Individual and combined haematotoxic effects of fumonisin B(1) and T-2 mycotoxins in rabbits

Food Chem Toxicol. 2014 Oct:72:257-64. doi: 10.1016/j.fct.2014.07.025. Epub 2014 Aug 1.

Abstract

Weaned rabbits were fed diets contaminated with 2 mg/kg diet T-2 toxin alone, or 10 mg/kg diet fumonisin B1 (FB1) alone, and both toxins in combination (2+10 mg/kg, resp.), as compared to a toxin free control. Samplings were performed after 2 and 4 weeks. Bodyweight of the T-2 fed group was lower after 4 weeks; the liver weight increased dramatically. Red blood cell (RBC) Na(+)/K(+) ATPase activity decreased after 4 weeks in the T-2 group, it increased in the FB1 group and antagonism was found by the combined treatment. The RBC membrane fatty acid profile was modified by both toxins similarly during the entire feeding. After 4 weeks T-2 alone and in combination (with FB1) was found to increase mean cell volume (MCV). The time-dependent alterations in the T-2 group were significant for MCV (increase) and the mean cell haemoglobin (increase). The active monovalent cation transport was altered by both mycotoxins. Most probably FB1 exerts its sodium pump activity modification via an altered ceramide metabolism (behenic acid decrease in the RBC membrane), while for T-2 toxin a moderate membrane disruption and enzyme (protein) synthesis inhibition was supposed (ca. 75% decrease of the sodium pump activity).

Keywords: Co-occurrence; Fatty acids; Mycotoxins; Red blood cell membrane; Sodium pump.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animal Feed
  • Animals
  • Body Weight / drug effects
  • Cell Membrane / chemistry
  • Erythrocytes / drug effects*
  • Erythrocytes / enzymology
  • Fatty Acids / chemistry
  • Fumonisins / toxicity*
  • Fusarium / chemistry
  • Liver / drug effects*
  • Male
  • Organ Size / drug effects
  • Rabbits
  • Sodium-Potassium-Exchanging ATPase / metabolism
  • T-2 Toxin / toxicity*

Substances

  • Fatty Acids
  • Fumonisins
  • fumonisin B1
  • Sodium-Potassium-Exchanging ATPase
  • T-2 Toxin