Evaluating <i>SEPHS2</i> expression and glutathione peroxidase as biomarkers in recurrent pregnancy loss: a new insight

Selenophosphate synthetase 2 (SEPHS2) activates selenophosphate, a donor for selenocysteine required for glutathione peroxidase (GPX) production. GPX protects placental tissue. Dysregulation of SEPHS2 and reduced GPX activity may contribute to oxidative stress–mediated placental dysfunction in recurrent pregnancy loss (RPL). To evaluate SEPHS2 gene expression and plasma GPX levels as prognostic biomarkers in women with idiopathic RPL and their association with oxidative imbalance. A total of 100 women with idiopathic RPL and 100 healthy women without history of RPL were included. SEPHS2 gene expression was quantified using quantitative reverse transcription polymerase chain reaction (qRT-PCR), and plasma GPX levels were measured using enzyme-linked immunosorbent assay (ELISA). SEPHS2 expression was significantly elevated in the RPL group compared with controls (mean fold change: 14 ± 11.4 vs. 5 ± 8), while plasma GPx levels were markedly reduced in women with RPL (5.57 ± 0.40 vs. 9.53 ± 3.28; P &lt; 0.001, 95% CI: 3.32–4.62). These findings indicate an association between increased SEPHS2 expression, reduced antioxidant activity, and recurrent pregnancy loss. Elevated SEPHS2 expression suggests disrupted selenoprotein-mediated antioxidant defense in RPL. SEPHS2 and GPX may serve as prognostic biomarkers. Lighting the importance of selenoproteins is vital for explaining the possible biological functions related to female reproductive efficacy and wellbeing.SEPHS2 and GPX could be used as prognostic markers for RPL.A decrease in GPX could be a cause of increased ROS among pregnant women, consequently causing progressive placental damage and pregnancy loss. Lighting the importance of selenoproteins is vital for explaining the possible biological functions related to female reproductive efficacy and wellbeing. SEPHS2 and GPX could be used as prognostic markers for RPL. A decrease in GPX could be a cause of increased ROS among pregnant women, consequently causing progressive placental damage and pregnancy loss.