Mycotoxins are secondary metabolites produced by many microfungi. Hitherto, over 300 mycotoxins with diverse structures have been identified. They contaminate most cereals and feedstuffs, which threaten human and animal health by exerting acute, sub-acute and chronic toxicological effects, with some considered as carcinogens. Many mycotoxins at low concentrations are able to induce the expression of cytochrome P450 and other enzymes implicated in the biotransformation and metabolization of mycotoxins and. Mycotoxins and their metabolites elicit different cellular disorders and adverse effects such as oxidative stress, inhibition of translation, DNA damage and apoptosis in host cells, thus causing various kinds of cytotoxicities. In this review, we summarize the biotransformation of mycotoxins in animal cells by CYP450 isoforms and other enzymes, their altered expression under mycotoxin exposure, and recent progress in mycotoxin cytotoxicity in different cell lines. Furthermore, we try to generalize the molecular mechanisms of mycotoxin effects in human and animal cells.

No abstract

No abstract

Aflatoxin B1 (AFB1) is a mycotoxin widely distributed in a variety of food commodities and exhibits strong toxicity toward multiple tissues and organs. However, little is known about its neurotoxicity and the associated mechanism. In this study, we observed that brain integrity was markedly damaged in mice after intragastric administration of AFB1 (300 μg/kg/day for 30 days). The toxicity of AFB1 on neuronal cells and the underlying mechanisms were then investigated in the neuroblastoma cell line IMR-32. A cell viability assay showed that the IC50 values of AFB1 on IMR-32 cells were 6.18 μg/mL and 5.87 μg/mL after treatment for 24 h and 48 h, respectively. ROS levels in IMR-32 cells increased significantly in a time- and AFB1 concentration-dependent manner, which was associated with the upregulation of NOX2, and downregulation of OXR1, SOD1, and SOD2. Substantial DNA damage associated with the downregulation of PARP1, BRCA2, and RAD51 was also observed. Furthermore, AFB1 significantly induced S-phase arrest, which is associated with the upregulation of CDKN1A, CDKN2C, and CDKN2D. Finally, AFB1 induced apoptosis involving CASP3 and BAX. Taken together, AFB1 manifests a wide range of cytotoxicity on neuronal cells including ROS accumulation, DNA damage, S-phase arrest, and apoptosis—all of which are key factors for understanding the neurotoxicology of AFB1.