Iron homeostasis: effects of different levels of protein iron on placental iron handling in sows.

Pregnant sows suffer from iron deficiency; however, excessive iron supplementation can induce tissue damage through ferroptosis. This study aimed to identify the optimal iron supplementation dose for gestating sows and investigate the mechanisms underlying iron deficiency and overdose, which contribute to reduced reproductive performance in sows. 84 sows with similar farrowing times were selected and stratified by body weight at day 85 of gestation. They were randomly assigned to one of three dietary treatments (n=28 per treatment): basal diet (L-Iron), basal diet supplemented with 0.13% protein iron (N-Iron) or 0.27% protein iron (H-Iron). Obviously, the rate of live-born piglets and placental vascular development in the N-Iron group were significantly higher than those in the l-Iron and H-Iron groups. Further analysis revealed that the expression levels of Transferrin (TF) and Transferrin receptor 1(TFR1) in the placenta of the H-Iron group were significantly reduced, while the expression levels of ferritin and nuclear receptor coactivator 4 were significantly increased. Importantly, the expression levels of lipid peroxidation and inflammatory markers such as lysophosphatidylcholine acyltransferase 3 and tumor necrosis factor-α were also significantly increased in the H-Iron group. In summary, our results indicate that supplementation of iron at an appropriate dose in iron-deficient pregnant sows promotes iron transfer between the sow and piglets and supports placental vascularization. Conversely, excessive iron supplementation leads to iron accumulation in the placenta, causing lipid peroxidation and mitochondrial damage, ultimately reducing the number of liveborn piglets.