Abstract

Ochratoxin A (OTA) is a powerful nephrotoxin and the severity of its damage to kidneys depends on both the dose and duration of exposure. According to the scientific data currently available, the mechanism of action still is not completely clarified, but it is supposed that oxidative stress is responsible for OTA-induced nephrotoxicity. Bioactive compound use has emerged as a potential approach to reduce chronic renal failure. Therefore, curcumin (CURC), due to its therapeutic effects, has been chosen for our study to reduce the toxic renal effects induced by OTA. CURC effects are 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. The end result of the experiment finds rats treated with OTA show alterations in biochemical and oxidative stress parameters in the kidney, related to a decrease in the Glomerular Filtration Rate (GFR). Conversely, the administration of CURC attenuates oxidative stress and prevents glomerular hyperfiltration versus the OTA group. Furthermore, kidney histological tests show a reduction in glomerular and tubular damage, inflammation and tubulointerstitial fibrosis. This study shows that CURC can mitigate OTA–induced oxidative damage in the kidneys of rats.

Highlights

  • Ochratoxin A (OTA) is a mycotoxin derived from the secondary metabolism of different fungi genera, in particular it originates from Aspergillus ochraceus, A. carbonarius, A. niger and Penicillium verrucosum, in tropical areas and in temperate climate regions, respectively [1]

  • The oral administration of OTA caused a significant reduction in body weights compared to the Control group at 7 and 14 days of treatment. (−16.1% and −22.2%, respectively)

  • The combination treatment with curcumin significantly attenuated the adverse effects of OTA after 14 days of treatment (5.1%)

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Summary

Introduction

Ochratoxin A (OTA) is a mycotoxin derived from the secondary metabolism of different fungi genera, in particular it originates from Aspergillus ochraceus, A. carbonarius, A. niger and Penicillium verrucosum, in tropical areas and in temperate climate regions, respectively [1]. OTA is often the cause of chronic toxicity, due to the prolonged intake of its small amounts, and manifests itself with carcinogenic, genotoxic, teratogenic, nephrotoxic and immunosuppressive effects [5,6,7] both on humans and numerous animal species. Added to an indirect contamination, which occurs with the ingestion by animals of naturally contaminated feed, subsequent passage, and accumulation of OTA in tissues (carry over), a direct contamination is possible. This kind of contamination is linked to the growth of molds producing OTA on the meat products

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