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.

中文翻译：

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丙烯酰胺诱导哺乳动物模型中骨结构的产前编程

摘要 丙烯酰胺（AA）是一种具有潜在致癌作用的化学物质。它在食品或动物食品中的存在源于其热处理。进行该实验是为了评估妊娠后半期怀孕母猪的 AA 暴露（3.0 毫克/千克体重/天）对后代骨骼发育的影响。作为模型动物，使用豚鼠。虽然新生儿足月体重不受母体 AA 治疗的影响，但在实验组中观察到骨较短，骨干横截面积减少。在股骨骨骺和干骺端以及关节和生长板软骨中观察到母体 AA 暴露的许多负面的后代性别依赖性影响。这些影响是由 AA 诱导的骨代谢改变引起的，如参与骨骼发育的众多蛋白质表达的变化所表明的：核因子κ-Β配体受体激活剂（RANKL）、金属蛋白酶组织抑制剂2（TIMP-2）、骨形态发生蛋白2（BMP-2）、血管内皮生长因子 (VEGF) 和软骨寡聚基质蛋白 (COMP)，它们的所有表达都被测量，并测定了未成熟胶原纤维的分布。根据结果​​，可以得出结论，怀孕母鼠暴露于 AA 对骨干中的致密骨结构、干骺端和骨骺中的骨小梁微结构以及关节和生长板软骨的结构产生负面影响。后代。AA 诱导的骨损伤增加了破骨细胞分化，正如通过 RANKL/OPG 比率的变化所观察到的那样，这反过来又通过降低其他蛋白质的表达来抑制成骨细胞功能。本研究的数据表明，母亲接触 AA 会导致出生后骨增加不足甚至骨丢失。