Mycotoxicosis has long been studied in humans and animals. Zearalenone-induced mycotoxicosis poses a growing problem in companion animals and livestock. The objective of this study was to determine whether intoxication with low doses of zearalenone (ZEA) and its biotransformation in selected animal species affects hematological and serum biochemical indices, as well as endocrine, intracrine and immunohistochemical parameters. Materials and Methods. Experiment I was performed on 36 gilts with a body weight of ± 20 kg. Half of the animals (18 gilts) were administered ZEA at a daily dose of 40 ìg/kg BW, and the remaining gilts were the placebo group. The experiment lasted 42 days. The animals were slaughtered at the end of the experiment (day 42), and samples were collected for laboratory analyses. Experiment II was performed on 30 clinically healthy pre-pubertal beagle bitches aged 70 days, with the initial body weight of ± 8 kg. The dogs were randomly divided into two experimental groups (EI and EII) and a control group (C). The experimental groups were administered per os ZEA doses of 50 and 75 ìg/kg BW, respectively, for 42 days. The control group bitches were administered placebo. The animals were subjected to ovariohysterectomy at the end of the experiment. Results and Discussion. The type of cell death induced by ZEA was very difficult to define in both groups of animals. Cell apoptosis and/or necrosis is determined by the cell’s energy resources, which reflect the level of mitochondrial metabolic activity. ZEA-induced damage of the cell membrane probably reduced the mitochondrial membrane potential. The above led to a decrease in ATP levels, which play an important role in the cell death process. In the presence of a toxic substance, such as ZEA, cell apoptosis and/or necrosis can be induced by the same factor as part of the hormetic response. The death of the cells studied here was induced by excessive Ca²⁺ levels in the mitochondria, mitochondrial dysfunction and a decrease or loss of mitochondrial metabolic activity in oocytes, follicular cells and interstitial cells in the ovaries of experimental bitches and gilts. Low doses of ZEA reduced the number of ERβ receptors, the only receptors in the ovaries, which activated epigenetic modification mechanisms and inhibited ovarian development. The increase in E2 concentrations was proportional to the degree of intoxication, which resulted from specific enzymatic regulation in the presence of ZEA as a competitive substrate that modulates the activity of enzymes participating in estrogen biosynthesis at the pre-receptor level and very low concentrations of á-zearalenol due to slow biotransformation of ZEA. Hyperestrogenism was observed, and the hormetic threshold dose level was clearly exceeded in the experimental groups. No changes were found in the hematological and serum biochemical parameters of the gilts and bitches.
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