Chronic ingestion of deoxynivalenol‐contaminated diet dose‐dependently decreases the area of myenteric neurons and gliocytes of rats

Abstract

Background Deoxynivalenol (DON), a mycotoxin produced by Fusarium spp., is commonly found in cereals ingested by humans and animals. Its ingestion is correlated with hepatic, hematologic, renal, splenic, cardiac, gastrointestinal, and neural damages, according to dose, duration of exposure and species. In this work, the effects of the ingestion of DON‐contaminated diet at concentrations considered tolerable for human and animal intake were assessed. Methods Male Wistar rats aging 21 days were allotted to five groups that were given, for 42 days, diets contaminated with different concentrations of DON (0, 0.2, 0.75, 1.75, and 2 mg kg−1 of chow). Food ingestion, bodyweight, oxidative status and morphometric analyses of gliocytes, and neurons of jejunal myenteric ganglia were recorded. Key Results At these concentrations, there was no food rejection, decrease in bodyweight gain, changes in oxidative status, or loss of either neurons or gliocytes. However, DON decreased gliocyte area, general neuronal population, nitrergic, cholinergic and NADH‐diaphorase positive subpopulations and, as a result, ganglion area. Conclusions & Inferences It was concluded that, even in the absence of visible effect, DON exposure reduces cell body area of gliocytes and neurons of the myenteric plexus of the rat jejunum.

Mycotoxins and the Enteric Nervous System

“…During a study performed on male Wistar rats ( Rattus novergicus ) aged 21 days, the influence of relatively low doses of DON on the ENS was described [ 14 ]. In that experiment, DON in various doses (from 0.2 mg/kg of chow to 2 mg/kg of chow) was given for 42 days, and the ENS was studied using immunohistochemistry and microscopic analysis.…”

“…In that experiment, DON in various doses (from 0.2 mg/kg of chow to 2 mg/kg of chow) was given for 42 days, and the ENS was studied using immunohistochemistry and microscopic analysis. It was shown that this mycotoxin does not affect the myenteric ganglia organization in the jejunum [ 14 ]. Between control animals and rats receiving DON there were no differences in the density of glial cells located in the myenteric plexus, or the population density of myenteric neurons.…”

“…Between control animals and rats receiving DON there were no differences in the density of glial cells located in the myenteric plexus, or the population density of myenteric neurons. Moreover, DON did not change the density of particular subpopulations of the myenteric neurons, i.e., cholinergic and nitrergic neurons [ 14 ]. However, all concentrations of DON studied in the above-mentioned experiment caused a decrease in the area of the general population of the myenteric neuronal cells, as well as cholinergic and nitrergic cell neurons.…”

“…However, all concentrations of DON studied in the above-mentioned experiment caused a decrease in the area of the general population of the myenteric neuronal cells, as well as cholinergic and nitrergic cell neurons. Moreover, DON also decreased the area of gliocytes located in the myenteric plexus [ 14 ] and decreased the myenteric ganglia area. It should be noted that during the cited study, besides changes in the ENS, the animals did not show any other symptoms of toxicity, including a decrease in body weight, diarrhea, loss of appetite or changes in the oxidative status [ 14 ].…”

“…Since mycotoxins are present in food and drinking water, the gastrointestinal (GI) tract is the part of the body that first comes into contact with these toxic factors [ 8 ]. A relatively large number of studies have described mycotoxin-induced morphological and functional changes in the GI tract, whose character depends on the type of mycotoxin, mammal species studied, as well as the degree and length of exposure to mycotoxins [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 ]. The most common effects of mycotoxins on the GI tract include inflammatory and necrotic changes, disturbances in secretory activity and metabolism of the enterocytes, damage to the intestinal barrier and dysfunction in intestinal absorption [ 10 , 11 , 16 , 20 ].…”