ArticleProceedings of the National Academy of Sciences of the United States of America2006
Free radical production requires both inducible nitric oxide synthase and xanthine oxidase in LPS-treated skin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
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- Ferroptosis as a Pathogenic Mechanism and Therapeutic Target in Autoimmune and Inflammatory Skin Diseases.Clinical reviews in allergy & immunology · 2026Review
- The Role of the Intestinal Microbiome in the Pathogenesis and Treatment of Hyperuricemia: A Review.Food science & nutrition · 2025Review
- Cysteine depletion triggers adipose tissue thermogenesis and weight loss.Nature metabolism · 2025Article
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- Genetic susceptibility to diabetic kidney disease is linked to promoter variants of XOR.Nature metabolism · 2023Article
- Oxidative stress and alopecia areata.Frontiers in medicine · 2023Review
- What Are Reactive Oxygen Species, Free Radicals, and Oxidative Stress in Skin Diseases?International journal of molecular sciences · 2021Review
- GRK2 deletion improves the function of skin flap following ischemia-reperfusion injury by regulating Drp1.American journal of translational research · 2021Article
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- Proximal Tubular Cell-Specific Ablation of Carnitine Acetyltransferase Causes Tubular Disease and Secondary Glomerulosclerosis.Diabetes · 2019Article
- IL-17A induces heterogeneous macrophages, and it does not alter the effects of lipopolysaccharides on macrophage activation in the skin of mice.Scientific reports · 2017Article
- Hydroxysafflor Yellow A Inhibits LPS-Induced NLRP3 Inflammasome Activation via Binding to Xanthine Oxidase in Mouse RAW264.7 Macrophages.Mediators of inflammation · 2016Article
- Effects of febuxostat on platelet-derived microparticles and adiponectin in patients with hyperuricemia.Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis · 2015Article
- Xanthine Oxidoreductase Function Contributes to Normal Wound Healing.Molecular medicine (Cambridge, Mass.) · 2015Article
- The role of uric acid in kidney fibrosis: experimental evidences for the causal relationship.BioMed research international · 2014Review
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- Nuclear factor-κB: a key regulator in health and disease of lungs.Archivum immunologiae et therapiae experimentalis · 2011Review
- Oxidative stress induces protein and DNA radical formation in follicular dendritic cells of the germinal center and modulates its cell death patterns in late sepsis.Free radical biology & medicine · 2011Article
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5 authors at 3 institutions in 1 country.
Funding
Abstract
Free radical formation has been investigated in diverse experimental models of LPS-induced inflammation. Here, using electron spin resonance (ESR) and the spin trap alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone, we have detected an ESR spectrum of alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone radical adducts in the lipid extract of mouse skin treated with LPS for 6 h. The ESR spectrum was consistent with the trapping of lipid-derived radical adducts. In addition, a secondary radical-trapping technique using dimethyl sulfoxide (DMSO) demonstrated methyl radical formation, revealing the production of hydroxyl radical. Radical adduct formation was suppressed by aminoguanidine, N-(3-aminomethyl)benzylacetamidine (1400W), or allopurinol, suggesting a role for both inducible nitric oxide synthase (iNOS) and xanthine oxidase (XO) in free radical formation. The radical formation was also suppressed in iNOS knockout (iNOS(-/-)) mice, demonstrating the involvement of iNOS. NADPH oxidase was not required in the formation of these radical adducts because the ESR signal intensity was increased by LPS treatment in NADPH oxidase knockout (gp91(phox-/-)) mice as much as it was in the wild-type mouse. Nitric oxide (*NO) end products were increased in LPS-treated skin. As expected, the *NO end products were not suppressed by allopurinol but were by aminoguanidine. Interestingly, nitrotyrosine formation in LPS-treated skin was also suppressed by aminoguanidine and allopurinol independently. Pretreatment with the ferric iron chelator Desferal had no effect on free radical formation. Our results imply that both iNOS and XO, but neither NADPH oxidase nor ferric iron, work synergistically to form lipid radical and nitrotyrosine early in the skin inflammation caused by LPS.
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