Selective toxicity of ochratoxin A in primary cultures from different brain regions

  title={Selective toxicity of ochratoxin A in primary cultures from different brain regions},
  author={Abdelhak Belmadani and Pieter S. Steyn and G{\'e}rard Tramu and A. M. Betbeder and Isabelle Baudrimont and Edmond Eku{\'e} Creppy},
  journal={Archives of Toxicology},
Abstract Ochratoxin A (OTA) is a mycotoxin produced by moulds from the Aspergillus and Penicillium genera. It is a natural contaminant of a wide variety of both human and animal foodstuffs. Via dietary intake, OTA passes into the blood of both humans and animals and accumulates in several organs, such as the kidney and the brain with selective toxicity in the ventral mesencephalon and in the cerebellum. In order to confirm the regional selectivity to OTA cytotoxicity in rat brain… 
Ochratoxin a reduces NMDA receptor subunits 2A and 2B concentrations in rat hippocampus: partial protective effect of melatonin
Subchronic administration of OTA reduced hippocampal NMDA receptor subunits 2A and 2B concentrations in rats and exhibited a partially protective effect on NR2A and NR2B against OTA, which was thought to affect cognitive functions.
Developmental Toxicity of Ochratoxin A in Rat Embryo Midbrain Micromass Cultures
There were no significant differences in the sensitivity of neurons in early and late stage of differentiation and astrocytes to the toxic activity of OTA, so OTA was classified as a strong teratogen and basic cytotoxicity should be connected.
Toxicity of Ochratoxin A and Its Modulation by Antioxidants: A Review
These studies demonstrated that antioxidants are able to counteract the deleterious effects of chronic consumption or exposure to OTA and confirmed the potential effectiveness of dietary strategies to counteract OTA toxicity.
Food-Origin Mycotoxin-Induced Neurotoxicity: Intend to Break the Rules of Neuroglia Cells
Various pathways in which common food-derived mycotoxins can induce glial toxicity and provide a novel perspective for future research on the neurodegenerative diseases are analyzed.
Efflux at the Blood-Brain Barrier Reduces the Cerebral Exposure to Ochratoxin A, Ochratoxin α, Citrinin and Dihydrocitrinone
C cerebral exposure of ochratoxin A, ochRatoxin α, citrinin and dihydrocitrinone is low and neurotoxicity is likely to play a subordinate role in their toxicity at common physiological concentrations, due to their slow transfer across the blood-brain barrier.
Ochratoxin A-induced DNA damage in human fibroblast: protective effect of cyanidin 3-O-beta-d-glucoside.
The ribotoxin deoxynivalenol affects the viability and functions of glial cells
The results suggest that environmental ribotoxins such as DON could, at low doses, cause modifications of brain homeostasis and possibly participate in the etiology of neurological diseases in which alterations of the glia are involved.


Subchronic effects of ochratoxin A on young adult rat brain and partial prevention by aspartame, a sweetener
Aspartame, a structural analogue of OTA largely modified the distribution and prevented the accumulation of Ota in the brain since the respective brain OTA contents decreased respectively to 9.0+6.0 ng/g of tissue, for the same duration of treatment.
Aspartame as a preventive agent of chronic toxic effects of ochratoxin A in experimental animals.
There is evidence of the implication of oxidative pathways in the OTA-induced cellular damage and the most threatening effects of OTA are nephrotoxicity and carcinogenicity.
Brain necrosis in mouse fetuses transplacentally exposed to the mycotoxin ochratoxin A.
Prevention of lipid peroxidation induced by ochratoxin A in Vero cells in culture by several agents.
Formation of ochratoxin A metabolites and DNA-adducts in monkey kidney cells.
Ochratoxin A-induced teratogenesis in rats: partial protection by phenylalanine
Results indicate that coadministered Phe provides partial prenatal protection from the teratogenic effects of OA, and OA-induced fetal malformations were significantly diminished in the presence of added Phe.
Toxic effects of potential environmental neurotoxins related to 1-methyl-4-phenylpyridinium on cultured rat dopaminergic neurons.
Dopaminergic rat mesencephalic neurons in culture were exposed to a group of potential environmental neurotoxins and exhibited highly selective dopaminergic toxicity, hence the requirements for a selective dopamineergic neurotoxin are rather strict.
Lipid peroxidation as a possible cause of ochratoxin A toxicity.
Effect of Ochratoxin A on enzyme activities and macromolecules synthesis in MDCK cells.
Both cellular macromolecules syntheses and enzymatic activities are inhibited by OTA in a dose-dependent manner after 24 h incubation, and the protection by 100 microM additional phenylalanine is optimal when MDCK cells were pretreated 4 h before the poisoning by Ota.
Inhibition of protein synthesis in mice by ochratoxin A and its prevention by phenylalanine.