ArticleToxicology and applied pharmacology2015
Phosphoramide mustard exposure induces DNA adduct formation and the DNA damage repair response in rat ovarian granulosa cells.
Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 64 citations in OpenAlex.
- SPATA22 heterozygous variants drive premature ovarian insufficiency: mechanism of granulosa cells dysfunction and therapeutic potential of N-acetylcysteine (NAC) treatment.Reproductive biology and endocrinology : RB&E · 2026Article
- BMSCs regulate RGS3 expression in ovarian stromal cells to improve ovarian stromal fibrosis and angiogenic microenvironment in cyclophosphamide-induced premature ovarian failure.Stem cell research & therapy · 2026Article
- Exosomes in oncofertility: emerging roles in chemotherapy-induced reproductive damage and fertility preservation.Reproduction & fertility · 2026Review
- Targeting a novel tamoxifen-using pathway to preserve ovarian reserve in rats with experimental chemotherapy-induced ovarian failure.BMC pharmacology & toxicology · 2026Article
- Inflammatory bowel disease leads to long-term ovarian dysfunction via immune-mediated follicular aging.Cellular and molecular life sciences : CMLS · 2026Article
- The role of mesenchymal stem cells and quercetin in preserving fertility in prepubertal male mice exposed to cyclophosphamide.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Prolonged Low-Dose Administration of FDA-Approved Drugs for Non-Cancer Conditions: A Review of Potential Targets in Cancer Cells.International journal of molecular sciences · 2025Review
- Metformin protects prepubertal mice ovarian reserve against cyclophosphamide via regulation of the PI3K/Akt/mTOR signaling pathway and Yap-1.Journal of ovarian research · 2024Article
- Article
- TP63 truncating mutation causes increased cell apoptosis and premature ovarian insufficiency by enhanced transcriptional activation of CLCA2.Journal of ovarian research · 2024Article
- Therapeutic potential of bone marrow mesenchymal stem cells in cyclophosphamide-induced infertility.Frontiers in pharmacology · 2023Article
- Premature ovarian insufficiency: a review on the role of oxidative stress and the application of antioxidants.Frontiers in endocrinology · 2023Review
- Low dosage use of cyclophosphamide improves the survival of patients with systemic lupus erythematosus.Clinical rheumatology · 2022Article
- Protective effects of a SIRT1 inhibitor on primordial follicle activation and growth induced by cyclophosphamide: insights from a bovine in vitro folliculogenesis system.Journal of assisted reproduction and genetics · 2022Article
- The Role of Mutant p63 in Female Fertility.International journal of molecular sciences · 2021Review
- After cyclophosphamide exposure, granulosa cells recover their anti-müllerian hormone-producing ability but not their numbers.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2021Article
- Determination of OHeliyon · 2021Article
- TRDMT1 participates in the DNA damage repair of granulosa cells in premature ovarian failure.Aging · 2021Article
- Synthesis of cyclophosphamide metabolites by a peroxygenase from Marasmius rotula for toxicological studies on human cancer cells.AMB Express · 2020Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Phosphoramide mustard (PM), the ovotoxic metabolite of the anti-cancer agent cyclophosphamide (CPA), destroys rapidly dividing cells by forming NOR-G-OH, NOR-G and G-NOR-G adducts with DNA, potentially leading to DNA damage. A previous study demonstrated that PM induces ovarian DNA damage in rat ovaries. To investigate whether PM induces DNA adduct formation, DNA damage and induction of the DNA repair response, rat spontaneously immortalized granulosa cells (SIGCs) were treated with vehicle control (1% DMSO) or PM (3 or 6μM) for 24 or 48h. Cell viability was reduced (P<0.05) after 48h of exposure to 3 or 6μM PM. The NOR-G-OH DNA adduct was detected after 24h of 6μM PM exposure, while the more cytotoxic G-NOR-G DNA adduct was formed after 48h by exposure to both PM concentrations. Phosphorylated H2AX (γH2AX), a marker of DNA double stranded break occurrence, was also increased by PM exposure, coincident with DNA adduct formation. Additionally, induction of genes (Atm, Parp1, Prkdc, Xrcc6, and Brca1) and proteins (ATM, γH2AX, PARP-1, PRKDC, XRCC6, and BRCA1) involved in DNA repair were observed in both a time- and dose-dependent manner. These data support that PM induces DNA adduct formation in ovarian granulosa cells, induces DNA damage and elicits the ovarian DNA repair response.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.