Evaluating <i>SEPHS2</i> expression and glutathione peroxidase as biomarkers in recurrent pregnancy loss: a new insight
BACKGROUND: 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). AIM: To evaluate SEPHS2 gene expression and plasma GPX levels as prognostic biomarkers in women with idiopathic RPL and their association with oxidative imbalance. METHODS: 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). RESULTS: 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 < 0.001, 95% CI: 3.32-4.62). These findings indicate an association between increased SEPHS2 expression, reduced antioxidant activity, and recurrent pregnancy loss. CONCLUSION: Elevated SEPHS2 expression suggests disrupted selenoprotein-mediated antioxidant defense in RPL. SEPHS2 and GPX may serve as prognostic biomarkers.
Authors
- Nesma M. Elaraby (ORCID: https://orcid.org/0000-0001-5872-9134)
- Taghreed A. Shalabi (ORCID: https://orcid.org/0000-0001-6212-7021)
- F. Hashemipour Hassan
- Mai M. Shaker
- Eman Reda Galal
- Fatma Elzahraa Sobhy Ammar
Institutions
- National Human Genome Research Institute (US)
- Al-Azhar University (ID)
- Al Azhar University (QA)
Publication Details
- Journal
- Biomarkers
- Published
- 2026-04-16
- DOI
- https://doi.org/10.1080/1354750x.2026.2659525
- Primary Topic
- Selenium in Biological Systems
- Type
- article
- Field-Weighted Citation Impact
- 0.00