ArticleThe Journal of reproduction and development2013
Oxidative stress produced by xanthine oxidase induces apoptosis in human extravillous trophoblast cells.
Article in The Journal of reproduction and development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Oxidative Stress in Pathogenesis of Preeclampsia: Mechanistic and Clinical Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Association between the serum uric acid-to-creatinine ratio index and the risk of preeclampsia in advanced maternal age pregnant women: a retrospective cohort study.Frontiers in cardiovascular medicine · 2026Article
- Oxidative Stress and Inflammation in Uterine-Vascular Adaptation During Pregnancy.Antioxidants (Basel, Switzerland) · 2025Review
- Effects of Molybdenum Supplementation in the Form of Ammonium and Sodium Salts on Trophoblast Cell Physiology and Gene Expression In Vitro.Journal of developmental biology · 2025Article
- The Role of Xanthine Oxidase in Pregnancy Complications: A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- HSPB8 binding to c-Myc alleviates hypoxia/reoxygenation-induced trophoblast cell dysfunction.Experimental and therapeutic medicine · 2024Article
- Temporal change of serum xanthine oxidase levels and its relation to clinical outcome of severe traumatic brain injury: a prospective cohort study.Neurosurgical review · 2023Article
- Assessment of Oxidative Stress-Induced Oral Epithelial Toxicity.Biomolecules · 2023Article
- Does the Micronutrient Molybdenum Have a Role in Gestational Complications and Placental Health?Nutrients · 2023Review
- Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia.Current hypertension reports · 2022Review
- Organometallic Folate Gold Nanoparticles Ameliorate Lipopolysaccharide-Induced Oxidative Damage and Inflammation in Zebrafish Brain.ACS omega · 2022Article
- MiR-133b regulates oxidative stress injury of trophoblasts in preeclampsia by mediating the JAK2/STAT3 signaling pathway.Journal of molecular histology · 2021Article
- Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications.Antioxidants (Basel, Switzerland) · 2021Review
- Tert-Butyl Hydroperoxide Stimulated Apoptosis Independent of Prostaglandin EReproductive sciences (Thousand Oaks, Calif.) · 2020Article
- Hydroxychloroquine Mitigates the Production of 8-Isoprostane and Improves Vascular Dysfunction: Implications for Treating Preeclampsia.International journal of molecular sciences · 2020Article
- Notoginsenoside R1 Protects Against the Acrylamide-Induced NeurotoxicityFrontiers in pharmacology · 2020Article
- High glutathionylation of placental endothelial nitric oxide synthase in preeclampsia.Redox biology · 2019Article
- New Insights into the Process of Placentation and the Role of Oxidative Uterine Microenvironment.Oxidative medicine and cellular longevity · 2019Review
- Oxidative Stress in Preeclampsia and Placental Diseases.International journal of molecular sciences · 2018Review
- Emerging Treatment Models in Rheumatology: Antiphospholipid Syndrome and Pregnancy: Pathogenesis to Translation.Arthritis & rheumatology (Hoboken, N.J.) · 2017Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress has been recognized as an important factor in the pathophysiology of preeclampsia. It has been reported that the expression of xanthine oxidase (XO) in the cytotrophoblast and plasma hydrogen peroxide (H(2)O(2)) level are significantly higher in preeclamptics than in control women. The aim of this study was to clarify the biological influence of reactive oxygen species (ROS) produced by XO on extravillous trophoblast (EVT) cells. TCL1 cells, a human immortalized EVT cell line, were incubated with xanthine and XO (X/XO). We then measured the cell number, urate level of the culture media and the apoptotic cell ratio. Similar experiments were performed with additional administration of allopurinol, catalase, L-NAME or D-NAME, and with administration of H(2)O(2) in substitution for X/XO. We assessed the effects of H(2)O(2) on invasion ability, tube-like formation and protein expression of HIF1A and ITGAV of TCL1. Finally, the apoptotic cell ratio using primary cultured trophoblasts was measured following exposure to H(2)O(2). X/XO decreased the relative cell number and increased the urate level and apoptotic cell ratio significantly. Elevation of the urate level and apoptotic cell ratio was attenuated by allopurinol and catalase, respectively. L-NAME and D-NAME had no influence on these effects. H(2)O(2) also decreased the relative cell number. Pretreatment with H(2)O(2) significantly inhibited the invasion ability, tube-like formation and HIF1A and ITGAV of TCL1. H(2)O(2) also induced apoptosis in primary cultured trophoblasts. In conclusion, ROS produced by XO induced apoptosis and affected EVT function including invasion and differentiation.
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