ArticleThe Biochemical journal2002
Selenium deficiency increases the expression of inducible nitric oxide synthase in RAW 264.7 macrophages: role of nuclear factor-kappaB in up-regulation.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.
- Contribution of oxidative stress in the mechanisms of postoperative complications and multiple organ dysfunction syndrome.Redox report : communications in free radical research · 2021Pooled it
- The effect of selenium supplementation on disease activity and immune-inflammatory biomarkers in patients with mild-to-moderate ulcerative colitis: a randomized, double-blind, placebo-controlled clinical trial.European journal of nutrition · 2023Trial
- Wound Healing Potential of Selenium and Nanoselenium.Biological trace element research · 2026Review
- Immune aging impairs muscle regeneration via macrophage-derived anti-oxidant selenoprotein P.EMBO reports · 2025Article
- The Modulatory Effect of Selol (Se IV) on Pro-Inflammatory Pathways in RAW 264.7 Macrophages.International journal of molecular sciences · 2025Article
- Recent advances in understanding oxidative stress in sepsis: pathogenic roles and antioxidant therapeutic prospects - a narrative review.Frontiers in pharmacology · 2025Review
- Selenium elicited an enhanced anti-inflammatory effect in primary bovine endometrial stromal cells with high cortisol background.BMC veterinary research · 2024Article
- Exploring the role of antioxidants in sepsis-associated oxidative stress: a comprehensive review.Frontiers in cellular and infection microbiology · 2024Review
- Selective Impact of Selenium Compounds on Two Cytokine Storm Players.Journal of personalized medicine · 2023Article
- Hydroxy-Selenomethionine, an Organic Selenium Source, Increases Selenoprotein Expression and Positively Modulates the Inflammatory Response of LPS-Stimulated Macrophages.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- Therapeutic Benefits of Selenium in Hematological Malignancies.International journal of molecular sciences · 2022Review
- The Role of Selenium in Pathologies: An Updated Review.Antioxidants (Basel, Switzerland) · 2022Review
- The Effects of Selenium on Bone Health: From Element to Therapeutics.Molecules (Basel, Switzerland) · 2022Review
- Zinc and Selenium in Inflammatory Bowel Disease: Trace Elements with Key Roles?Biological trace element research · 2021Review
- Systemic treatment with alpha-tocopherol and/or sodium selenite decreases the progression of experimental periodontitis.Clinical oral investigations · 2021Article
- Macrophage Selenoproteins Restrict Intracellular Replication ofFrontiers in immunology · 2021Article
- Associations between Trace Elements and Cognitive Decline: An Exploratory 5-Year Follow-Up Study of an Elderly Cohort.International journal of environmental research and public health · 2020Article
- Understanding the Redox Biology of Selenium in the Search of Targeted Cancer Therapies.Antioxidants (Basel, Switzerland) · 2020Review
- Simultaneous detection of the enzyme activities of GPx1 and GPx4 guide optimization of selenium in cell biological experiments.Redox biology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The inducible isoform of nitric oxide synthase (iNOS) is implicated in atherosclerosis, malignancy, rheumatoid arthritis, tissue and reperfusion injuries. A key determinant of the pro-oxidant versus protective effects of NO is the underlying redox status of the tissue. Selenoproteins, such as glutathione peroxidases (GPxs) and thioredoxin reductases, are key components of cellular defence and promote optimal antioxidant/oxidant balance. In this study, we have investigated the relationship between Se status, iNOS expression and NO production in Se-deficient and Se-supplemented RAW 264.7 macrophage cell lines. The cellular GPx activity, a measure of Se status, was 17-fold lower in Se-deficient RAW 264.7 cells and the total cellular oxidative tone, as assessed by flow cytometry with 2',7'-dichlorodihydrofluorescein diacetate, was higher in the Se-deficient cells than the Se-supplemented cells. Upon lipopolysaccharide (LPS) stimulation of these cells in culture, we found significantly higher iNOS transcript and protein expression levels with an increase in NO production in Se-deficient RAW 264.7 cells than the Se-supplemented cells. Electrophoretic mobility-shift assays, nuclear factor-kappaB (NF-kappaB)-luciferase reporter assays and Western blot analyses indicate that the increased expression of iNOS in Se deficiency could be due to an increased activation and consequent nuclear localization of the redox-sensitive transcription factor NF-kappaB. These results suggest an inverse relationship between cellular Se status and iNOS expression in LPS-stimulated RAW 264.7 cells and provide evidence for the beneficial effects of dietary Se supplementation in the prevention and/or treatment of oxidative-stress-mediated inflammatory diseases.
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Registered trials
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