Efficacy of methylprednisolone on T-2 toxin-induced cardiotoxicity in vivo: A pathohistological study

Antidotal Potency of the Novel, Structurally Different Adsorbents in Rats Acutely Intoxicated with the T-2 Toxin

“…Furthermore, in our previous studies, Mycosorb ® , Minazel-Plus ® , and Mycofix-plus ® , given in the same dose, showed a promising protective potential against the adverse influence of the T-2 toxin in rats [ 18 , 19 , 45 ]. Throughout this study, Mycosorb ® administered at the same dose of 1 g/kg p.o., shortly after treatment with the T-2 toxin, significantly reduced the LD 50 value ( Table 1 ), indicating that the applied dose was very safe and therapeutically effective only in case of T-2 poisoning.…”

“…Although the body mass and food and water consumption of the Minazel-Plus ® - and Mycofix-plus ® -treated rats were also markedly decreased in comparison with the control animals, it was still greater than in the group treated with the T-2 toxin only, especially during the last three weeks of the trial. When a relatively high single dose of the T-2 toxin was administered, a significant decrease in body weight and food and water consumption was observed compared with the control group [ 19 , 44 ]. This could be explained by the loss of appetite, complete feed refusal, and substantial lesions in the tunica mucosa of the gastrointestinal tract accompanied by prolonged bloody diarrhea, which prevented food and water intake and its utilization [ 45 , 54 , 55 ].…”

“…The ligands, mainly β-D-glucans, derived from the yeast cell’s wall, expressed the most potent functional efficiency in forming a complex with various mycotoxins in naturally or artificially contaminated animal feed [ 56 , 61 , 62 , 63 , 64 ]. It is assumed that the protective role of the applied organic adsorbent is a consequence of generating a tight biological complex with the T-2 toxin or its active metabolites, suppressing their negative impact on the gastric mucosal cells, and thus alleviating the production of pro-inflammatory substances [ 9 , 17 , 18 ] and the further release of reactive oxygen species and cytokines (TNF-α, IL-1, and IL-6) [ 21 , 65 , 66 ] as crucial mediators of oxidative stress and further development of the inflammatory reaction.…”

“…The oral intake of naturally infected food and feed with various toxic parts of Fusarium fungi can result in severe mycotoxicosis with signs of intoxication similar to T-2 toxin effects [ 8 , 9 , 10 , 11 , 12 ]. In humans and animals, the T-2 toxin causes general signs of the so-called shock-like syndrome, accompanied with emesis, lowered weight gain, lethargy, bloody diarrhea, gastric and intestinal disorders, haemorrhaging, immunosuppression, cardiomyopathy, and finally death [ 13 , 14 , 15 , 16 , 17 , 18 ]. Furthermore, similarly to acute radiation syndrome [ 19 , 20 , 21 ], inflammatory reaction, caused by the T-2 toxin, is a consequence of phospholipase A2 activation, successive prostaglandins, and reactive oxygen species (ROS) production [ 15 , 22 , 23 ].…”

“…In humans and animals, the T-2 toxin causes general signs of the so-called shock-like syndrome, accompanied with emesis, lowered weight gain, lethargy, bloody diarrhea, gastric and intestinal disorders, haemorrhaging, immunosuppression, cardiomyopathy, and finally death [ 13 , 14 , 15 , 16 , 17 , 18 ]. Furthermore, similarly to acute radiation syndrome [ 19 , 20 , 21 ], inflammatory reaction, caused by the T-2 toxin, is a consequence of phospholipase A2 activation, successive prostaglandins, and reactive oxygen species (ROS) production [ 15 , 22 , 23 ]. Intensive accumulation of ROS may lead to DNA damage, protein oxidation, and lipid peroxidation [ 24 , 25 , 26 ].…”