Acrylamide-Induced Prenatal Programming of Bone Structure in Mammal Model

Abstract

Abstract Acrylamide (AA) is a chemical substance with a potentially carcinogenic effect. Its presence in food or animal food arises from its thermal processing. The experiment was conducted to evaluate the effect of AA exposure (3.0 mg/kg. b.w./day) of pregnant dams during the second half of the pregnancy on bone development in offspring. As an model animal, guinea pig was used. While term body weight of newborns was not influenced by maternal AA treatment, shorter bones with reduced bone diaphysis cross-sectional area were observed in experimental group. Numerous negative, offspring sex-dependent effects of maternal AA exposure were observed in femoral epiphysis and metaphysis as well as the articular and growth plate cartilages. These effects resulted from the AA-induced alterations in bone metabolism, as indicated by the changes in the expression of numerous proteins involved in bone development: receptor activator of nuclear factor kappa-Β ligand (RANKL), tissue inhibitor of metalloproteinases 2 (TIMP-2), bone morphogenetic protein 2 (BMP-2), vascular endothelial growth factor (VEGF), and cartilage oligomeric matrix protein (COMP), all of whose expression was measured as well as distribution of immature collagen fibres was determined. Based on the results, it can be concluded that the exposure of pregnant dams to AA negatively affected the structure of compact bone in bone diaphysis, microarchitecture of trabecular bone in metaphysis and epiphysis as well as the structure of the articular and growth plate cartilages in their offspring. The AA-induced bone impairment increased osteoclast differentiation, as observed through the change in the RANKL/OPG ratio, which in turn inhibited osteoblast function by decreasing the expression of other proteins. The data of the present study suggests that maternal AA exposure can result in insufficient bone gain and even bone loss after the birth.