Etiology and History of Study
The disease is caused by microscopic mold fungi — the pathogens Aspergillus flavus and Aspergillus parasiticus. The name of the toxin group itself is an acronym formed from the Latin name of the main producer: Aspergillus flavus toxins.
These dangerous metabolites were first discovered in 1960. The catalyst for large-scale research was a sudden outbreak of a previously unknown disease in Great Britain, which drew scientists' attention to Aspergillus toxins.
Characteristics of Toxins and Sources of Contamination
Aflatoxins represent a complex group of chemical compounds. Several main fractions of these metabolites are distinguished: $B_1$, $B_2$, $B_{2a}$, $G_1$, $G_2$, $G_{2a}$, $M_1$, and $M_2$. The primary epidemiological danger of aflatoxins lies in their high toxicity and thermostability. They are not destroyed even by thorough heat treatment of food products.
The problem has a wide geographical distribution. Human infection occurs via the alimentary route through contaminated food:
- Plant-based products: toxins are most frequently found in cereals, peanuts, carrots, beans, and cocoa.
- Animal-based products: aflatoxins can accumulate in animal tissues and biological fluids; therefore, meat, milk, and various types of cheese can serve as sources of poisoning.
Clinical Presentation of Acute Poisoning
Acute aflatoxicosis is characterized by an extremely rapid development of symptoms and high mortality. The pathological process affects multiple body systems simultaneously:
- Damage to internal organs: pronounced gastrointestinal dysfunctions are observed. However, the key link in the pathogenesis is severe hepatotoxicity. The toxins cause hepatic tissue necrosis, which can subsequently progress to cirrhosis. Furthermore, there is a high risk of developing primary liver cancer.
- Neurological symptoms: patients suffer from generalized motor lethargy, and they develop convulsive syndrome and paresis.
- Vascular and tissue disorders: the toxic effect on the vascular wall leads to hemorrhages (multiple bleedings) and extensive edema.
Spectrum of Other Aspergillus Mycotoxins
In addition to classical aflatoxins, various species of the genus Aspergillus are capable of producing a number of other dangerous toxic substances.
| Mycotoxin | Producer species (Aspergillus) |
|---|---|
| Ochratoxins A, B, C | A. ochraceus |
| Patulin | A. terreus, A. niveus, A. candidum |
| Gliotoxin | A. giganteus, A. fumigatus |
| Sterigmatocystin | A. versicolor, A. nidulans |
| Tremorgen | A. clavatus, A. flavus, A. candidum |
| Cytochalasins | A. clavatus |
| Citrinin | A. terreus, A. niveus, A. candidum |
Briefly: answers to topical questions
What is the molecular mechanism of the hepatotoxic and carcinogenic action of aflatoxin B1?
The molecular mechanism of aflatoxin B1 action involves its biotransformation in the liver to form an active alkylating metabolite. Microsomal oxidation of the toxin occurs under the action of the cytochrome P450 system.
- Aflatoxin B1 8,9-epoxide is a potent alkylating agent that covalently binds to DNA nitrogenous bases (primarily guanine).
This interaction causes mutations in tumor suppressor genes (e.g., p53). As a result, malignant transformation of hepatocytes is initiated, leading to the development of primary liver cancer.
What pathomorphological and histological changes develop in liver tissues during aflatoxicosis?
Pathomorphological changes in the liver during aflatoxicosis are characterized by severe toxic tissue damage with a high risk of malignancy. The following processes develop in the tissues:
- Necrosis — the death of hepatocytes, which is a key link in hepatotoxicity.
- Cirrhosis — the outcome of progressive liver damage.
- Vascular and tissue disorders — the occurrence of hemorrhages (bleedings) and edema.
- Carcinogenesis — the development of primary liver cancer.
These changes are accompanied by a rapid development of symptoms and high mortality.
What methods are used for the laboratory indication of aflatoxins in food products and biological material?
Laboratory indication of aflatoxins includes extraction of the mycotoxin from a sample using an organic solvent and its subsequent identification. The following methods are used for analyzing crops, food products, feed, and raw materials of animal origin:
- Physicochemical — chromatography and spectrophotometry.
- Immunological — enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA).
- Biological assays (bioassays) — the use of chicken embryos, cell cultures, sensitive microorganisms, laboratory animals (rats, mice, guinea pigs), and birds (ducklings, pigeons).
The name "Aflatoxin" is easy to remember through the acronym: A-fla-toxin = Aspergillus flavus toxins. This immediately suggests the main causative agent and the nature of the poison.
Class and exam questions
Can products containing aflatoxins be detoxified by boiling or frying?
No, aflatoxins have pronounced thermostability. They are not destroyed during heat treatment, so contaminated products remain toxic.
What effect do aflatoxins have on the liver?
Hepatotoxicity is a key link in poisoning. The metabolites cause liver necrosis, which can progress to cirrhosis, and also significantly increase the risk of primary liver cancer.
Are animal-based products dangerous in cases of aflatoxicosis?
Yes. Aflatoxins can accumulate in the tissues of animals that have consumed contaminated feed. Therefore, meat, milk, and cheese can also serve as fully fledged sources of human poisoning.
What else to study on this topic
- Features of the chemical structure of aflatoxin fractions (B1, B2, G1, G2, M1, M2)
- Pathogenesis of convulsive syndrome and paresis in acute aflatoxicosis
- Mechanisms of hemorrhagic and edematous manifestations of the toxic effect of Aspergillus
- Comparative characteristics of ochratoxins and patulin: impact on the macroorganism
- Diagnostic criteria for the transition of toxic liver necrosis to cirrhosis
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