EnviroTOX Suite of Panels

Deeper Insights into the Body's Toxic Burden

EnviroTOX panels provide practitioners with a powerful tool for detecting toxic exposures and their health impacts. Beginning with our foundational panel of EnviroTOX consisting of the Organic Acids Test, TOXDetect Profile and Glyphosate Test with subsequent panels building upon with MycoTOX Profile and Metals – Toxic Elements.

Our EnviroTOX panels streamline the identification process, allowing for the collection of extensive data from a single, convenient urine sample. Maximize efficiency, reduce costs, and gain unparalleled visibility into toxic environmental factors affecting health.

Limited Time Introductory Pricing Available!

Order now before it expires on August 31st, 2024! The discounted rate will be automatically applied in your portal.

Urine
Turnaround Time: 1-2 weeks

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

* Available in English, Spanish, Japanese, German, French, Italian, Korean, Polish, Portuguese, Chinese

What Patients Might Benefit from the EnviroTOX Panels?

Continuous and increasing exposure to toxicants is posing serious health threats including:

  • ADHD
  • Alzheimer’s Disease
  • Anxiety
  • Asthma
  • Autism Spectrum Disorders
  • Cancers
  • Cardiovascular Disease
  • Chronic Fatigue
  • Cognitive Dysfunction
  • Depression
  • Diabetes
  • Headaches
  • Immune Dysfunction
  • Infertility
  • Inflammatory Bowel Disease
  • Obesity
  • Memory Loss/Disturbances
  • Mood Changes
  • Neurological Symptoms
  • Parkinson's Disease
  • Respiratory Problems
  • Sinus/Nasal Congestion

Details

Why Test?

Toxic substances in our environment pose detrimental health risks, from pollutants in the air to chemicals in everyday products. Identifying and mitigating constant exposure is crucial for optimizing patient outcomes. Our EnviroTOX panels provide comprehensive assessments, including evaluations for mycotoxins and heavy metals, which disrupt balance and harm organ systems. The Organic Acids Test within these panels uncovers their health impacts, offering valuable insights into their effects on overall well-being.

Understanding the Power of Panels:

  • Comprehensive Assessment: Analyzes exposure to an array of toxic substances and their health impacts for a holistic view of patient health.
  • Tailored Insights: Testing is tailored to individual’s patient profile allowing for personalized interventions based on specific exposure patterns.
  • Simplified Process: Bundling essential tests offers time and cost savings, requiring just a single urine sample collection for convenience.

Analytes

Select the EnviroTOX Panel that Best Meets your Patients’ Needs:

Beginning with our foundational panel of EnviroTOX consisting of the Organic Acids Test, TOXDetect Profile and Glyphosate Test with subsequent panels building upon with MycoTOX Profile and Metals – Toxic Elements, practitioners gain extensive insights into toxic exposure, providing greater assessment of total body burden.

EnviroTOX EnviroTOX Complete EnviroTOX Complete + Metals
96 Analytes 107 Analytes 127 Analytes
Organic Acids Test:
Intestinal Microbial Overgrowth
Oxalate Metabolites
Glycolytic Cycle Metabolites
Mitochondrial Krebs Cycle Metabolites
Mitochondrial Amino Acids Metabolites
Neurotransmitter Metabolites
Pyrimidine Folate Metabolism
Ketone and Fatty Acid Oxidation
Nutritional Markers
Indicators of Detoxification
Amino Acid Metabolites
Mineral Metabolism

TOXDetect Profile:
Phthalates
VOCs – Volatile Organic Compounds
Pesticides
Triphenyl Phosphate
Acrylamide
Perchlorate
Bisphenol S (BPS)

Glyphosate Test:
Glyphosate

MycoTOX Profile:
Aflatoxin
Ochratoxin
Trichothecene
Zearalenone
Chaetoglobosin A
Citrinin
Enniatin B
Gliotoxin
Mycophenolic Acid
Sterigmatocystin
 
Metals – Toxic Elements:
20 Toxic Elements

Sample Reports

The EnviroTOX Panels provide individual test reports for each test included in the panel. These reports are designed to offer easy-to-interpret results and comprehensive insights into your patients’ 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 environmental toxicants and the MosaicDX EnviroTOX Panels. These resources enhance patient understanding, decision-making, and overall health journey:

  • Patient Brochure: A comprehensive guide that explains the importance of environmental toxicants testing and how the EnviroTOX Panels can benefit patients.

Frequently Asked Questions

If you or a patient has had a TOXDetect Profile and/or a Glyphosate Test run and found moderate-high levels of any compounds, there are things you can do to help your body eliminate the toxins and to prevent future exposures. The first steps to reducing the amount of toxins presently in the body are to switch to eating only organic food and drinking water that has common toxins, including pesticides filtered out. Most conventional food crops are exposed to larger and larger doses of pesticides and herbicides, and by switching to organic you will prevent exposure to hundreds of these toxicants. Many of these chemicals have also contaminated our water supplies. Installing a high-quality water filtration system in the home that eliminates them is important to do and there are several options available.  

The next step to avoiding future exposures is to change the products you use on a daily basis – from food and beverage containers to beauty and cleaning products. Instead of using plastic water bottles and food containers, switch to glass or metal. Never microwave food in plastic or Styrofoam containers and do not drink hot beverages from plastic or Styrofoam cups. Make sure your shampoo, soaps, lotions, and other beauty products are free of phthalates. Use cleaning products made from natural ingredients or make your own at home.  

To eliminate toxins from the body, we highly recommend exercise and the use of saunas, especially infrared sauna therapy to rid many chemicals through sweat. Infrared sauna is superior to conventional sauna because it reaches deeper into the body, increasing the circulation in the blood vessels, and causing the body to start to releasing many of the chemicals stored in body fat.  

There are two supplements that are particularly useful in helping the body detoxify. The first is glutathione, or its precursor N-acetyl cysteine. Glutathione is one of the most common molecules used by the body to eliminate toxic chemicals. If you are constantly exposed to toxicants your stores of glutathione could be depleted. The second supplement is vitamin B3 (niacin). Some may not enjoy the flushing that can happen when taking niacin, however, this flushing is from the blood vessels dilating, which is useful in the detoxification process.  If sensitive to the flushing, start with the lowest recommended dose and work up from there.

Several substances measured by the TOXDetect Profile may come from various sources of exposure. The panel cannot determine the specific origin of the toxicant, but it can provide information on the most common sources. By collaborating with your healthcare provider, you can investigate and eliminate potential sources of exposure. 

•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.

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

The Organic Acids Test by Mosaic Diagnostics evaluates levels of oxalates in urine. Oxalate (and its acid form, oxalic acid), is an organic acid that is primarily derived from three sources: the diet, fungus (such as Aspergillus and Penicillium), possibly Candida, and also human metabolism. Oxalic acid is the most acidic organic acid in body fluids and is used commercially to remove rust from car radiators. Antifreeze (ethylene glycol) is toxic primarily because it is converted to oxalate in the body. Two different types of genetic diseases are known in which oxalates are high in the urine, hyperoxalurias type I and type II, which can also be determined from the Organic Acids Test. 

Foods especially high in oxalates are often foods thought to be otherwise healthy, including spinach, beets, chocolate, peanuts, wheat bran, tea, cashews, pecans, almonds, berries, and many others. People now frequently consume “green smoothies” in an effort to eat “clean” and get healthy, however, they may actually be sabotaging their health. The most common components of green smoothies are spinach, kale, Swiss chard, and arugula, all of which are loaded with oxalates. These smoothies also often contain berries or almonds, which have high amounts of oxalates as well. Oxalates are not found in meat or fish at significant concentrations. Daily adult oxalate intake is usually 80-120 mg/d. A single green smoothie with two cups of spinach contains about 1,500 mg of oxalate, a potentially lethal dose. 

High Oxalate Food List

Fruit
Vegetables
Blackberries 
Beans (baked, green, dried, kidney)
Leeks
Blueberries
Beets
Okra
Carambola
Beet greens
Olives
Concord grapes
Beet root
Parsley
Currents
Carrots
Peppers (chili and green)
Dewberries
Celery
Pokeweed
Elderberries
Chicory
Potatoes (baked, boiled, frieds)
Figs
Collards
Rutabaga
Fruit cocktail
Dandelion greens
Spinach
Gooseberry
Eggplant
Summer squash
Kiwis
Escarole
Sweet potato
Lemon peel
Kale
Swiss chard
Orange peel
 
Zucchini
Raspberries
 
 
Rhubarb
 
 
Canned strawberries
 
 
Tamarillo
 
 
Tangerines
 
 
Fats, Nuts Seeds
Dairy
Misc.
Nuts
Chocolate milk
Chocolate
Nut butters
Soy cheese
 
Sesame seeds
Soy milk
 
Tahini
Soy yogurt
 
Soy nuts
 
 
Drinks
Starch
Dark or “robust” beer
Amaranth
Wheat bran
Black tea
Buckwheat
Wheat germ
Chocolate milk
Cereal (bran or high fiber)
Whole wheat bread
Cocoa
Crisp bread (rye or wheat)
Whole wheat flour
Instant coffee
Fruit cake
Hot chocolate
Grits
Ovaltine
Pretzels
Soy drinks
Taro

External sources of oxalates include ethylene glycol, the main component of antifreeze. Antifreeze is toxic mainly because of the oxalates formed from it. In addition, some foods also contain small amounts of ethylene glycol. Vitamin C (ascorbic acid or ascorbate) can be converted to oxalates but the biochemical conversion system is saturated at low levels of vitamin C so that no additional oxalate is formed until very large doses (greater than 4 g per day) are consumed. The high correlation between arabinose and oxalates indicate that intestinal yeast/fungal overgrowth is likely the main cause for elevated oxalates in the autistic spectrum population. The deposition of oxalates in critical tissues such as brain and blood vessels, the oxidative damage caused by oxalate salts, and the deposition of oxalate mercury complexes in the tissues.

Mosaic Diagnostics offers written interpretations within test reports and complimentary consultations with our clinical educators for qualified practitioners. To schedule a consultation, simply sign in to your MosaicDX account and book a consultation online. 

We encourage all patients to discuss results with your practitioner.

Our Resources tab also contains educational materials that you may find useful, we also offer MosaicEDGE workshops for qualified practitioners to better understand the fundamentals of lab testing.

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.

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.

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. 

Molds thrive in warm, damp, and humid conditions, and exposure to mold-rich environments may result in a variety of health effects ranging from mild to severe depending on an individual’s sensitivity or underlying allergy to mold.

Given their ubiquitous presence, testing should be considered in anyone with signs and/or symptoms of mold exposure – or an environmental history for a known current or past exposure to mold.

Individuals at highest risk for health problems when exposed to mold include those with:

  • Underlying immune system dysfunction (history of atopy, immune suppression, or immunodeficiency)
  • Underlying chronic lung disease
  • Infants, young children, and the elderly
  • Workers employed in jobs that result in high and ongoing levels of exposure (farm/dairy workers, lumber/wood workers, winemakers).

Have a question? We've got answers.

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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).