Toxicopathological studies on the effects of T-2 mycotoxin and their interaction in juvenile goats

Abstract

Food and feeds contaminated with mycotoxins have been a threat to the rearing industry by causing some of the most fatal toxic reactions not only in the farm animals but also in humans who consume them. Toxicity to juvenile goats was induced by feed contamination with T-2 toxin (at 10 and 20 ppm dosage; group I and II, respectively). The toxicity impact was assessed on days 15 and 30 post treatment with respect to growth performance, oxidative stress, apoptotic studies and detailed pathomorphology. The study revealed that apart from the obvious clinical toxicosis (weakness, lethargy, and retardation in growth), the toxin fed groups also exhibited significant haematological (reduced hemoglobin, total leukocyte and thrombocyte counts) and biochemical changes (increased levels of oxidative stress markers with concomitant decrease in levels of serum and tissue catalase and superoxide dismutase). The pathomorphological and histological alterations suggested that the liver and intestine were the most affected organs. Ultra-structurally, varying degrees of degeneration, cytoplasmic vacuolations and pleomorphic mitochondria were observed in the hepatocytes and the enterocytes of the intestine. Kidney also revealed extensive degeneration of the cytoplasmic organelles with similar condensation of the heterochromatin whereas the neuronal degeneration was characterized by circular, whirling structures. In addition, the central vein and portal triad of the hepatocytes, cryptic epithelial cells of the intestine, MLNs in the lymphoid follicles, PCT and DCT of the nephronal tissues and the white pulp of the spleen exhibited extensive apoptosis. In this study, it was also observed that the expression of HSPs, pro-apoptotic proteins and pro-inflammatory cytokines were significantly upregulated in response to the toxin treatment. These results suggest that the pathogenesis of T-2 toxicosis in goats employs oxidative, apoptotic and inflammatory mechanisms.

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

“…On the other hand, organic adsorbents like Mycosorb ® have consequently been recommended as an alternative solution to adsorb numerous mycotoxins, including the T-2 toxin, but without spoiling the nutrient bioavailability or inducing adverse health effects in animals [ 56 ]. In agreement with other researchers, we observed [ 34 , 37 , 42 , 44 ] a significant lowering of the rats’ body weight and food and water consumption from the first week after the application of T-2 toxin. 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.…”

“…In this regard, we found typical clinical signs of intoxication in rats like vomiting, emesis, food refusal, diarrhea, decreased body surface temperature, lethargy, and weakness after 4 days of T-2 toxin administration at a single dose of 1.67 mg/kg p.o. Namely, the described clinical signs exhibited by the T-2 toxin-poisoned animals were similar to the symptoms reported earlier in calves [ 48 , 49 ], sheep [ 50 ], pigs [ 51 ], and goats [ 34 ]. Typical symptoms of T-2 toxicosis in lambs were expressed in the form of recurrent diarrhea associated with infection of the Eimeria species [ 50 ].…”

“…Partial or complete feed refusal, prolonged bloody diarrhea, and decreased gastrointestinal absorptive capacity were also registered in cattle [ 53 , 54 , 55 ]. Because of the complete refusal of feed, reduction of protein synthesis, and consequent weight loss, many organs were damaged, primarily the kidneys and liver, as well as the gastrointestinal and lymphatic tissue [ 4 , 34 ]. As noted by other scientists [ 42 , 44 ], we also observed a complete absence of previously mentioned clinical signs of T-2 toxin intoxication following the therapeutic administration of Mycosorb ® , Minazel-Plus ® , and Mycofix-plus ® over the whole research period.…”

“…There is a strong belief that T-2 toxic effects are a consequence of certain subcellular changes [ 4 , 5 , 30 , 31 ]. Thus, during a histopathology examination of the gastrointestinal tissue of rats, prominent mucosal lesions in an exceeding sort of petechiae and ulcerations were determined, presumably because of augmented capillary permeability and hemorrhages, and therefore a build-up of cells involved in inflammation was noted [ 32 , 33 , 34 ].…”

“…As mentioned earlier, these intensive gastric injuries are not only thanks to a local toxic effect [ 9 , 20 ], but to biliary excretion and enterohepatic recirculation of the T-2 and HT-2 toxins as well, [ 15 , 21 ] causing generalized toxic effects [ 34 ]. By providing the previously demonstrated mechanism of gastric toxicity induced by the T-2 toxin, an approach that supports the use of adsorbents seems to be rational.…”