Abstract

Simple SummaryCereal, which is the main ingredient of animal feed, is often contaminated with mold, which produces heat-resistant, carcinogenic, and harmful metabolites/toxins called fumonisins. Feed contamination with fumonisins is a worldwide problem; however, the dietary intake of fumonisins is difficult to estimate because their concentrations in many products are unknown. The effects of consuming fumonisin-contaminated feed on animal health are not fully known, and the economic losses that are related to health care or animal husbandry are difficult to calculate as fumonisins are found commonly in foods, including those that are intended for infants or pregnant dams. The involuntary intake of moldy feed leads to a serious health risk with long-term effects. The research on prenatal exposure to fumonisins is limited. Previous studies have shown that prenatal fumonisins exposure causes abnormalities in the bone and enteric nervous system development. Therefore, it is very important to study the effects of prenatal exposure to fumonisins on the general development of offspring at different periods of life, including weaning.Cereals are often contaminated with fumonisins, which are the toxic byproducts of mold. The aim of the study was to determine the effect of maternal exposure to fumonisins on the development and the liver function of the offspring at weaning. Two doses of fumonisins (60 and 90 mg/kg b.w.) were tested. The changes in the basal blood morphology, the biochemical parameters, the absolute and relative weights of the vital organs, and the changes in the cardiac and biceps brachii muscle histology were studied. The liver damage was assessed by evaluating the liver morphology and the common clinical liver panel. Maternal fumonisin intoxication caused a decrease in the body weight at birth and an increase in the heart, liver, kidney, lungs, ovaries, and testes weights. The cytokines and hormones, as well as the red blood cell counts and hemoglobin levels, were elevated in a dose-dependent manner following the exposure to fumonisins. Maternal exposure caused degenerative morphological and structural changes in the liver, as well as inflammation in the striated muscles, such as the heart and biceps brachii, and disproportionate development of the rat offspring in a dose-dependent manner. Moreover, FB exposure resulted in the disproportional development of the rat offspring in a dose-dependent manner, which was probably caused by the bodily hormonal dysregulation. Prenatal fumonisin exposure can be a pathological precursor for serious diseases, such as obesity and diabetes, later in life.

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