What is mycotoxicosis?

Mycotoxicosis refers to poisoning or toxic effects resulting from exposure to mycotoxins, which are toxic secondary metabolites produced by certain fungi. These fungi can grow on various food commodities, including grains, nuts, fruits, and vegetables, as well as in indoor environments such as buildings with water damage or high humidity levels. Mycotoxins are produced by molds belonging to genera such as Aspergillus, Penicillium, Fusarium, and others.


Exposure to mycotoxins can occur through ingestion of contaminated food or beverages, inhalation of airborne spores or toxins, or direct contact with contaminated surfaces. The health effects of mycotoxicosis can vary depending on the type and amount of mycotoxin ingested, the duration of exposure, and individual susceptibility factors.


Some common mycotoxins and their associated health effects include:


  • Aflatoxins: Produced primarily by Aspergillus species, aflatoxins are potent carcinogens and hepatotoxins. Chronic exposure to aflatoxins through contaminated food, particularly grains, nuts, and legumes, has been linked to liver cancer, liver damage, immune suppression, and growth impairment.


  • Ochratoxin: Produced by several species of Aspergillus and Penicillium fungi, ochratoxin is associated with nephrotoxicity (kidney damage), carcinogenicity, and immunosuppression. Chronic exposure to ochratoxin through contaminated cereals, coffee, wine, and spices has been implicated in kidney disease and urinary tract cancer.


  • Fumonisins: Produced primarily by Fusarium species, fumonisins are associated with esophageal cancer, neural tube defects, and other developmental abnormalities. Fumonisins can contaminate maize (corn) and maize-based products, posing a risk to populations reliant on maize as a dietary staple.


  • Trichothecenes: Produced by various Fusarium species, trichothecenes are potent mycotoxins with immunosuppressive, cytotoxic, and genotoxic effects. Trichothecenes can cause vomiting, diarrhea, neurotoxicity, and immunosuppression in humans and animals. Exposure to trichothecenes may occur through ingestion of contaminated cereals, grains, and animal feed.


  • Patulin: Produced by Penicillium and Aspergillus fungi, patulin is associated with gastrointestinal irritation, immunosuppression, and genotoxicity. Patulin can contaminate fruits, particularly apples, and apple-based products such as juices and ciders.


What is the relationship between mycotoxicosis and oxidative stress?

The relationship between mycotoxicosis and oxidative stress involves complex interactions between mycotoxins, cellular metabolism, inflammation, and antioxidant defenses. While the precise mechanisms linking mycotoxicosis to oxidative stress are not fully understood, several factors suggest potential connections between these processes:


  • Direct Generation of Reactive Oxygen Species (ROS): Some mycotoxins have been shown to directly generate reactive oxygen species (ROS) within cells. For example, aflatoxins, ochratoxin A, and patulin have been reported to induce oxidative stress by promoting ROS production through various mechanisms, including disruption of mitochondrial function, activation of NADPH oxidases, and inhibition of antioxidant enzymes.


  • Induction of Inflammatory Responses: Mycotoxins can trigger inflammatory responses in tissues and organs, leading to the activation of immune cells and the release of pro-inflammatory cytokines and chemokines. Chronic inflammation is associated with increased oxidative stress, as inflammatory cells such as macrophages and neutrophils produce ROS as part of their antimicrobial defense mechanisms. Mycotoxin-induced inflammation may contribute to oxidative damage and tissue injury in affected individuals.


  • Disruption of Antioxidant Defenses: Mycotoxins can disrupt antioxidant defenses within cells, leading to impaired scavenging of ROS and increased susceptibility to oxidative stress. For example, mycotoxins such as aflatoxins and ochratoxin A have been shown to inhibit antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, which play critical roles in neutralizing ROS and protecting cells from oxidative damage.


  • Induction of Apoptosis and Cell Death: Mycotoxins can induce apoptosis (programmed cell death) and necrosis in cells and tissues, leading to the release of ROS and oxidative stress. Apoptosis and necrosis pathways are closely linked to oxidative stress, as ROS can activate signaling pathways that regulate cell survival and death. Mycotoxin-induced cell death may further exacerbate tissue injury and inflammation, contributing to the pathogenesis of mycotoxicosis.


  • DNA Damage and Genotoxicity: Some mycotoxins are genotoxic and can induce DNA damage, chromosomal abnormalities, and mutations in cells. DNA damage resulting from mycotoxin exposure can trigger oxidative stress by activating DNA repair mechanisms and generating ROS during repair processes. Persistent DNA damage and oxidative stress may contribute to carcinogenesis and other long-term health effects associated with mycotoxicosis.


Overall, oxidative stress is believed to play a significant role in the pathogenesis and progression of mycotoxicosis, contributing to tissue injury, inflammation, and organ dysfunction.