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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Free radical production requires both inducible nitric oxide synthase and xanthine oxidase in LPS-treated skin
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Free radical production requires both inducible nitric oxide synthase and xanthine oxidase in LPS-treated skin

机译：自由基的产生需要LPS处理的皮肤中的一氧化氮合酶和黄嘌呤氧化酶

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摘要

Free radical formation has been investigated in diverse experimental models of LPS-induced inflammation. Here, using electron spin resonance (ESR) and the spin trap α-(4-pyridyl-1-oxide)-N-tert-butylnitrone, we have detected an ESR spectrum of α-(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)benzyl-acetamidine (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.
机译：已在LPS诱导的炎症的各种实验模型中研究了自由基的形成。在这里，我们使用电子自旋共振（ESR）和自旋阱α-（4-吡啶基-1-氧化物）-N-叔丁基硝酮，检测到了α-（4-吡啶基-1-氧化物）-的ESR光谱。 LPS处理6h的小鼠皮肤脂质提取物中的N-叔丁基硝氮自由基加合物。 ESR谱图与脂质衍生的自由基加合物的捕获一致。此外，使用二甲基亚砜（DMSO）的二次自由基捕获技术证明了甲基自由基的形成，揭示了羟基自由基的产生。自由基加合物的形成被氨基胍，N-（3-氨基甲基）苄基-乙am（1400W）或别嘌呤醇抑制，表明诱导型一氧化氮合酶（iNOS）和黄嘌呤氧化酶（XO）在自由基形成中均起作用。在iNOS基因敲除（iNOS〜（-/-））小鼠中，自由基的形成也受到抑制，证明了iNOS的参与。这些自由基加合物的形成不需要NADPH氧化酶，因为通过LPS处理，NADPH氧化酶敲除（gp91〜（phox- /-））小鼠的ESR信号强度与野生型小鼠一样多。经LPS处理的皮肤中一氧化氮（〜·NO）终产物增加。不出所料，别嘌呤醇不会抑制〜·NO终产物，而是被氨基胍抑制。有趣的是，LPS处理的皮肤中硝基酪氨酸的形成也被氨基胍和别嘌呤醇独立抑制。用铁螯合剂Desferal预处理对自由基的形成没有影响。我们的结果表明，iNOS和XO均不能协同作用，在LPS引起的皮肤炎症早期形成脂质自由基和硝基酪氨酸，但NADPH氧化酶和三价铁均不能协同作用。

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