Prenatal exposure to aflatoxin B₁ (AFB₁) poses a significant risk to fetal development and is associated with reduced birth weight in humans. Experimental studies consistently show that AFB₁ induces fetal abnormalities, with skeletal malformations and ossification defects being the most common. However, the specific impact of AFB₁ on fetal osteogenesis remains unclear. Given this knowledge gap, this study aimed to review the existing literature concerning the pathogenesis of AFB₁ and its potential influence on bone development. The primary mechanisms implicated in AFB₁’s impact on bone include dysfunction in vitamin D and calcium metabolism, alterations in parathyroid hormone production and function, induction of inflammatory responses, and oxidative stress. Collectively, these mechanisms have the potential to impair osteoblast and osteoclast function and, consequently, compromise ossification. Based on these findings, studies should explore and elucidate the effects of AFB₁. Elucidating these mechanisms is crucial for mitigating the deleterious impacts of AFB₁ on fetal skeletal development.

Aflatoxin (AF) exposure during pregnancy may compromise maternal health and fetal development. This study aimed to evaluate the effects of gestational exposure to AF in pregnant Wistar rats and the mitigating effect of a functional yogurt (FY) containing inactivated biomass of Lacticaseibacillus rhamnosus and Saccharomyces cerevisiae. Animals were exposed to total AF (sum AFB₁, AFB₂, AFG₁ and AFG₂: 1.0 mg/kg/day) from gestational day (GD) 6 to 15, with or without FY supplementation. Maternal and reproductive parameters, fetal development, cranial ossification and placental growth factor (PlGF) immunostaining were evaluated, along with determination of AF metabolites in maternal and fetal samples. AF exposure reduced maternal weight gain during GD6–GD15 and fetal weight at GD20. Delayed cranial ossification occurred in 51.4 and 15.6% of fetuses in AF and AF + FY groups, respectively, with most severe alterations occurring in the AF group. Serum aflatoxin M₁ (AFM₁) concentrations were lower (p = 0.002) in AF + FY than in AF groups. AF metabolites were quantified less frequently in maternal liver from FY-supplemented animals (p = 0.015), while placentas or fetal livers from the AF + FY group had no quantifiable levels of AF metabolites. PlGF immunostaining was highest in AF group and lowest in the FY group (p = 0.0007). In conclusion, FY containing L. rhamnosus and S cerevisiae biomasses attenuated some AF-induced effects on fetal development, particularly delayed cranial ossification.