Advances in the Effect of Mycotoxin on Lipid Peroxide and Antioxidant Status of Animals

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Mycotoxins".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 1478

Special Issue Editors


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Guest Editor
Department of Preventive Medicine and Public Health, Food Science, Toxicology and Forensic Medicine, University of Valencia, 46100 Valencia, Spain
Interests: mycotoxins; antioxidant activity; antifungal activity; lactic acid bacteria; biopreservation; simulated gastrointestinal digestion; bioaccessibility; bioavailability
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Guest Editor
Technical and RD Department, BIONTE NUTRITION, 43204 Reus, Spain
Interests: mycotoxins; animal nutrition; feed; oxidative stress; biomarkers of exposure; biomarkers of effect; feed additive; anti-mycotoxins agent

E-Mail Website
Guest Editor
Department of Preventive Medicine and Public Health, Food Science, Toxicology and Forensic Medicine, University of Valencia, 46100 Valencia, Spain
Interests: mycotoxins; in vitro toxicity; lactic acid bacteria; biopreservation; simulated gastrointestinal digestion; bioaccessibility; bioavailability

Special Issue Information

Dear Colleagues,

Mycotoxins are secondary fungal metabolites found as contaminants in agricultural commodities and feed. Mycotoxins are considered a major risk for animal health worldwide. Oxidative stress is behind the toxicity of mycotoxins. In fact, the imbalance between free radicals (ROS) and the antioxidant capacity of the animals can cause chemical damage to DNA, membranes, proteins and lipids. The generation of ROS (as superoxide anion, hydroxyl radical or perhydroxyl radical) activates p53, p38, mitogen-activated protein kinases (MAPKs), and caspases, up-regulates Bax expression and down-regulates the Bcl2 protein, inducing cell apoptosis. Furthermore, the overproduction of ROS may lead to the release of calcium and free iron into the cytoplasm, generating highly reactive radicals that damage DNA and membranes due to the polyunsaturated fatty acid residues of phospholipids contents. In turn, lipid peroxidation may also damage some organelles including peroxisomes, mitochondria, and the endoplasmic reticulum, causing detrimental changes in the main targets of ROS, involving the enzymatic systems of the electron-transport chain and antioxidant mechanisms as Nrf2, GPx, SOD and CAT expression. Therefore, the lipid peroxidation may also lead to cell apoptosis under a vicious cycle promoting ROS generation. Moreover, the production of ROS can promote the up-regulation of NF-ᴋB expression and the synthesis of pro-inflammatory cytokines, such as TNF, IL-1, IL-6, and IL-8, leading to ROS overproduction. Hence, the oxidative stress induced by mycotoxins is a harmful feedback process that increases the cellular damage and determines the toxicity of mycotoxins.

Prof. Dr. Giuseppe Meca
Dr. Insaf Riahi
Dr. Laura Escrivá Llorens
Guest Editors

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Keywords

  • mycotoxins
  • oxidative stress
  • apoptosis
  • lipid peroxidation
  • animal health

Published Papers (1 paper)

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Research

13 pages, 3351 KiB  
Article
Involvement of Autophagy and Oxidative Stress-Mediated DNA Hypomethylation in Transgenerational Nephrotoxicity Induced in Rats by the Mycotoxin Fumonisin B1
by Nouf Aldawood, Sarah Almustafa, Saleh Alwasel, Waleed Aldahmash, Abir Ben Bacha, Abdullah Alamri, Mohammad Alanazi and Abdel Halim Harrath
Toxins 2023, 15(11), 663; https://doi.org/10.3390/toxins15110663 - 17 Nov 2023
Viewed by 1224
Abstract
Fumonisin B1 (FB1), a mycotoxin produced by Fusarium verticillioides, is one of the most common pollutants in natural foods and agricultural crops. It can cause chronic and severe health issues in humans and animals. The aim of this study was to evaluate [...] Read more.
Fumonisin B1 (FB1), a mycotoxin produced by Fusarium verticillioides, is one of the most common pollutants in natural foods and agricultural crops. It can cause chronic and severe health issues in humans and animals. The aim of this study was to evaluate the transgenerational effects of FB1 exposure on the structure and function of the kidneys in offspring. Virgin female Wistar rats were randomly divided into three groups: group one (control) received sterile water, and groups two and three were intragastrically administered low (20 mg/kg) and high (50 mg/kg) doses of FB1, respectively, from day 6 of pregnancy until delivery. Our results showed that exposure to either dose of FB1 caused histopathological changes, such as atrophy, hypercellularity, hemorrhage, calcification, and a decrease in the glomerular diameter, in both the first and second generations. The levels of the antioxidant markers glutathione, glutathione S-transferase, and catalase significantly decreased, while malondialdehyde levels increased. Moreover, autophagy was induced, as immunofluorescence analysis revealed that LC-3 protein expression was significantly increased in both generations after exposure to either dose of FB1. However, a significant decrease in methyltransferase (DNMT3) protein expression was observed in the first generation in both treatment groups (20 mg/kg and 50 mg/kg), indicating a decrease in DNA methylation as a result of early-life exposure to FB1. Interestingly, global hypomethylation was also observed in the second generation in both treatment groups despite the fact that the mothers of these rats were not exposed to FB1. Thus, early-life exposure to FB1 induced nephrotoxicity in offspring of the first and second generations. The mechanisms of action underlying this transgenerational effect may include oxidative stress, autophagy, and DNA hypomethylation. Full article
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