Abstract

Ochratoxin A (OTA) is a powerful mycotoxin found in various foods and feedstuff, responsible for subchronic and chronic toxicity, such as nephrotoxicity, hepatotoxicity, teratogenicity, and immunotoxicity to both humans and several animal species. The severity of the liver damage caused depends on both dose and duration of exposure. Several studies have suggested that oxidative stress might contribute to increasing the hepatotoxicity of OTA, and several antioxidants, including curcumin (CURC), have been tested to counteract the toxic hepatic action of OTA in various classes of animals. Therefore, the present study was designed to evaluate the protective effect of CURC, a bioactive compound with different therapeutic properties on hepatic injuries caused by OTA in rat animal models. CURC effects were examined in Sprague Dawley rats treated with CURC (100 mg/kg), alone or in combination with OTA (0.5 mg/kg), by gavage daily for 14 days. At the end of the experiment, rats treated with OTA showed alterations in biochemical parameters and oxidative stress in the liver. CURC dosing significantly attenuated oxidative stress and lipid peroxidation versus the OTA group. Furthermore, liver histological tests showed that CURC reduced the multifocal lymphoplasmacellular hepatitis, the periportal fibrosis, and the necrosis observed in the OTA group. This study provides evidence that CURC can preserve OTA-induced oxidative damage in the liver of rats.

Highlights

  • The oral administration of ochratoxin A (OTA) caused a significant increase in ALT, AST, and alkaline phosphatase (ALP) activities and caused a significant reduction in the concentration of total protein compared to the Control group (CONTROL) group after

  • The activities of superoxide dismutase (SOD), CAT, and glutathione peroxidase (GPx) were significantly decreased in the liver of OTA-treated rats in comparison to the CONTROL group

  • Cotreatment with curcumin group (CURC) showed a good recovery of SOD, CAT, and GPx activities compared to the OTA group

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Summary

Introduction

Oxidative stress has become a new hot spot in the context of mycotoxin mechanism of action [1]. Oxidative stress is hypothesized to be one of the main causes in the development of many disorders such as chronic kidney disease, hepatic inflammation, hypercholesterolemia, diabetes, and hepatic cirrhosis [2]. Oxidative stress involves an excessive production of free radicals, which, in turn, induce oxidative damage to cellular biomolecules, including proteins, lipids, and nucleic acids, in numerous tissues [3]. Several studies indicate that oxidative stress plays critical roles in the toxicity of ochratoxin A (OTA) [4,5]. More than 300 mycotoxins have been identified; 4.0/).

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