Do diacetoxyscirpenol, ochratoxin A, and patulin come from different fungi and promote oxidative or mitochondrial stress?

Diacetoxyscirpenol (DAS), ochratoxin A (OTA), and patulin are fungal mycotoxins with distinct dominant producer patterns and experimental evidence of cellular stress effects. The overall claim is well supported for fungal origin and for OTA/patulin mitochondrial-redox effects, but is more tentative for DAS.

Producer patterns

• DAS is principally produced by several Fusarium species, including F. sporotrichioides, F. sambucinum, F. poae, F. langsethiae, and F. equiseti. Trichothecene-pathway genetics, including a proposed TRI8-dependent terminal deacetylation, support this assignment.
• OTA is chiefly produced by Aspergillus (notably sections Circumdati and Nigri) and Penicillium, including P. verrucosum and P. nordicum.
• Patulin occurs in Penicillium, Aspergillus, and Byssochlamys; P. expansum is a major food-relevant producer, and patL disruption abolishes detectable patulin production in this species. These groups overlap, so they are not wholly taxonomically separate.

Oxidative and mitochondrial mechanisms

• OTA has the most direct evidence: in primary human kidney proximal-tubule cells, concentrations as low as 10 nM increased mitochondrial ROS and reduced oxidative phosphorylation, maximal respiration, and ATP production. Other human-cell work found ROS elevation, mitochondrial membrane-potential loss, and ATP depletion.
• Patulin increased ROS, impaired oxidative phosphorylation, depleted ATP, and disrupted membrane potential in HEK293 cells; glutathione or N-acetylcysteine attenuation supports a redox-mediated contribution. Similar ROS-associated injury occurred in 293T cells.
• DAS is less certain: increased ROS, cytotoxicity, and apoptosis were reported only during combined DAS/T-2/HT-2 exposure, precluding toxin-specific mitochondrial conclusions.

Bottom line

• OTA and patulin convincingly induce overlapping but partly distinguishable oxidative and bioenergetic stress in cultured human cells; DAS remains only tentatively implicated. These findings do not establish mitochondrial injury at ordinary human exposure levels.