Core Viewpoint - The latest research published in Nature reveals that maternal iron deficiency during pregnancy can lead to significant impacts on fetal sex development, specifically causing XY mouse embryos to develop ovaries instead of testes [2][14]. Group 1: Research Findings - The study conducted by a team from Osaka University demonstrates that iron, particularly ferrous ions (Fe²⁺), plays a crucial role in activating male sex determination genes [2][11]. - The Sry gene, located on the Y chromosome, is essential for male development and is activated during a specific time window in embryonic development [3][11]. - Iron metabolism is linked to the expression of the Sry gene, where iron deficiency leads to increased suppression of Sry expression due to epigenetic modifications [5][11]. Group 2: Mechanisms of Action - The research indicates that iron accumulates in key cells responsible for sex determination, with iron-related gene expression significantly higher in these cells compared to others [6][11]. - Experiments showed that blocking iron supply resulted in decreased Sry expression and a shift in XY embryos towards female characteristics [7][11]. - Maternal iron deficiency, induced through dietary means or iron chelation, resulted in a notable percentage of XY offspring exhibiting sex reversal [8][9][11]. Group 3: Implications for Human Health - The findings suggest that severe maternal iron deficiency could be an underrecognized environmental risk factor for certain cases of 46-XY disorders of sex development in humans [14]. - The study emphasizes the importance of adequate iron intake during pregnancy to prevent anemia and ensure proper fetal sex development [14]. - This research challenges traditional views on iron's role, highlighting its influence on gene expression and fetal development, thus calling for nutritional interventions during pregnancy [14].