Abstract

The aims of the current study were to determine the half-lethal concentration of ochratoxin A (OTA) as well as the levels of lactate dehydrogenase release and DNA fragmentation induced by OTA in primary porcine fibroblasts, and to examine the role of α-tocopherol in counteracting its toxicity. Cells showed a dose-, time- and origin-dependent (ear vs. embryo) sensitivity to ochratoxin A. Pre-incubation for 3 h with 1 nM α-tocopherol significantly (P < 0.01) reduced OTA cytotoxicity, lactate dehydrogenase release and DNA damage in both fibroblast cultures. These findings indicate that α-tocopherol supplementation may counteract short-term OTA toxicity, supporting its defensive role in the cell membrane.

Highlights

  • Ochratoxin A (OTA) is a mycotoxin produced by Aspergillus and Penicillum species

  • We first investigated the LC50 of OTA after 24 h and 48 h of treatment in ear and embryo porcine fibroblasts and found that the LC50 differed between the two cell types

  • The fibroblasts derived from ear were the most sensitive to OTA cytotoxicity

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Summary

Introduction

Ochratoxin A (OTA) is a mycotoxin produced by Aspergillus and Penicillum species. It occurs in several agricultural products and causes diseases both in humans and animals [1]. OTA has been implicated in renal and hepatic toxicity, neurotoxicity, teratogenicity, and immunotoxicity [2], and it is considered by the International Agency for Research on Cancer as possibly carcinogenic (group 2B) to humans [3], making consistent exposure to OTA a cause of serious concern. OTA is responsible for acute, subchronic and chronic intoxications, and the effects, correlated with the latter two, are of major concern for financial losses in the agriculture and food industry [5]. The main clinical patterns associated with OTA intoxication in swine are impaired renal function, depression, anorexia, decreased weight gain and productivity [6]

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