Abstract
Among many mycotoxins, T-2 toxin, macrocyclic trichothecenes, fumonisin B1 (FB1) and ochratochin A (OTA) are known to have the potential to induce neurotoxicity in rodent models. T-2 toxin induces neuronal cell apoptosis in the fetal and adult brain. Macrocyclic trichothecenes bring about neuronal cell apoptosis and inflammation in the olfactory epithelium and olfactory bulb. FB1 induces neuronal degeneration in the cerebral cortex, concurrent with disruption of de novo ceramide synthesis. OTA causes acute depletion of striatal dopamine and its metabolites, accompanying evidence of neuronal cell apoptosis in the substantia nigra, striatum and hippocampus. This paper reviews the mechanisms of neurotoxicity induced by these mycotoxins especially from the viewpoint of oxidative stress-associated pathways.
Highlights
Mycotoxins are fungal metabolites known to be harmful toward human and animal health
T-2 toxin is a well-known inhibitor of protein synthesis through its high binding affinity to peptidyl transferase which is an integral part of the 60 s ribosomal subunit [9,10,11]
In the study by Sehata et al [36] on the fetal brain, the expression of MEKK1 gene increased at 12 and 24 h, and the expression of c-jun gene at 24 h after T-2 toxin treatment. These findings suggest that the mitogen-activated protein kinases (MAPKs)-Jun N-terminal kinase (JNK)-c-jun pathway might be involved in T-2 toxin-induced apoptosis in the fetal brain
Summary
Mycotoxins are fungal metabolites known to be harmful toward human and animal health. Disorders caused by mycotoxins have been reported in digestive, urinary, immune and reproduction systems [1], and many in vivo and in vitro studies have been performed in order to clarify the mechanisms of mycotoxin-induced toxicity in these systems. 2011, 12 that, in many cases, membrane-active properties of various mycotoxins determine their toxicity and incorporation of mycotoxins into membrane structures causes various detrimental changes, resulting in alterations in second messenger systems through damaging membrane receptors. Detrimental effects of mycotoxins on DNA and RNA and protein synthesis together with proapoptotic action further compromise important metabolic pathways and changes in physiological functions including growth, development and reproduction occur. Compared with the amount of research on digestive, urinary, immune and reproduction systems, there are few reports of the effects of mycotoxins on neuronal tissues. This paper reviews the mechanisms of neurotoxicity experimentally induced in rats and mice by T-2 toxin, macrocyclic trichothecenes, fumonisin B1 (FB1) and ochratoxin A (OTA) especially from the viewpoint of oxidative stress-associated pathways
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