Abstract

Background:Alflatoxin B1 (AFB1) is the most hepatotoxic and hepatocarcinogenic of the aflatoxins and occurs as a contaminant in a variety of foods. The toxicity of AFB1 has been shown to be associated with a wide range of pathological events, such as enhanced apoptosis and oxidative events. Currently there is no treatment for mycotoxin exposure. The aim of this study was to evaluate the potential ability of picolinyl-L-phenylalaninate (PLP), picolinyl-L-tryptophanate (PLT), and nicotinyl-L-tryptophanate (NLT) Schiff base amino acid derivatives to act against damaging effects of AFB1 using a rat model of mycotoxicosis. For this purpose, a range of markers of immune and antioxidant systems in liver and blood plasma samples, as well as the apoptotic rate in neutrophils and monocytes was assessed.Methods:Mongrel white pubescent rats (with 180-200g b/w) were used in all experiments. Concentration of the markers of immune and antioxidant systems was measured in plasma by ELISA, using commercially available kits according to manufacturers’ instructions. The rate of apoptosis in neutrophils and monocytes was analyzed by flow cytometry.Results:AFB1 induced mycotoxicosis caused significant elevation of malonic dialdehyde contents (plasma and liver: p = 0.0001 compared with untreated rats), the levels of superoxide dismutase (p=0.005), total non-enzymatic water-soluble antioxidants (p = 0.0001), and terminal complement complex (p = 0.021). Moreover, the increased rates of early and late apoptosis in neutrophils and monocytes were observed as well. Treatment with PLP, PLT and NLT were shown to mitigate these effects, though to a different extent.Conclusions:The results obtained in this study clearly demonstrated that chronic AFB1 exposure induced oxidative cell damage, immunosuppression and apoptosis of circulating immune cells. The oral administration of Schiff base cyclic amino acid derivatives was capable of minimizing the detrimental effects of mycotoxicosis by possessing multi-mechanistic effects that target AFB1-induced pathological events.

Highlights

  • Aflatoxin B1 (AFB1) is a mycotoxin produced by Aspergillus flavus and related fungi that grow in staple foods, including cereals and nuts, such as corn, rice and peanuts[1], especially in areas with appropriate conditions of moisture and heat where these fungi are ubiquitous

  • We assessed the intensity of Alflatoxin B1 (AFB1)-induced lipid peroxidation and the effects of the Schiff bases

  • AFB1 induced a significant increase of Malonic dialdehyde (MDA) both in plasma (59%, p = 0.0001) and liver (85%, p = 0.0001) in rats of mycotoxicosis group (Figure 2), which suggests about activation of lipid peroxidation processes

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Summary

Introduction

Aflatoxin B1 (AFB1) is a mycotoxin produced by Aspergillus flavus and related fungi that grow in staple foods, including cereals and nuts, such as corn, rice and peanuts[1], especially in areas with appropriate conditions of moisture and heat where these fungi are ubiquitous. The toxicity of AFB1 has been shown to be associated with a wide range of pathological events, such as enhanced apoptosis and oxidative events. The aim of this study was to evaluate the potential ability of picolinyl-L-phenylalaninate (PLP), picolinyl-L-tryptophanate (PLT), and nicotinyl-L-tryptophanate (NLT) Schiff base amino acid derivatives to act against damaging effects of AFB1 using a rat model of mycotoxicosis. For this purpose, a range of markers of immune and antioxidant systems in liver and blood plasma samples, as well as the apoptotic rate in neutrophils and monocytes was assessed. The oral administration of Schiff base cyclic amino acid version 1 published 10 Aug 2017

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