Abstract

The heat shock protein (Hsp70) level was assessed after 14 days of oral gavage-exposure to fumonisin B1 (FB1: 150 µg/animal/day), deoxynivalenol (DON: 30 µg/animal/day) and zearalenone (ZEN: 150 µg/animal/day), alone or in combinations (in additive manner: FD = FB1 + DON, FZ = FB1 + ZEN, DZ = DON + ZEN and FDZ = FB1 + DON + ZEN) in the liver, kidneys and lung of 24 adult male Wistar rats (n = 3/group). The liver was the most responsive tissue, as compared with kidney and lung. Except of DZ-treatment, mycotoxins elevated the Hsp70 levels in livers. The highest Hsp70-levels (≈ twofold) were in the DON, FD, FZ and FDZ treatments (additive effects). In the kidney, alterations (↑ ≈ twofold) were detected in ZEN, FD, FZ and DZ treatments. The least responsive organ was the lung (↑ only in FDZ, antagonistic effect). DON and ZEA exposures have altered the reduced glutathione concentration (↓) and glutathione peroxidase activity (↓) in the blood serum. The serum malondialdehyde level increased only after exposure to FD (synergistic effect), as compared with the DZ group (antagonistic effect). When the blood clinical chemistry was assessed, significant alterations were in alanine aminotransferase (80% increase in FDZ, antagonistic effect) and total protein (↓ ZEN). Results varied according to the organ, toxin type and interactions. Furthermore, oxidative stress was not the only key player behind the Hsp70 increase, in which another mechanism is suggested.

Highlights

  • Fusarium mycotoxins, namely deoxynivalenol (DON), fumonisins (FBs) and zearalenone (ZEN), are frequently occurring in animal feed (Gruber-Dorninger et al 2019)

  • We found several treatments to increase the Hsp70 level (P < 0.05), as compared with the control (Fig. 2)

  • Mycotoxin effects vary between the different cells, depending on the toxin types and their plausible interactions

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Summary

Introduction

Namely deoxynivalenol (DON), fumonisins (FBs) and zearalenone (ZEN), are frequently occurring in animal feed (Gruber-Dorninger et al 2019). Fusarium mycotoxins vary in disruption level on the cellular redox balance system; ZEN > F­ B1 > DON (El GolliBennour and Bacha 2011). The redox sensors, namely the heat shock proteins (Hsps), have remarkable cytoprotective mechanisms; they act as molecular chaperones In response to the different lethal stimuli, Hsp can increase the cellular survival chance by aiding the protein assembling and folding through mitigating the mitochondrial damage, nuclear fragmentation and stress-induced caspase-cascade (Jee 2016; Mosser et al 1997). The base of this anti-apoptotic effect is the socalled Hsp70-mediated modulation of the proteasome

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