Mycotoxins Flashcards
(15 cards)
Mycotoxins
Toxic compounds produced by fungi that contaminate food causing health risks.
Aflatoxins
Highly toxic mycotoxins produced by Aspergillus sp. found in maize and peanuts, causing liver damage and cancer.
Amanitins
Toxic compounds produced by fungi Amanita (death cap) leading to liver and kidney failure.
Chemical nature of aflatoxins
Aflatoxins are polyketide-derived, small and hydrophobic with a fused coumarin-lactane structure, allowing for lipid penetration.
Chemical nature of amanitins
Octapeptide backbone with unusual amino acid bnding to a tryptathione bridge, making them highly resistant to enzymatic degradation.
Mechanism of aflatoxins
- Ingestion: Aflatoxins enter gut
- Absorption: Metabolized in liver by cytochrome P450 enzymes.
- Toxic metabolites: Form reactive intermediates
- DNA binding: Causes mutations
- Liver damage: Leads to hepatocyte death, cirrhosis, or hepatocellular carcinoma.
Mechanisms of amanitins
- Ingestion: Amanitin enters the bloodstream
- Hepatocyte uptake: Transported to the liver
- RNA polymerase II inhibition: Blocks mRNA synthesis
- Hepatocyte damage: oxidative stress
- Liver failure: widespread hepatocyte necrosis.
Two Aspergillus species that make aflatoxins
Aspergillus flavus - aflatoxin B1 most deadly
Aspergillus parasiticus - multiple types.
Categorification of Alatoxins
Categories are done based on UV light.
Categories of aflatoxins
AFB1 - most toxic an carcinogenic
AFB2 - slightly less toxic AFB1
AFG1 - green fluorescence of AFB1
AFG2 - slightly less toxic AFG1
AFM1 - Hydroxylated metabolite of AFB1, found in milk.
Types of P450 enzyme
CYP1A2 and CYP3A4, which convert AFB1 to aflatoxin-8,9-epoxide, causing liver damage.
AFB1 adduct
AFB1-N7-guanine which disrupts base pairing, specifaclly in p53 tumour suppressor.
Oxidative stress
Reactive oxygen species cause lipid peroxification, DNA lyses.
Proteinsynthesis inhibition.
Reduced ribosomal functions induces incorrect protein creation.
Apoptosis induction
AFBI can increase production of pro-apoptopic pathways.