zearalenol and beauvericin

Coffee silverskin and spent coffee have been evaluated in a neuroblastoma cell line (SH-SY5Y cells) against beauvericin (BEA) and α-zearalenol (α-ZEL)-induced cytotoxicity with different strategies of treatment. First, the direct treatment of mycotoxins and coffee by-products extracts in SH-SY5Y cells was assayed. IC

Topics: Cell Death; Cell Line, Tumor; Coffee; Cytoprotection; Depsipeptides; Dose-Response Relationship, Drug; Humans; Inhibitory Concentration 50; Neurons; Neuroprotective Agents; Plant Extracts; Seeds; Time Factors; Zeranol

Beauvericin (BEA), α-zearalenol (α-ZEL) and β-zearalenol (β-ZEL), are produced by several Fusarium species that contaminate cereal grains. These mycotoxins can cause cytotoxicity and neurotoxicity in various cell lines and they are also capable of produce oxidative stress at molecular level. However, mammalian cells are equipped with a protective endogenous antioxidant system formed by no-enzymatic antioxidant and enzymatic protective systems such as glutathione peroxidase (GPx), glutathione S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD). The aim of this study was evaluating the effects of α-ZEL, β-ZEL and BEA, on enzymatic GPx, GST, CAT and SOD activity in human neuroblastoma cells using the SH-SY5Y cell line, over 24 h and 48 h with different treatments at the following concentration range: from 1.56 to 12.5 μM for α-ZEL and β-ZEL, from 0.39 to 2.5 μM for BEA, from 1.87 to 25 μM for binary combinations and from 3.43 to 27.5 μM for tertiary combination. SH-SY5Y cells exposed to α-ZEL, β-ZEL and BEA revealed an overall increase in the activity of i) GPx, after 24 h of exposure up to 24-fold in individual treatments and 15-fold in binary combination; ii) GST after 24 h of exposure up to 10-fold (only in combination forms), and iii) SOD up to 3.5- and 5-fold in individual and combined treatment, respectively after 48 h of exposure. On the other hand, CAT activity decreased significantly in all treatments up to 92% after 24 h except for β-ZEL + BEA, which revealed the opposite.

Topics: Catalase; Cell Line, Tumor; Depsipeptides; Enzyme Assays; Glutathione Peroxidase; Glutathione Transferase; Humans; Mycotoxins; Peroxidases; Superoxide Dismutase; Zeranol

Beauvericin (BEA) and zearalenone derivatives, α-zearalenol (α-ZEL), and β-zearalenol (β-ZEL), are produced by several

Topics: Cell Death; Cell Line, Tumor; Depsipeptides; Dose-Response Relationship, Drug; Drug Synergism; Humans; Inhibitory Concentration 50; Neurons; Neurotoxins; Time Factors; Zeranol

The co-presence of mycotoxins from fungi of the genus Fusarium is a common fact in raw food and food products, as trace levels of them or their metabolites can be detected, unless safety practices during manufacturing are carried out. Zearalenone (ZEA), its metabolites α-zearalenol (α-ZEL) and β-zearalenol (β-ZEL) and, beauvericin (BEA) are co/present in cereals, fruits or their products which is a mixture that consumer are exposed and never evaluated in neuronal cells. In this study the role of oxidative stress and intracellular defense systems was assessed by evaluating reactive oxygen species (ROS) generation and glutathione (GSH) ratio activity in a human neuroblastoma cell line, SH-SY5Y cells, treated individually and combined with α-ZEL, β-ZEL and BEA. It was further examined the expression of genes involved in cell apoptosis (CASP3, BAX, BCL2) and receptors of (endogenous or exogenous) estrogens (ERβ and GPER1), by RT-PCR in those same conditions. These results demonstrated elevated ROS levels in combinations where α-ZEL was involved (2.8- to 8-fold compared to control); however, no significant difference in ROS levels were detected when single mycotoxin was tested. Also, the results revealed a significant increase in GSH/GSSG ratio at all concentrations after 24 h. Expression levels of CASP3 and BAX were up regulated by α-ZEL while CASP3 and BCL2 were down regulated by β-ZEL, revealing how ZEA´s metabolites can induce the expression of cell apoptosis genes. However, BEA down-regulated the expression of BCL2. Moreover, β-ZEL + BEA was the only combination treatment which was able to down regulate the levels of cell apoptosis gene expression. Relying to our findings, α-ZEL, β-ZEL and BEA, induce injury in SH-SY5Y cells elevating oxidative stress levels, disturbing the antioxidant activity role of glutathione system and finally, causing disorder in the expressions and activities of the related apoptotic cell death genes.

Topics: Apoptosis; Caspase 3; Cell Culture Techniques; Cell Line, Tumor; Depsipeptides; Gene Expression; Glutathione; Humans; Oxidation-Reduction; Oxidative Stress; Reactive Oxygen Species; Up-Regulation; Zearalenone; Zeranol