Myco-Metabolic Panel

Uncovering Mold & Mycotoxin Exposures and Their Toxic Health Impacts

The Myco-Metabolic Panel integrates the MycoTOX Profile with the Organic Acids Test (OAT), providing synergistic insights into toxic mold exposure and its negative impacts on critical bodily functions like energy production, detoxification, and nutrients.

This powerful combination equips practitioners with patient insights to develop personalized and comprehensive treatment plans for mold exposure, while directly addressing underlying health issues for improved outcomes.

Our high-complexity laboratory is committed to delivering accurate and reliable results in coordination with these top licensure programs:
Urine
Turnaround Time: 1-2 weeks

Turnaround times are estimates. Detailed order tracking is available in the MosaicDX Portal.

What Patients Might Benefit from the Myco- Metabolic Panel?

Symptoms and disease states associated with mycotoxin exposure, nutritional deficiencies, and other metabolic imbalances include the following:

  • ADHD
  • Allergic Conjunctivitis
  • Alzheimer's
  • Anxiety
  • Asthma
  • Autism Spectrum Disorders
  • Bronchitis
  • Cognitive Impairments
  • Chronic Fatigue
  • Depression
  • Diabetes
  • Digestive Issues
  • Fibromyalgia
  • Headaches
  • Infertility
  • Inflammatory Bowel Disease
  • Intestinal Permeability
  • Insulin Resistance
  • Lyme
  • Multiple Sclerosis
  • Neurological Disorders
  • Nutrient Deficiencies
  • Obesity
  • Schizophrenia
  • Shortness of Breath
  • Sinus/Nasal Congestion
  • Skin Conditions
  • Sneezing
  • Sore Throat
  • Tick-Born Infections

Details

Why Test?

Mold exposure is more common and can have significant health consequences than you may realize, but with MosaicDX’s testing, you can make informed decisions to improve your quality of life.

With the Myco-Metabolic Panel, you can take control of your health, uncovering mycotoxin exposure and its negative impacts on bodily processes critical to good health. This comprehensive test combination offers clarity and valuable insights for you and your practitioner to effectively address health challenges.

  • Evaluates the 11 most prevalent and harmful mycotoxins produced by molds.
  • Comprehensive view of 76 key markers tied to gut health, neurotransmitters, energy production, nutritional status, detoxification capability, and beyond.
  • Convenient, at-home sampling for everyone, without invasive procedures.
  • Utilizes cutting-edge technology to deliver highly specific and accurate test results.

What are Mycotoxins?

Mycotoxins are toxic metabolites produced by certain types of molds – microscopic filamentous fungi that are pervasive in both outdoor and indoor environments. Mycotoxins pose a serious public health threat, and can cause a number of chronic health problems, such as kidney damage, liver damage, immune suppression, and certain types of cancer. Mycotoxins have also been associated with a number of complex chronic conditions

What are Organic Acids?

Organic acids are products of the body’s metabolic pathways. Evaluation of these downstream metabolites from various metabolic pathways provides insight into key physiologic areas that can contribute to the development of chronic diseases and conditions:

• Gut Health
• Mitochondrial Dysfunction
• Neurotransmitter Status
• Detoxification
• Macronutrient Breakdown
• Nutritional Status

Analytes

The Myco-Metabolic Panel is composed of The Organic Acids Test and MycoTOX Profile, this panel provides a comprehensive view of the 76 key markers in the OAT along with 11 of the most prevalent and harmful mycotoxins produced by molds.

Organic Acids
Citramalic
5-Hydroxymethyl-2-furoic
3-Oxoglutaric
Furan-2,5-dicarboxylic
Furancarbonylglycine
Tartaric
Arabinose
Carboxycitric
Tricarballylic
2-Hydroxyphenylacetic
4-Hydroxyphenylacetic
4-Hydroxybenzoic
4-Hydroxyhippuric
Hippuric
3-Indoleacetic
Succinic
HPHPA (Clostridia marker)
4-Cresol (C. difficile)
DHPPA (beneficial bacteria)
Glyceric
Glycolic
Oxalic
Lactic
Pyruvic
2-Hydroxybutyric
Fumaric
Malic
2-Oxoglutaric
Aconitic
Citric
Homovanillic Acid (HVA)
Vanillmandelic Acid (VMA)
HVA/VMA Ratio
5-Hydroxyindoleacetic (5-HIAA)
Quinolinic
Kynurenic
HVA/DOPAC Ratio
Dihydroxyphenylacetic (DOPAC)
Uracil
Thymine
3-Hydroxybutyric
Acetoacetic
4-Hydroxybutyric
Ethylmalonic
Methylsuccinic
Adipic
Suberic
Sebacic
Methylmalonic (Vitamin B12)
Pyridoxic (Vitamin B6)
Pantothenic (Vitamin B5)
Glutaric (Vitamin B2-Riboflavin)
Ascorbic (Vitamin C)
3-Hydroxy-3-methylglutaric (Vitamin Q10-CoQ10)
N-Acetylcysteine (Glutathione precursor and chelating agent)
Methylcitric (Vitamin H-Biotin)
Pyroglutamic
Orotic
2-Hydroxyhippuric
2-Hydroxyisovaleric
2-Oxoisovaleric
3-Methyl-2-oxovaleric
2-Hydroxyisocaproic
2-Oxoisocaproic
2-Oxo-4-methiolbutyric
Mandelic
Phenyllactic
Phenylpyruvic
Homogentisic
4-Hydroxyphenyllactic
N-Acetylaspartic
Malonic
3-Methylglutaric
3-Hydroxyglutaric
3-Methylglutaconic
Phosphoric

 

MycoTOX Profile

An aflatoxin of concern, AFM1, is a hydroxylated metabolite of AFB1 and is secreted in the milk of both humans and animals.

Ochratoxin A (OTA) which is the most prevalent, toxic, and clinically relevant fungal toxin of this mycotoxin group. While it has been associated with numerous negative health impacts, the kidney has been noted to be its main target organ – and studies indicate its association with nephrotoxicity in humans and animals.

Tricothecenes are extremely potent inhibitors of protein synthesis and have been described to have wide-ranging negative systemic effects including immunotoxicity (immunosuppression), gastrointestinal toxicity, neurotoxicity, and dermatologic manifestations.

The main toxic effect of Zearalenone relates to its endocrine disruptive capabilities and as such, resultant negative reproductive effects in humans and animals.

Chaetomium globosum is frequently isolated from materials found in water-damaged buildings – and is often referred to as ‘black mold.’

ENB has been shown to have endocrine disrupting properties as well as the ability to cross the blood brain barrier in in vitro assays.

Airborne Aspergillus fungal spores are ubiquitous in many environments making potential exposure to gliotoxin common. Gliotoxins have been found on linoleum flooring and wallpaper in water damaged buildings, as well as silage and other animal food stocks.

MPA is used as an immunosuppressive drug for the prevention of transplant rejection in the form of sodium mycophenolate (Myfortic™, Novartis) and a pro-drug, mycophenolate mofetil (CellCept™, Roche) – and as a result, its levels may be elevated on diagnostics in patients using these pharmaceuticals.

Sterigmatocystin is a precursor of aflatoxin B1 in fungi capable of producing aflatoxins. Despite the similarity of chemical structure of these two mycotoxins, Sterigmatocystin has been noted to be a less potent carcinogen than Aflatoxin B1 (AFB1). It is classified as a Group 2B carcinogen by the International Agency for Research on Cancer.

Exposure to CTN has been linked to the development of nephropathy, which is caused by CTN’s ability to increase the permeability of mitochondrial membranes in the kidneys. Rat studies have demonstrated that CTN is carcinogenic. Furthermore, several studies have linked exposure to CTN with a suppression of the immune response.

Sample Reports

The Myco-Metabolic Panel provides individual test reports for the Organic Acids Test and MycoTOX Profile. These test reports offer valuable insights for practitioners seeking comprehensive understanding of their patients’ potential mold and mycotoxin exposure and health impacts.

Test Prep and Instructions

MosaicDX offers patient-friendly sample collection kits that make testing simple. Each kit includes:

  • Visual, step-by-step instructions for test preparation and sample collection.
  • Personalized shipping cards.
  • Pediatric collection bags if needed.

With just one easy urine sample collection, patients can confidently and accurately collect their samples.

Patient Resources

Explore our assets designed to help practitioners educate and support patients about mold exposure and the MosaicDX Myco-Metabolic Panel. These resources enhance patient understanding, decision-making, and overall health journey:

  • Patient Brochure: A comprehensive guide that explains the importance of mycotoxin testing and how the Myco-Metabolic Panel can benefit patients.

Frequently Asked Questions

Acremonium sp.
Aureobasidium
F. graminearum
Phoma sp.
Alternaria
Chaetomium
F. incarnatum
Rhodotorula
A. flavipes
Cladosporium
F. moniliforme
Scopulariopsis
Aspergillus flavus
Cunninghamella
F. solani
Stachybotrys
A. fumigatus
Cylindrocarpon
F. verticillioides
S. chartarum
A. niger
Dendrodochium
Myrothecium roridum
Trichoderma viride
A. ochraceus
Exophiala
M. verrucaria
Ulocaldium
A. parasiticus
Fusarium avenaceum
Penicillium carbonarius
Verticillium
A. sydowii
F. cerealis
P. nordicum
 
A. versicolor
F. clumonrum
P. stoloniferum
 
A. viridictum
F. equiseti
P. verrucosum
 

Mycotoxins are low molecular weight, secondary metabolites of fungal (mold) compounds which are increasingly recognized as a global health threat given their role in precipitating both acute and chronic adverse health outcomes.

  • Common fungi sources of mycotoxins include species such as Fusarium, Aspergillus, Penicillium, Alternaria, and Claviceps. To date nearly 400 potentially toxic mycotoxins produced by more than 100 fungi species have been identified, although research has focused on the most toxigenic in the public health, veterinary, and agricultural realms.
  • Exposure to mycotoxins may occur through a variety of routes such as inhalation, ingestion, and dermal contact from airborne mold spores, food contamination, and water-damaged building environments.
  • Susceptibility to mycotoxins is influenced by a patient’s age, sex, presence of other underlying diseases and/or exposures, nutritional status, and length of exposure.
  • While mycotoxin toxicity may present as an acute state marked by rapid onset with potential life-threatening illness, most of the negative health impacts observed in the developed (Western) world are due to chronic, low-dose exposures. These long-term exposures have been associated with a variety of systemic effects (mycotoxicoses) in both humans and animals – and most commonly manifest as nephrotoxicity, hepatotoxicity, immunosuppression, carcinogenicity, and teratogenicity.

Acute mycotoxin effects are characterized by rapid onset and toxic response in the target organ most affected by the offending agent.

As an example, consumption of large doses of aflatoxins can result in life-threatening, acute poisoning (aflatoxicosis) due to detrimental impact on the liver.

Acute mycotoxin effects are more frequently observed in economically poorer global areas where sub-optimal food cultivation, harvesting, and storage practices are common; malnutrition is a constant presence; and a poor regulatory environment exists.

Chronic mycotoxin effects are characterized by lower exposure doses over longer periods of time – and symptoms attributed to chronic mycotoxin exposure are wide-ranging in their impact on an array of physiologic systems and functions.

As expected with the clinical standard of care, results from any diagnostic test – including those of the MycoTOX profile – should always be considered within the context of each patient’s unique history and clinical presentation. Given that, the information provided on potential therapeutic support for patients with mycotoxin exposure is provided for educational purposes only.

In general, practitioners working with patients with mold and/or mycotoxin exposure focus on three key clinical areas:

  • Addressing Mycotoxin Exposure
  • Supporting the Foundations of Health
  • Judicious Use of Supplements and/or Pharmaceuticals

Address Mycotoxin Exposure

First-Line Remediation/Defense: Removal/Avoidance of the Offending Agent

The first line of defense against mycotoxin exposure – as with any toxin or toxicant – is identification and remediation of the source of exposure with the goal of preventive exposure strategies going forward.

Support the Foundations of Health

Focus on Critical Lifestyle and Physiologic Elimination Functions

Optimize Elimination

  • Gut Function
    • Support phase 1 and 2 liver detoxification
    • Provide treatments aimed at abnormalities in gut microflora and functioning; probiotics, treating infections and avoiding food allergens.
  • Hydration
    • Support elimination/excretion via the kidney
  • Sweating (movement, saunas, etc.)
    • Support elimination/excretion via dermal routes

Optimize Nutrition

  • Focus on a whole foods diet to maximize fiber and nutrient density

Judicious Use of Supplements and/or Pharmaceuticals

Personalization of the therapeutic journey is key as each patient’s presentation and history is unique.

Clinicians working with patients with mycotoxin exposure and/or symptoms may consider working with the following:

  • Foundational support
    • Multivitamin/mineral, probiotic (acidophilus + bifidus strains), antioxidants, and essential fatty acids
  • Detoxification support
    • NAC, glutathione
  • Binders
  • Anti-fungals
    • These pharmaceuticals should be assessed for use on a clinical case-by-case basis ONLY given challenges related to their potential, significant side-effects.

Application of the creatinine correction is a technique to reduce excessive variation in urine test results due to differences in fluid intake prior to collection of urine samples. Dividing the amount of a substance in urine by creatinine corrects for cases in which the patient may be dehydrated or excessively hydrated. In the case of dehydration, failure to perform creatinine correction might indicate that the person has toxic levels of mycotoxins when, in fact, the values are high just due to dehydration. With creatinine correction, such an error is avoided.

Together they provide necessary information about mycotoxin burden, nutritional need, mitochondrial function and detox capability in one, easy, urine sample.

Mold OvergrowthOrganic Acids Test:
GI tract invasive growth of metabolites of mycotoxins – aspergillus and fusarium
MycoTOX Profile:
Toxicity can happen independently or simultaneously with growth and colonization
Mycotoxin Potential ExposureX – 2 metabolites metabolite indicators aspergillus and fusariumX – 20 tests
Mycotoxin Toxic BurdenX
Mycotoxin Specific InfoX
Nutritional NeedX
Mitochondrial functionX
Detox capabilityX

Mycotoxins are toxic metabolites produced by certain types of molds – microscopic filamentous fungi that are pervasive in both outdoor and indoor environments. Common routes of exposure to these low-molecular weight compounds include inhalation, dermal contact, and ingestion via common contaminated food sources (corn, cereals, ground and tree nuts, spices, dried fruits, apples, coffee, meat, milk, and eggs).

Attention is increasingly being given to indoor air pollution resulting not only from the influx of irritant agents (spores, pollens) from the outdoor environment, but also from the growth of molds, fungi and bacteria on almost all indoor materials (drywall, paint, wallpaper, carpeting, etc.) when excessive moisture is present in high humidity geographic areas or water-damaged buildings. The growth of these biological agents in damp environments leads to the production of spores, cells, fragments and volatile organic compounds which have been linked to a wide range of health hazards, including exacerbation of asthma as well as allergic and infectious respiratory diseases infections.

Adverse health effects may be acute or chronic in nature, and the degree of impact can vary depending on the age, sex, genetics, and underlying health status of the exposed individual, as well as the duration and dose magnitude of the offending substance and their synergistic effects with other mycotoxins.

Because mycotoxins are byproducts of mold metabolism, clinicians assessing symptomatic patients with known mold exposure – or with an environmental history concerning for mold exposure – will also need to consider the concomitant presence of mycotoxins and their potential negative health impact as well.

The MycoTOX profile is designed to accurately detect mycotoxins produced by various toxic molds. However, it does not indicate the location or source of the mold, whether it is in your home, workplace, or elsewhere. Mycotoxin exposure can come from both dietary and environmental sources. Spoiled food is a dietary source, while living or working in water-damaged buildings, airborne or physical contact with outdoor molds, and airborne dust in buildings containing mold spores are environmental sources. 

Currently, there are no established guidelines for retesting mycotoxins after intervention. However, some healthcare providers recommend retesting at 3-6 months, 12 months, and annually as part of a wellness screen. Individuals with severe mold and mycotoxin-related illnesses may require more frequent testing. 

Patients with high toxic levels are at greater risk of concomitant exposure from all toxins. For patients with specific exposure history, practitioners can order individual panels or combine profiles to identify or more rapidly reduce or remove multiple sources of toxin exposure:

These test can all be done from one urine sample:

The OAT or MOAT is typically not affected by antibiotics or antifungal medications, unless they contain certain fruits like apples, grapes, pears, or cranberries. However, it’s important for both the patient and practitioner to consider the purpose of the test when deciding whether to avoid these medications. For instance, if the practitioner is interested in evaluating the effectiveness of a particular therapy, it may be acceptable for the patient to continue taking the medication during the test. On the other hand, if the patient wants to determine their metabolic condition without any influence from medication, it’s advisable to discontinue the antibiotics or antifungals for a period of 1-2 weeks before the test. 

Use of organic acids to provide insight into functional metabolic imbalances has evolved from historic diagnostic testing to investigate inborn errors of metabolism (IEM).

While the OAT is not designed specifically to diagnose classically defined IEMs, persistent marked elevations in OAs noted on the profile may indicate an undiagnosed underlying metabolic pathway defect. As such, further clinical investigation via an individual patient’s clinical presentation and the results of complementary laboratory tests may be warranted to guide more specific testing.

IEM are a class of inborn errors of metabolic pathways that are marked by accumulation (and usually toxic) organic acid metabolites in blood (i.e., organic acidemias) and increased excretion of organic acids in urine (i.e., organic acidurias). While individual IEMs are rare that typically become apparent clinically during the newborn period or early infancy, though milder – and even asymptomatic – forms may emerge in adolescence and adulthood.

Because of the life-threatening metabolic disturbances (acidosis and ketosis) that are associated with IEMs, an entire field of preconception and postnatal screening has arisen. Current newborn screening includes assessment of 34 core conditions which allows for early treatment intervention should a positive finding result.

Almost all organic acids used for human testing are measured by a combination of gas or liquid chromatography linked with mass spectrometry. Organic acids are most commonly analyzed in urine because they are not extensively reabsorbed in the kidney tubules after glomerular filtration. Thus, organic acids in urine are often present at 100 times their concentration in the blood serum and thus are more readily detected in urine. This is why organic acids are rarely tested in blood or serum. The number of organic acids found in urine is enormous. Over 1,000 different organic acids have been detected in urine since this kind of testing started.

•Organic acidic products of cellular metabolism that are excreted in urine (in mammals)

oProduced by living organisms including humans, bacteria, and fungi

oEvaluation of these downstream products of metabolic pathways provides insight into potential nutrient deficiencies, inflammation, toxicity, and other imbalances that could be contributing to clinical complaints

•Origins of Organic Acid Testing

oTo rule out rare Inborn Errors of Metabolism (IEM)- usually in infancy

oElevations of these organic acids (OA) reflect dysfunction in specific metabolic pathways

§Accumulation of these toxic metabolites can by life-threatening

§Symptoms observed in the newborn period include poor feeding and weight gain; nausea and vomiting; neuromuscular issues (e.g., poor tone, seizures); and susceptibility to infection

Use of OAs have evolved from investigating IEM to providing insight into functional metabolic imbalances.

The following tests provide valuable insight into metabolism, nutrient needs, food sensitivities and metal toxicity.

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Clinical References

MYCOTOXINS

  • Janik E, Niemcewicz M, Ceremuga M, Stela M, Saluk-Bijak J, Siadkowski A, et al. Molecular Aspects of Mycotoxins-A Serious Problem for Human Health. Int J Mol Sci. 2020;21(21).
  • Bennett JW, Klich M. Mycotoxins. Clin Microbiol Rev. 2003;16(3):497-516.
  • AFLATOXIN M1 (AFM1)

  • Cinar A, Onbaşı E. Mycotoxins: The Hidden Danger in Foods. IntechOpen; 2020.
  • S G, Kitya D, Lubega A, Ogwal-Okeng J, W W, B D. Review of the Biological and Health Effects of Aflatoxins on Body Organs and Body Systems. InTech; 2013.
  • Fallah A, Rahnama MR, Jafari T, et al. Seasonal variation of aflatoxin M1 contamination in industrial and traditional Iranian dairy products. Food Control 2011;22(10):1653-6.
  • Polizzi V, Delmulle B, Adams A, Moretti A, Susca A, Picco AM, et al. JEM Spotlight: Fungi, mycotoxins and microbial volatile organic compounds in mouldy interiors from water-damaged buildings. J Environ Monit. 2009;11(10):1849-58.
  • Coulombe RA. The Toxicology of Aflatoxins: Human Health, Veterinary and Agricultural Significance. D.L. Eaton aJDG, editor: Academic Press; 1994.
  • Dhakal A, Hashmi MF, Sbar E. Aflatoxin Toxicity.  StatPearls. Treasure Island (FL): StatPearls Publishing Copyright © 2022, StatPearls Publishing LLC.; 2022.
  • Pickova D, Ostry V, Toman J, Malir F. Aflatoxins: History, Significant Milestones, Recent Data on their Toxicity and Ways to Mitigation. Toxins. 2021;13(6):399.
  • Bennett JW, Klich M. Mycotoxins. Clin Microbiol Rev. 2003;16(3):497-516.
  • Janik E, Niemcewicz M, Ceremuga M, Stela M, Saluk-Bijak J, Siadkowski A, et al. Molecular Aspects of Mycotoxins-A Serious Problem for Human Health. Int J Mol Sci. 2020;21(21).
  • Kolf-Clauw M, Sassahara M, Lucioli J, Rubira-Gerez J, Alassane-Kpembi I, Lyazhri F, et al. The emerging mycotoxin, enniatin B1, down-modulates the gastrointestinal toxicity of T-2 toxin in vitro on intestinal epithelial cells and ex vivo on intestinal explants. Arch Toxicol. 2013;87(12):2233-41.
  • Liew WP, Mohd-Redzwan S. Mycotoxin: Its Impact on Gut Health and Microbiota. Front Cell Infect Microbiol. 2018;8:60.
  • Alizadeh A, Braber S, Akbari P, Garssen J, Fink-Gremmels J. Deoxynivalenol Impairs Weight Gain and Affects Markers of Gut Health after Low-Dose, Short-Term Exposure of Growing Pigs. Toxins (Basel). 2015;7(6):2071-95.
  • Osselaere A, Santos R, Hautekiet V, De Backer P, Chiers K, Ducatelle R, et al. Deoxynivalenol impairs hepatic and intestinal gene expression of selected oxidative stress, tight junction and inflammation proteins in broiler chickens, but addition of an adsorbing agent shifts the effects to the distal parts of the small intestine. PLoS One. 2013;8(7):e69014.
  • Mehrzad J, Fazel F, Pouyamehr N, Hosseinkhani S, Dehghani H. Naturally Occurring Level of Aflatoxin B(1) Injures Human, Canine and Bovine Leukocytes Through ATP Depletion and Caspase Activation. Int J Toxicol. 2020;39(1):30-8.
  • Ubagai T, Tansho S, Ito T, Ono Y. Influences of aflatoxin B1 on reactive oxygen species generation and chemotaxis of human polymorphonuclear leukocytes. Toxicol In Vitro. 2008;22(4):1115-
  • CHAETOGLOBOSIN A (CHA)

  • Fogle MR, Douglas DR, Jumper CA, Straus DC. Growth and mycotoxin production by Chaetomium globosum. Mycopathologia. 2007;164(1):49-56.
  • Salo JM, Kedves O, Mikkola R, Kredics L, Andersson MA, Kurnitski J, et al. Detection of Chaetomium globosum, Ch. cochliodes and Ch. rectangulare during the Diversity Tracking of Mycotoxin-Producing Chaetomium-like Isolates Obtained in Buildings in Finland. Toxins. 2020;12(7):443.
  • Li H, Xiao J, Gao YQ, Tang JJ, Zhang AL, Gao JM. Chaetoglobosins from Chaetomium globosum, an endophytic fungus in Ginkgo biloba, and their phytotoxic and cytotoxic activities. J Agric Food Chem. 2014;62(17):3734-41.
  • Zhang G, Zhang Y, Qin J, Qu X, Liu J, Li X, et al. Antifungal Metabolites Produced by Chaetomium globosum No.04, an Endophytic Fungus Isolated from Ginkgo biloba. Indian J Microbiol. 2013;53(2):175-80.
  • Chen J, Zhang W, Guo Q, Yu W, Zhang Y, He B. Bioactivities and Future Perspectives of Chaetoglobosins. Evidence-Based Complementary and Alternative Medicine. 2020;2020:1-10.
  • Knudsen PB, Hanna B, Ohl S, Sellner L, Zenz T, Dohner H, et al. Chaetoglobosin A preferentially induces apoptosis in chronic lymphocytic leukemia cells by targeting the cytoskeleton. Leukemia. 2014;28(6):1289-98.
  • Shinohara C, Chikanishi T, Nakashima S, Hashimoto A, Hamanaka A, Endo A, et al. Enhancement of fibrinolytic activity of vascular endothelial cells by chaetoglobosin A, crinipellin B, geodin and triticone B. J Antibiot (Tokyo). 2000;53(3):262-8.
  • CITRININ (Cihydrocitrinone DHC)

  • Jh D. The Occurrence, Properties and Significance of Citrinin Mycotoxin. Journal of Plant Pathology & Microbiology. 2015;6(11).
  • Xu B-j, Jia X-q, Gu L-j, Sung C-k. Review on the qualitative and quantitative analysis of the mycotoxin citrinin. Food Control. 2006;17(4):271-85.
  • Eisenbrand PDG. Toxicological evaluation of red mould rice: An update. 2013.
  • Liao C-D, Chen Y-C, Lin H-Y, Chiueh L-C, Shih DY-C. Incidence of citrinin in red yeast rice and various commercial Monascus products in Taiwan from 2009 to 2012. Food Control. 2014;38:178-83.
  • J.A.L. Kiebooms BH, , C. Thiry. A quantitative UHPLC-MS/MS method for citrinin and ochratoxin A detection in food, feed and red yeast rice food supplements. World Mycotoxin Journal. 2016.
  • Viegas S, Assunção R, Nunes C, Osteresch B, Twarużek M, Kosicki R, et al. Exposure Assessment to Mycotoxins in a Portuguese Fresh Bread Dough Company by Using a Multi-Biomarker Approach. Toxins (Basel). 2018;10(9).
  • Martins ML, Gimeno A, Martins HM, Bernardo F. Co-occurrence of patulin and citrinin in Portuguese apples with rotten spots. Food Addit Contam. 2002;19(6):568-74.
  • Lhotská I, Šatínský D, Havlíková L, Solich P. A fully automated and fast method using direct sample injection combined with fused-core column on-line SPE-HPLC for determination of ochratoxin A and citrinin in lager beers. Anal Bioanal Chem. 2016;408(12):3319-29.
  • Bailly JD, Querin A, Le Bars-Bailly S, Benard G, Guerre P. Citrinin production and stability in cheese. J Food Prot. 2002;65(8):1317-21.
  • Zhang H, Ahima J, Yang Q, Zhao L, Zhang X, Zheng X. A review on citrinin: Its occurrence, risk implications, analytical techniques, biosynthesis, physiochemical properties and control. Food Res Int. 2021;141:110075.
  • Kamle M, Mahato DK, Gupta A, Pandhi S, Sharma N, Sharma B, et al. Citrinin Mycotoxin Contamination in Food and Feed: Impact on Agriculture, Human Health, and Detection and Management Strategies. Toxins. 2022;14(2):85.
  • Bouslimi A, Ouannes Z, Golli EE, Bouaziz C, Hassen W, Bacha H. Cytotoxicity and oxidative damage in kidney cells exposed to the mycotoxins ochratoxin a and citrinin: individual and combined effects. Toxicol Mech Methods. 2008;18(4):341-9.
  • Ostry V, Malir F, Ruprich J. Producers and important dietary sources of ochratoxin A and citrinin.Toxins (Basel). 2013;5(9):1574-86.
  • Bennett JW, Klich M. Mycotoxins. Clin Microbiol Rev. 2003;16(3):497-516.
  • ENNIATIN B (ENB)

  • Prosperini A, Berrada H, Ruiz MJ, Caloni F, Coccini T, Spicer LJ, et al. A Review of the Mycotoxin Enniatin B. Front Public Health. 2017;5:304.
  • Carl Batt PP. Encyclopedia of Food Microbiology (Second Edition): Academic Press; 2014.
  • Korkalainen M, Täubel M, Naarala J, Kirjavainen P, Koistinen A, Hyvärinen A, et al. Synergistic proinflammatory interactions of microbial toxins and structural components characteristic to moisture-damaged buildings. Indoor Air. 2017;27(1):13-23.
  • Bertero A, Moretti A, Spicer LJ, Caloni F. Fusarium Molds and Mycotoxins: Potential Species-Specific Effects. Toxins (Basel). 2018;10(6).
  • Pérez-Fuentes N, Alvariño R, Alfonso A, González-Jartín J, Gegunde S, Vieytes MR, et al.Enniatins A1 and B1 alter calcium homeostasis of neuronal cells leading to apoptotic death. Food Chem Toxicol. 2022;168:113361.
  • Pérez-Fuentes N, Alvariño R, Alfonso A, González-Jartín J, Gegunde S, Vieytes MR, et al. Single and combined effects of regulated and emerging mycotoxins on viability and mitochondrial function of SH-SY5Y cells. Food Chem Toxicol. 2021;154:112308.
  • Alonso-Garrido M, Escrivá L, Manyes L, Font G. Enniatin B induces expression changes in the electron transport chain pathway related genes in lymphoblastic T-cell line. Food Chem Toxicol. 2018;121:437-43.
  • Jonsson M, Jestoi M, Anthoni M, Welling A, Loivamaa I, Hallikainen V, et al. Fusarium mycotoxin enniatin B: Cytotoxic effects and changes in gene expression profile. Toxicol In Vitro. 2016;34:309-20.
  • Krug I, Behrens M, Esselen M, Humpf HU. Transport of enniatin B and enniatin B1 across the blood-brain barrier and hints for neurotoxic effects in cerebral cells. PLoS One. 2018;13(5):e0197406.
  • Chiminelli I, Spicer LJ, Maylem ERS, Caloni F. Emerging mycotoxins and reproductive effects in animals: A short review. J Appl Toxicol. 2022;42(12):1901-9.
  • Kalayou S, Ndossi D, Frizzell C, Groseth PK, Connolly L, Sørlie M, et al. An investigation of the endocrine disrupting potential of enniatin B using in vitro bioassays. Toxicol Lett. 2015;233(2):84-94.
  • Alonso-Garrido M, Tedeschi P, Maietti A, Font G, Marchetti N, Manyes L. Mitochondrial transcriptional study of the effect of aflatoxins, enniatins and carotenoids in vitro in a blood brain barrier model. Food Chem Toxicol. 2020;137:111077.
  • Meca G, Sospedra I, Valero MA, Mañes J, Font G, Ruiz MJ. Antibacterial activity of the enniatin B, produced by Fusarium tricinctum in liquid culture, and cytotoxic effects on Caco-2 cells. Toxicol Mech Methods. 2011;21(7):503-12.
  • GLIOTOXIN (GTX)

  • Nguyen VT, Lee JS, Qian ZJ, Li YX, Kim KN, Heo SJ, et al. Gliotoxin isolated from marine fungus Aspergillus sp. induces apoptosis of human cervical cancer and chondrosarcoma cells. Mar Drugs. 2013;12(1):69-87.
  • Gliotoxin (T3D3604)  [2-22-23]. Available from: http://www.t3db.ca/toxins/T3D3604.
  • Keller LA, Keller KM, Monge MP, Pereyra CM, Alonso VA, Cavaglieri LR, et al. Gliotoxin contamination in and pre- and postfermented corn, sorghum and wet brewer’s grains silage in Sao Paulo and Rio de Janeiro State, Brazil. J Appl Microbiol. 2012;112(5):865-73.
  • Bloom E, Nyman E, Must A, Pehrson C, Larsson L. Molds and mycotoxins in indoor environments–a survey in water-damaged buildings. J Occup Environ Hyg. 2009;6(11):671-8.
  • Tachampa K, Takeda M, Khamdang S, Noshiro-Kofuji R, Tsuda M, Jariyawat S, et al. Interactions of organic anion transporters and organic cation transporters with mycotoxins. J Pharmacol Sci. 2008;106(3):435-43.
  • Brown R, Priest E, Naglik JR, Richardson JP. Fungal Toxins and Host Immune Responses.Frontiers in Microbiology. 2021;12.
  • Waring P, Beaver J. Gliotoxin and related epipolythiodioxopiperazines. Gen Pharmacol. 1996;27(8):1311-6.
  • Gardiner DM, Waring P, Howlett BJ. The epipolythiodioxopiperazine (ETP) class of fungal toxins: distribution, mode of action, functions and biosynthesis. Microbiology (Reading). 2005;151(Pt 4):1021-32.
  • Niide O, Suzuki Y, Yoshimaru T, Inoue T, Takayama T, Ra C. Fungal metabolite gliotoxin blocks mast cell activation by a calcium- and superoxide-dependent mechanism: implications for immunosuppressive activities. Clin Immunol. 2006;118(1):108-16.
  • Fujihara S, Ward C, Dransfield I, Hay RT, Uings IJ, Hayes B, et al. Inhibition of nuclear factor-kappaB activation un-masks the ability of TNF-alpha to induce human eosinophil apoptosis. Eur J Immunol. 2002;32(2):457-66.
  • Suen YK, Fung KP, Lee CY, Kong SK. Gliotoxin induces apoptosis in cultured macrophages via production of reactive oxygen species and cytochrome c release without mitochondrial depolarization. Free Radic Res. 2001;35(1):1-10.
  • Gayathri L, Akbarsha MA, Ruckmani K. In vitro study on aspects of molecular mechanisms underlying invasive aspergillosis caused by gliotoxin and fumagillin, alone and in combination.Scientific Reports. 2020;10(1).
  • Fragaki G, Stefanaki I, Dais P, Mikros E. Conformational properties of the macrocyclic trichothecene mycotoxin verrucarin A in solution. Magn Reson Chem. 2008;46(12):1102-11.
  • Kwon-Chung KJ, Sugui JA. What do we know about the role of gliotoxin in the pathobiology of Aspergillus fumigatus? Med Mycol. 2009;47 Suppl 1(Suppl 1):S97-103.
  • N.J. Mitchell AGM-C, A. Romoser, T.D. Phillips, A.W. Hayes. Mycotoxin: Elsevier; 2014.
  • MYCOPHENOLIC ACID (MPA)

  • Vaali K, Tuomela M, Mannerström M, Heinonen T, Tuuminen T. Toxic Indoor Air Is a Potential Risk of Causing Immuno Suppression and Morbidity-A Pilot Study. J Fungi (Basel). 2022;8(2).
  • Mahmoudian F, Sharifirad A, Yakhchali B, Ansari S, Fatemi SS. Production of Mycophenolic Acid by a Newly Isolated Indigenous Penicillium glabrum. Curr Microbiol. 2021;78(6):2420-8.
  • Allison AC. Mechanisms of action of mycophenolate mofetil. Lupus. 2005;14 Suppl 1:s2-8.
  • Gillot G, Jany JL, Dominguez-Santos R, Poirier E, Debaets S, Hidalgo PI, et al. Genetic basis for mycophenolic acid production and strain-dependent production variability in Penicillium roqueforti.Food Microbiol. 2017;62:239-50.
  • Dietrich R, Märtlbauer E. Development and application of monoclonal antibodies against the mycotoxin mycophenolic acid. Mycotoxin Res. 2015;31(4):185-90.
  • Baum B, Mohr A, Pfaffl M, Bauer J, Hewicker-Trautwein M. Morphological findings in lymphatic tissues of sheep following oral application of the immunosuppressive mycotoxin mycophenolic acid. Mycopathologia. 2005;160(2):167-75.
  • OCHRATOXIN A (OTA)

  • Bui-Klimke TR, Wu F. Ochratoxin A and human health risk: a review of the evidence. Crit Rev Food Sci Nutr. 2015;55(13):1860-9.
  • Doi K, Uetsuka K. Mechanisms of mycotoxin-induced neurotoxicity through oxidative stress-associated pathways. Int J Mol Sci. 2011;12(8):5213-37.
  • Baudrimont I, Ahouandjivo R, Creppy EE. Prevention of lipid peroxidation induced by ochratoxin A in Vero cells in culture by several agents. Chem Biol Interact. 1997;104(1):29-40.
  • Sava V, Velasquez A, Song S, Sanchez-Ramos J. Adult hippocampal neural stem/progenitor cells in vitro are vulnerable to the mycotoxin ochratoxin-A. Toxicol Sci. 2007;98(1):187-97.
  • Omotayo OP, Omotayo AO, Mwanza M, Babalola OO. Prevalence of Mycotoxins and Their Consequences on Human Health. Toxicol Res. 2019;35(1):1-7.
  • Wang H, Chen Y, Zhai N, Chen X, Gan F, Li H, et al. Ochratoxin A-Induced Apoptosis of IPEC-J2 Cells through ROS-Mediated Mitochondrial Permeability Transition Pore Opening Pathway. J Agric Food Chem. 2017;65(48):10630-7.
  • Peng M, Liu J, Liang Z. Probiotic Bacillus subtilis CW14 reduces disruption of the epithelial barrier and toxicity of ochratoxin A to Caco-2 cells. Food Chem Toxicol. 2019;126:25-33.
  • Yang X, Gao Y, Yan Q, Bao X, Zhao S, Wang J, et al. Transcriptome Analysis of Ochratoxin A-Induced Apoptosis in Differentiated Caco-2 Cells. Toxins (Basel). 2019;12(1).
  • Hope JH, Hope BE. A review of the diagnosis and treatment of Ochratoxin A inhalational exposure associated with human illness and kidney disease including focal segmental glomerulosclerosis. J Environ Public Health. 2012;2012:835059.
  • Petzinger E, Ziegler K. Ochratoxin A from a toxicological perspective. J Vet Pharmacol Ther. 2000;23(2):91-8.
  • Wu Q, Dohnal V, Huang L, Kuča K, Wang X, Chen G, et al. Metabolic pathways of ochratoxin A.Curr Drug Metab. 2011;12(1):1-10.
  • Sorrenti V, Di Giacomo C, Acquaviva R, Barbagallo I, Bognanno M, Galvano F. Toxicity of Ochratoxin A and Its Modulation by Antioxidants: A Review. Toxins. 2013;5(10):1742-66.
  • Polizzi V, Delmulle B, Adams A, Moretti A, Susca A, Picco AM, et al. JEM Spotlight: Fungi, mycotoxins and microbial volatile organic compounds in mouldy interiors from water-damaged buildings. J Environ Monit. 2009;11(10):1849-58.
  • Bennett JW, Klich M. Mycotoxins. Clin Microbiol Rev. 2003;16(3):497-516.
  • Cinar A, Onbaşı E. Mycotoxins: The Hidden Danger in Foods. IntechOpen; 2020.
  • STERIGMATOCYSTIN (STC)

  • Díaz Nieto CH, Granero AM, Zon MA, Fernández H. Sterigmatocystin: A mycotoxin to be seriously considered. Food Chem Toxicol. 2018;118:460-70.
  • Tuomi T, Reijula K, Johnsson T, Hemminki K, Hintikka E-L, Lindroos O, et al. Mycotoxins in Crude Building Materials from Water-Damaged Buildings. Applied and Environmental Microbiology. 2000;66(5):1899-904.
  • Bing Huei Chen BSI. Nanomaterial-based sensors for mycotoxin analysis in food. Novel appraoches of nanotechnology in foods. Fu Jen University, Department of Food Science2016. 387 – 423 p.
  • Polizzi V, Delmulle B, Adams A, Moretti A, Susca A, Picco AM, et al. JEM Spotlight: Fungi, mycotoxins and microbial volatile organic compounds in mouldy interiors from water-damaged buildings. J Environ Monit. 2009;11(10):1849-58.
  • Sterigmatocystin (T3D3663): T3DB;  [Available from: http://www.t3db.ca/toxins/T3D3663.
  • Essigmann JM, Barker LJ, Fowler KW, Francisco MA, Reinhold VN, Wogan GN. Sterigmatocystin-DNA interactions: identification of a major adduct formed after metabolic activation in vitro. Proc Natl Acad Sci U S A. 1979;76(1):179-83.
  • Sivakumar V, Thanislass J, Niranjali S, Devaraj H. Lipid peroxidation as a possible secondary mechanism of sterigmatocystin toxicity. Hum Exp Toxicol. 2001;20(8):398-403.
  • Stark AA. Mutagenicity and carcinogenicity of mycotoxins: DNA binding as a possible mode of action. Annu Rev Microbiol. 1980;34:235-62.
  • Zingales V, Fernández-Franzón M, Ruiz MJ. Sterigmatocystin: Occurrence, toxicity and molecular mechanisms of action – A review. Food Chem Toxicol. 2020;146:111802.
  • Gao W, Jiang L, Ge L, Chen M, Geng C, Yang G, et al. Sterigmatocystin-induced oxidative DNA damage in human liver-derived cell line through lysosomal damage. Toxicol In Vitro. 2015;29(1):1-7.
  • Wang JS, Groopman JD. DNA damage by mycotoxins. Mutat Res. 1999;424(1-2):167-81.
  • Misumi J. The mechanisms of gastric cancer development produced by the combination of Helicobacter pylori with Sterigmatocystin, a mycotoxin. Nihon Rinsho. 2004;62(7):1377-86.
  • Reijula K, Tuomi T. Mycotoxins of aspergilli: exposure and health effects. Front Biosci. 2003;8:s232-5.
  • Cao W, Wang H, Zhang X, Sun X. Mutation of p53 and Ki-ras gene in human fetal lung fibroblast cells in vitro by sterigmatocystin. Wei Sheng Yan Jiu. 2000;29(3):175-7.
  • Viegas C, Nurme J, Piecková E, Viegas S. Sterigmatocystin in foodstuffs and feed: aspects to consider. Mycology. 2020;11(2):91-104.
  • Chu FS. Encyclopedia of Food Sciences and Nutrition (Second Edition). Caballero B, editor: Academic Press; 2003.
  • Tabata S. Yeasts and Molds | Mycotoxins: Aflatoxins and Related Compounds. Fuquay JW, editor. Academic Press2011.
  • TRICOTHECENES

  • Doi K, Uetsuka K. Mechanisms of mycotoxin-induced neurotoxicity through oxidative stress-associated pathways. Int J Mol Sci. 2011;12(8):5213-37.
  • Ráduly Z, Price RG, Dockrell MEC, Csernoch L, Pócsi I. Urinary Biomarkers of Mycotoxin Induced Nephrotoxicity—Current Status and Expected Future Trends. Toxins. 2021;13(12).
  • Nathanail AV, Varga E, Meng-Reiterer J, Bueschl C, Michlmayr H, Malachova A, et al. Metabolism of the Fusarium Mycotoxins T-2 Toxin and HT-2 Toxin in Wheat. Journal of Agricultural and Food Chemistry. 2015;63(35):7862-72.
  • Adhikari M, Negi B, Kaushik N, Adhikari A, Al-Khedhairy AA, Kaushik NK, et al. T-2 mycotoxin: toxicological effects and decontamination strategies. Oncotarget. 2017;8(20):33933-52.
  • Polak-Sliwinska M, Paszczyk B. Trichothecenes in Food and Feed, Relevance to Human and Animal Health and Methods of Detection: A Systematic Review. Molecules. 2021;26(2).
  • Tuomi T, Reijula K, Johnsson T, Hemminki K, Hintikka EL, Lindroos O, et al. Mycotoxins in crude building materials from water-damaged buildings. Appl Environ Microbiol. 2000;66(5):1899-904.
  • Bloom E, Nyman E, Must A, Pehrson C, Larsson L. Molds and mycotoxins in indoor environments–a survey in water-damaged buildings. J Occup Environ Hyg. 2009;6(11):671-8.
  • Dai C, Das Gupta S, Wang Z, Jiang H, Velkov T, Shen J. T-2 toxin and its cardiotoxicity: New insights on the molecular mechanisms and therapeutic implications. Food Chem Toxicol. 2022;167:113262.
  • Pei X, Zhang W, Jiang H, Liu D, Liu X, Li L, et al. Food-Origin Mycotoxin-Induced Neurotoxicity: Intend to Break the Rules of Neuroglia Cells. Oxid Med Cell Longev. 2021;2021:9967334.
  • Zhang J, You L, Wu W, Wang X, Chrienova Z, Nepovimova E, et al. The neurotoxicity of trichothecenes T-2 toxin and deoxynivalenol (DON): Current status and future perspectives. Food Chem Toxicol. 2020;145:111676.
  • Ren Z, He H, Zuo Z, Xu Z, Wei Z, Deng J. ROS: Trichothecenes’ handy weapon? Food Chem Toxicol. 2020;142:111438.
  • Pierron A, Alassane-Kpembi I, Oswald IP. Impact of mycotoxin on immune response and consequences for pig health. Anim Nutr. 2016;2(2):63-8.
  • Rocha O, Ansari K, Doohan FM. Effects of trichothecene mycotoxins on eukaryotic cells: a review.Food Addit Contam. 2005;22(4):369-78.
  • Zhang J, Liu X, Su Y, Li T. An update on T2-toxins: metabolism, immunotoxicity mechanism and human assessment exposure of intestinal microbiota. Heliyon. 2022;8(8):e10012.
  • R. F. Medical Aspects of Chemical and Biological Warfare. TMM1997.
  • Karunasena E, Larrañaga MD, Simoni JS, Douglas DR, Straus DC. Building-associated neurological damage modeled in human cells: a mechanism of neurotoxic effects by exposure to mycotoxins in the indoor environment. Mycopathologia. 2010;170(6):377-90.
  • Wu QH, Wang X, Yang W, Nüssler AK, Xiong LY, Kuča K, et al. Oxidative stress-mediated cytotoxicity and metabolism of T-2 toxin and deoxynivalenol in animals and humans: an update.Arch Toxicol. 2014;88(7):1309-26.
  • Li Y, Wang Z, Beier RC, Shen J, De Smet D, De Saeger S, et al. T-2 toxin, a trichothecene mycotoxin: review of toxicity, metabolism, and analytical methods. J Agric Food Chem. 2011;59(8):3441-53.
  • Dai C, Xiao X, Sun F, Zhang Y, Hoyer D, Shen J, et al. T-2 toxin neurotoxicity: role of oxidative stress and mitochondrial dysfunction. Arch Toxicol. 2019;93(11):3041-56.
  • Wu Q, Wang X, Nepovimova E, Wang Y, Yang H, Li L, et al. Antioxidant agents against trichothecenes: new hints for oxidative stress treatment. Oncotarget. 2017;8(66):110708-26.
  • Bennett JW, Klich M. Mycotoxins. Clin Microbiol Rev. 2003;16(3):497-516.
  • Kolf-Clauw M, Sassahara M, Lucioli J, Rubira-Gerez J, Alassane-Kpembi I, Lyazhri F, et al. The emerging mycotoxin, enniatin B1, down-modulates the gastrointestinal toxicity of T-2 toxin in vitro on intestinal epithelial cells and ex vivo on intestinal explants. Arch Toxicol. 2013;87(12):2233-41.
  • Liew WP, Mohd-Redzwan S. Mycotoxin: Its Impact on Gut Health and Microbiota. Front Cell Infect Microbiol. 2018;8:60.
  • Alizadeh A, Braber S, Akbari P, Garssen J, Fink-Gremmels J. Deoxynivalenol Impairs Weight Gain and Affects Markers of Gut Health after Low-Dose, Short-Term Exposure of Growing Pigs. Toxins (Basel). 2015;7(6):2071-95.
  • Osselaere A, Santos R, Hautekiet V, De Backer P, Chiers K, Ducatelle R, et al. Deoxynivalenol impairs hepatic and intestinal gene expression of selected oxidative stress, tight junction and inflammation proteins in broiler chickens, but addition of an adsorbing agent shifts the effects to the distal parts of the small intestine. PLoS One. 2013;8(7):e69014.
  • ZEARALENONE

  • Janik E, Niemcewicz M, Ceremuga M, Stela M, Saluk-Bijak J, Siadkowski A, et al. Molecular Aspects of Mycotoxins-A Serious Problem for Human Health. Int J Mol Sci. 2020;21(21).
  • Ropejko K, Twarużek M. Zearalenone and Its Metabolites-General Overview, Occurrence, and Toxicity. Toxins (Basel). 2021;13(1).
  • Kowalska K, Habrowska-Górczyńska DE, Piastowska-Ciesielska AW. Zearalenone as an endocrine disruptor in humans. Environ Toxicol Pharmacol. 2016;48:141-9.
  • Beezhold D. Analysis of mycotoxins in dust samples from a water damaged building. 2000.
  • Jing S, Liu C, Zheng J, Dong Z, Guo N. Toxicity of zearalenone and its nutritional intervention by natural products. Food Funct. 2022;13(20):10374-400.
  • Brown R, Priest E, Naglik JR, Richardson JP. Fungal Toxins and Host Immune Responses.Frontiers in Microbiology. 2021;12.
  • Marin DE, Motiu M, Taranu I. Food contaminant zearalenone and its metabolites affect cytokine synthesis and intestinal epithelial integrity of porcine cells. Toxins (Basel). 2015;7(6):1979-88.
  • Kotowicz N. The Importance of Fusarium Fungi in Wheat Cultivation – Pathogenicity and Mycotoxins Production: A Review. Journal of Animal &Plant Sciences. 2014;21(2).
  • Omotayo OP, Omotayo AO, Mwanza M, Babalola OO. Prevalence of Mycotoxins and Their Consequences on Human Health. Toxicol Res. 2019;35(1):1-7.
  • Ráduly Z, Price RG, Dockrell MEC, Csernoch L, Pócsi I. Urinary Biomarkers of Mycotoxin Induced Nephrotoxicity—Current Status and Expected Future Trends. Toxins. 2021;13(12).