ArticleJournal of ovarian research2026
Sphingosine-1-phosphate mitigates radiation-induced ovarian injury in rats by suppressing ferroptosis via activating the Nrf2-GCLC-GPX4 axis.
Article in Journal of ovarian research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOvarian tissue is highly sensitive to ionizing radiation; even low-dose exposure can lead to premature ovarian failure and infertility. However, the molecular mechanisms underlying radiation-induced ovarian damage and potential protective interventions remain incompletely defined.
methodsUsing a rat model of abdominal irradiation, we investigated whether sphingosine-1-phosphate (S1P) protects against radiation-induced ovarian injury by modulating ferroptosis. Rats were pretreated with S1P, with or without the glutamate-cysteine ligase catalytic subunit (GCLC) inhibitor L-buthionine sulfoximine (BSO) or the ferroptosis inhibitor ferrostatin-1 (Fer-1). Ovarian histopathology, follicle counts, serum hormone levels, inflammatory and oxidative stress markers, and ferroptosis-related proteins were analyzed.
resultsS1P treatment significantly alleviated radiation-induced structural and functional ovarian damage by preserving ovarian architecture, increasing follicle number (notably primordial follicles), normalizing serum hormone levels, and reducing inflammatory cytokines. Mechanistically, S1P mitigated mitochondrial injury and oxidative stress by decreasing iron accumulation, lipid peroxidation, and reactive oxygen species (ROS) levels, while restoring glutathione (GSH), superoxide dismutase (SOD), and mitochondrial membrane potential. Mechanistically, S1P enhanced the expression of GCLC and glutathione peroxidase 4 (GPX4), suppressed transferrin receptor 1 (TfR1) expression, and transiently activated nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. Pharmacological inhibition of GCLC by BSO abolished these protective effects, confirming the essential role of the Nrf2-GCLC-GPX4 axis in regulating ferroptosis and redox balance.
conclusionsS1P protects against radiation-induced ovarian injury by suppressing ferroptosis through upregulation of GCLC and GPX4 downstream of Nrf2 activation. These findings identify S1P as a potential therapeutic agent for preserving ovarian function during radiotherapy and highlight the GCLC-GSH-GPX4 pathway as a critical target for ovarian radioprotection.
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