Deoxynivalenol

Infertility associated with dietary contaminants has raised increasing concern, particularly regarding the effects of mycotoxins such as deoxynivalenol (DON) and α-zearalenol (α-ZOL). These fungal metabolites are commonly found in food and known for their toxicological effects in both humans and animals. However, the impact of combined exposure to DON and α-ZOL at low concentrations on reproductive tissues remains poorly understood. This study aimed to evaluate the individual and combined effects of DON (10 μM) and α-ZOL (0.68 μM) on porcine reproductive tissues using an ex vivo model. Uterine and ovarian explants were collected from eight sows at slaughterhouses and incubated for 8 and 12 h, respectively. Samples were then subjected to histological and immunohistochemical analyses to assess tissue integrity, apoptosis (caspase-3), oxidative stress, and the expression of key markers including IL-10, TNF-α, E-cadherin, COX-2, VEGF, and sex hormone receptors (E1, P4). All treatments induced significant tissue damage compared to controls. In uteri, epithelial desquamation and increased caspase-3 expression were observed, along with decreased expression of cytokines, adhesion molecules, and hormone receptors. In the ovaries, follicular degeneration and altered E1 expression patterns were detected. The combined treatment led to more severe alterations and reduced antioxidant capacity, suggesting a synergistic toxic effect. These findings demonstrate that both uterine and ovarian tissues are vulnerable to DON and α-ZOL and that combined exposure exacerbates reproductive toxicity. The porcine ex vivo model proved to be a reliable tool for assessing the toxicological impact of environmental contaminants on reproductive health.

Deoxynivalenol (DON) contamination in animal feed threatens livestock health due to chronic low-dose exposure and masked forms. 15-acetyl-deoxynivalenol (15ADON), a major masked form, exhibits stronger toxicity than DON in cell models, yet in vivo data, particularly in poultry, remain scarce. To address this gap, 1-day-old chickens were fed diets containing 3 mg/kg DON, 3 mg/kg 15ADON, or a combination of 1.5 mg/kg each. Immunotoxicity and cecal microbiota were evaluated through immune parameters and 16S rRNA sequencing. To examine cumulative effects, chickens were also exposed to low-dose DON at different developmental stages. Both DON and 15ADON induced evident immunotoxicity, including immune organ damage. Compared with controls, 15ADON reduced antibody titers against infectious bronchitis and Marek's disease viruses by 30 % and IgM levels by 50 % during early immune development. Co-exposure produced no synergistic effects, whereas prolonged low-dose DON exposure initially enhanced antibody production but later caused a 20-50 % decline relative to controls. Microbiota analysis revealed an increased abundance of Lactobacillus in DON and 15ADON treated groups, while overall microbial richness and diversity remained unchanged. These findings demonstrate that 15ADON exerts comparable immunotoxicity to DON, highlight the importance of exposure timing and duration, and reveal masked mycotoxins as underappreciated risks in poultry production. Our results provide valuable in vivo evidence to support the reassessment of regulatory limits and further investigation into masked mycotoxin toxicity.