RESUMO
Selenium deficiency has been considered to increase the risk of gestational complications. Our previous work showed that maternal selenium deficiency suppressed proliferation, induced autophagy dysfunction, and apoptosis in the placenta of mice. However, other effects of maternal selenium deficiency on the placenta and the underlying mechanisms remain unclear. In the present study, dietary selenium deficiency in dams significantly suppressed glutathione peroxidase (GSH-Px) activity, total antioxidant capacity (T-AOC), and increased malondialdehyde (MDA) content in the placentae, confirming the oxidative stress in the placenta. By transcriptome sequencing analysis, the DEGs were involved in many biological processes, including ion transport, lipid metabolic process, immune response, transmembrane transport, and others. According to the KEGG analysis, the DEGs were primarily enriched in metabolic pathways, PI3K-Akt signaling pathway, and others. Among these, the steroid hormone biosynthesis pathway enriched the most DEGs. Hsd3b1, an ER enzyme involved in progesterone synthesis, was validated downregulated. Consistently, the progesterone content in the serum of the selenium-deficient group was decreased. Ion transporters and transmembrane transporters, such as Heph, Trf, Slc39a8, Slc23a1, Atp7b, and Kcnc1, were reduced in the selenium-deficient placentae. Immune response-related genes, including Ccl3, Ccl8, Cxcl10, and Cxcl14, were increased in the selenium-deficient placentae, along with an increase in macrophage number. These results suggested that maternal selenium deficiency may impair progesterone biosynthesis, reduce nutrient transporters expression, and promote immune response by increasing the oxidative stress of the placentae. This present study provides a novel insight into the possible cause of placenta disorder during pregnancy.
