Source 1
  ⚖ When the balance tips

  too much — If moulds grow on foods for a long time in warmth and moisture, they form more mycotoxins, which largely survive heating.

  too little — If few moulds grow, few mycotoxins form; the body needs them for no task.

  established physiology · Source 1, 2

• Aflatoxin M1 — in urine and milk Part of the aflatoxin is given an OH group at a different position by CYP1A2. This aflatoxin M1 appears in urine and in milk. It is more water-soluble. Source 2↓ depletes The OH group makes aflatoxin more water-soluble; as aflatoxin M1 it leaves the body with the urine and passes into milk in mammals. established physiology Source 2
  ⚖ When the balance tips

  too much — If a lot of aflatoxin B1 is absorbed, aflatoxin M1 in urine and milk rises too.

  too little — If little is absorbed, only a little aflatoxin M1 appears.

  established physiology · Source 2

• Ochratoxin A — second common mycotoxin Ochratoxin A consists of a ring system and the amino acid phenylalanine. It too is produced by moulds on grain, coffee and wine. The gut absorbs it well. Source 4, 1↑ supplies Ochratoxin A reaches the gut with grain, coffee and wine and is absorbed well there; breakdown later starts at the phenylalanine part. established physiology Source 4, 1
  ⚖ When the balance tips

  too much — If more ochratoxin A arrives, it rises slowly in the blood and stays there for a long time, because albumin holds on to it.

  too little — If little arrives, the amount in the blood stays low but falls only slowly.

  established physiology · Source 4, 5

Cofactors in this pathway

• Glutathione — Glutathione S-transferases attach it to the aflatoxin epoxide and make it water-soluble; it is used up Source 3, 2In the ORY catalogue as a laboratory value: Glutathion (GSH)
• NADPH — Electron donor of the cytochrome P450 enzymes CYP1A2 and CYP3A4; without NADPH, no epoxide Source 2, 6
• Oxygen — Provides the oxygen atom that the P450 enzymes attach as an epoxide or OH group Source 2, 3
• Iron — Central atom in the haem of the cytochrome P450 enzymes and binds the oxygen there Source 6In the ORY catalogue as a laboratory value: Eisen
• Vitamin B2 (FAD, FMN) — Flavin cofactors of P450 reductase, which passes electrons from NADPH to the P450 enzymes Source 6
• Zinc — Metal in the active site of carboxypeptidase A, which separates ochratoxin A into two parts; without zinc, no cleavage Source 7, 4In the ORY catalogue as a laboratory value: Zink
• Acetyl-CoA — Donor of the acetyl group in the last step towards the mercapturic acid; it then passes into urine Source 3

Sources

1. Sweeney MJ, Dobson AD. Molecular biology of mycotoxin biosynthesis. FEMS Microbiol Lett 1999 · PubMed 10386364
2. Dohnal V, Wu Q, Kuča K. Metabolism of aflatoxins: key enzymes and interindividual as well as interspecies differences. Arch Toxicol 2014 · PubMed 25027283
3. Deng J, Zhao L, Zhang NY et al. Aflatoxin B(1) metabolism: Regulation by phase I and II metabolizing enzymes and chemoprotective agents. Mutat Res Rev Mutat Res 2018 · PubMed 30454686
4. Ringot D, Chango A, Schneider YJ, Larondelle Y. Toxicokinetics and toxicodynamics of ochratoxin A, an update. Chem Biol Interact 2006 · PubMed 16293235
5. Duarte SC, Pena A, Lino CM. Human ochratoxin a biomarkers--from exposure to effect. Crit Rev Toxicol 2011 · PubMed 21401326
6. Iyanagi T, Xia C, Kim JJ. NADPH-cytochrome P450 oxidoreductase: prototypic member of the diflavin reductase family. Arch Biochem Biophys 2012 · PubMed 22982532
7. Kim DH. Chemistry-based design of inhibitors for carboxypeptidase A. Curr Top Med Chem 2004 · PubMed 15320722

Whole pathway: Mycotoxins

Related pathways

• Glutathione — mercapturic acid
• 8-OHdG — Glutathion (GSH), Eisen
• Copper — Glutathion (GSH), Eisen
• Borrelia — Eisen, Zink
• Calprotectin — Eisen, Zink

As of 2026-09-16. Draft written by Claude to schema v2; sources checked in PubMed; expert approval pending
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