Phytic Acid Exposure Alters AflatoxinB1‐Induced Reproductive and Oxidative Toxicity in Albino Rats (Rattus norvegicus)

Abdelaziz S. Abu El-Saad,Hamada M. Mahmoud

doi:10.1093/ecam/nem137

Abstract

The increased use of feed in Egypt's aquaculture and animal industries raises concerns about the possible presence of mycotoxins in feedstuffs. The use of alternative medicine, such as botanicals and nutritional supplements, has become popular with inflammatory cases. The present study aimed to testify the role played by phytic acid (IP6) in enhancing the reproductive and oxidative toxicity induced in aflatoxinB1 (AFB1) treated white male albino rats (Rattus norvegicus) throughout treatment and withdrawal periods. One hundred and twenty white male albino rats were grouped into four groups. Group 1, was injected with 300 μg kg−1 body wt of AFB1 once every 3 days for 15 days and left uninjected for another 15 days to study the withdrawal effect. Group 2, was injected with 300 μg kg−1 body wt of AFB1 once every 3 days for 15 days and treated simultaneously with IP6 daily for another 15 days. Group 3, was treated daily with IP6 (40 mg kg−1 body wt) for 15 days and with no treatment for other 15 days. Group 4, injected with equivalent volume of sterile phosphate buffer saline solution as a control group. Sera were taken at the experimental intervals and assayed for testosterone hormone, follicular-stimulating hormone (FSH) and luteinizing hormone (LH) to determine the toxicological impact of AFB1 and the possibility of amelioration by phytic acid on the reproductive performance of the studied animal. The effects of AFB1 treatment on the absolute and relative weight of testis as well as its histopathologic effect on the testis and the possibility of amelioration by IP6 treatment were evaluated. The activities of enzymatic and non-enzymatic anti-oxidants, in addition to lipid peroxidation were measured in the testis’ homogenate of AFB1-treated rats. A decrease in sex hormone levels, an increase in testicular lipid peroxidation product levels and a significant decrease in testicular glutathione content, catalase and total peroxidase and superoxide dismutase activities were recorded. The histopathologic alterations revealed a degeneration and highly mitotic division within the spermatogenic nuclei, in addition to some karyomegaly and nuclear pyknosis. It is concluded that the reduction in the toxicity of free radicals by phytic acid might be responsible for the protective influence observed.

Highlights

Numerous toxigenic fungi and their metabolites have been identified from a variety of substrates
The present study aimed to investigate the reproductive and oxidative toxicity induced in AFB1-treated white male albino rats (Rattus norvegicus) and to evaluate the role of phytic acid exposure as well as the withdrawal period, in inducing alterations on such toxicological impacts of AFB1
Testis absolute weight was significantly decreased as a result of administration of AFB1 and/or phytic acid at all experimental periods

Summary

Introduction

Numerous toxigenic fungi and their metabolites have been identified from a variety of substrates Most of these are produced by genera of Aspergilli, Peniallia and Fusaria and are most often isolated from cereal grains or corn, ß 2007 The Author(s). Mycotoxins are among the most common food contaminants in animal feed, causing great economic loss in animal mass production and aquaculture [1,2,3,4]. Luyendy et al [5], Cupid et al [6] and Meki et al [7,8] reported that aflatoxinB1 (AFB1) is a food contaminant fungal toxin that has been implicated as a causative agent in human acute hepatotoxicity, hepatic and extrahepatic carcinogenesis, due to the fact of its formation of AFB1-macromolecular adducts (AFB1-DNA and AFB1albumin). The oxidative damage has been postulated to play a major role in the mechanisms associated with AFB1-induced cytotoxicity and carcinogenicity in mammalian species and indicates that oxidation of AFB1 generates free radical species via the metabolic pathways and an iron-mediated redox mechanism [9]

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Conclusion