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Citrinin is a polyketide mycotoxin produced by various fungal species, primarily from the genera Penicillium, Aspergillus, and Monascus (1, 2). It is frequently encountered as a contaminant in food commodities such as grains, fruits, and red yeast rice, the latter being a common dietary supplement (3). Unlike standard therapeutic targets such as receptors or enzymes, citrinin is a toxic secondary metabolite that exerts deleterious effects on cellular systems rather than acting as a site for therapeutic drug action (4). Its primary mechanism of toxicity involves the disruption of mitochondrial function, specifically the inhibition of the respiratory chain and the subsequent induction of oxidative stress through the generation of reactive oxygen species (ROS) (5). Citrinin is notoriously nephrotoxic, primarily affecting the renal proximal tubules, and has also been associated with hepatotoxicity, genotoxicity, and potential teratogenic effects (6). There are currently no clinical drugs designed to target citrinin; management focuses on food safety regulation and limiting human exposure (7).
Inhibits mitochondrial respiration and induces oxidative stress by increasing reactive oxygen species (ROS) production, leading to cellular apoptosis and necrosis (5).
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