Protective effect of modified glucomannans and organic selenium against antioxidant depletion in the chicken liver due to T-2 toxin-contaminated feed consumption Julia E. Dvorska a , Athanasios C. Pappas b , Filiz Karadas c , Brian K. Speake b , Peter F. Surai b,d, ⁎ a Sumy National University, Sumy, Ukraine b Avian Science Research Centre, SAC, Scotland, UK c Department of Animal Science, Faculty of Agriculture, University of Yuzuncu Yil, Van, Turkey d Department of Nutrition, Sant-Istvan University, Godollo, Hungary Received 17 September 2006; received in revised form 4 February 2007; accepted 4 February 2007 Available online 12 February 2007 Abstract The aim of this work was to assess the effect of T-2 toxin on the antioxidant status of the chicken and to study possible protective effects of modified glucomannan (Mycosorb™) and organic selenium (Sel-Plex™). Inclusion of T-2 toxin in the chickens' diet (8.1 mg/kg for 21 days) was associated with significant decreases in the concentrations of selenium (Se)(by 32.2%), α-tocopherol (by 41.4%), total carotenoids (by 56.5%), ascorbic acid (by 43.5%) and reduced glutathione (by 56.3%) in the liver, as well as a decrease in the hepatic activity of Se-dependent glutathione peroxidase (Se-GSH-Px) (by 36.8%). However, inclusion of modified glucomannans into the T-2 toxin-contaminated diet provided a partial protection against the detrimental effects of the mycotoxin on the antioxidant defences in the chicken liver. For example, the Se concentration in the liver was restored completely, although the Se-GSH-Px activity in the liver increased to only 81% of its control value. These protective effects of modified glucomannas were associated with a 45% reduction of lipid peroxidation in the liver in comparison to the effects of T-2 toxin alone. A combination of modified glucomannas with organic Se was shown to provide further protection against toxin-induced antioxidant depletion and lipid peroxidation in the chicken liver. Thus, the data clearly indicate a major protective effect of the mycotoxin-binder in combination with organic Se against the detrimental consequences of T-2 toxin-contaminated feed consumption by growing chickens. © 2007 Elsevier Inc. All rights reserved. Keywords: Antioxidants; Chicken; Glucomannan; Mycotoxin; Peroxidation; Selenium; T-2 toxin 1. Introduction Mycotoxin contamination of various feed and food com- modities is a global problem (Schollenberger et al., 2006). More than 300 mycotoxins have been characterised (Fink-Gremmels, 1999) and this number is growing quickly. The trichothecene group of mycotoxins accounts for over one hundred fungal metabolites, of which T-2 toxin, produced by the Fusarium fungus, was the first to be studied (Leeson et al., 1995; Bondy and Pestka, 2000). The adverse effects of trichothecene toxins on animal health is expressed in a diverse range of symptoms including skin lesions, immunosuppression, hepatotoxicity, nephrotoxicity, neurotoxicity, genotoxicity and even death (Hollinger and Ekperigin, 1999). Recently four major molecular mechanisms of mycotoxin toxicity, including T-2 toxin, were suggested (Surai, 2006): 1) inhibition of DNA, RNA and protein synthesis simultaneously with direct damage to DNA; 2) promotion of lipid peroxidation; 3) promotion of apoptosis and 4) effect on gene expression. While a variety of different strategies to combat mycotox- icosis have been developed, the most promising are based on the addition of adsorbents to contaminated feed. The adsorbent material selectively binds mycotoxins during digestion, pre- venting their absorption from the gastrointestinal tract, thereby decreasing the toxic effects (Devegowda et al., 1998; Chowdh- ury and Smith, 2005; Karaman et al., 2005). Of several different Comparative Biochemistry and Physiology, Part C 145 (2007) 582 – 587 www.elsevier.com/locate/cbpc ⁎ Corresponding author. Avian Science Research Centre, SAC, Scotland, UK. Tel.: +44 7808812073; fax: +44 1780 764505. E-mail address: psurai@alltech.com (P.F. Surai). 1532-0456/$ - see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.cbpc.2007.02.005