In Vivo Measurement of Reactive Oxygen Species Generated in Skin under Ultraviolet Light Irradiation

紫外线照射下皮肤产生的活性氧的体内测量

• 批准号: 12672168
• 负责人: UEDA Jun-ichi
• 金额: $ 2.5万
• 依托单位: National Institute of Radiological Sciences
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2001
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12672168/
• 关键词: ultraviolet light; skin; reactive oxygen species; free radical; in vivo ESR; surface-soil-type resonator; hairless mouse; PBN; In vitro ESR; ニトロキシルラジカル; スピンプローブ; サーフェイス・コイル型共振器

Distinct electron spin resonance(ESR) signal of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) adduct of hydroxyl radical (OH) was observed in uroporphyrin or hematoporphyrin photodynamic reactions in the presence of reducing reagents, although no adduct of OH was observed using 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline-N-oxide (DEPMPO) as a spin-trapping agent. Both DMPO and DEPMPO adducts of OH appeared, as the spin-trapping was performed with DEPMPO in the presence of DMPO. The results indicate that the DMPO-mediated generation of OH occurs during the spin-trapping in photodynamic reactions. Thus, in vivo ESR spectroscopy with a nitroxyl spin probe was employed to detect reactive oxygen species generated in skin.An aqueous solution of carbamoyl-PROXYL was injected intravenously to an anesthetized hair-removed ddY mouse or hairless mouse, and L-band ESR spectra of the probe were recorded at the dorsal region of the mice. A surface-coil-type resonator was used to detect carbamoyl-PROXYL in skin. The decay rate of the ESR signal increased by irradiation with UV light (UVA+B). The enhancement of signal decay was suppressed by pre-administration of a spin-trapping reagent, N-t-butyl-α-phenylnitrone (PBN), while PBN did not change the decay rate for non-irradiated mouse. Peroxyl radical caused the decay of carbamoyl-PROXYL signal in vitro, and the decay was inhibited by PBN. These observations suggest that peroxyl radical was generated in skin of mouse under ultraviolet light irradiation.

在尿卟啉和血卟啉光动力反应中，在还原剂存在下，观察到了5，5-二甲基-1-吡咯啉-N-氧化物（DMPO）与羟基自由基（OH）加合物的电子自旋共振（ESR）信号，而在5-（二乙氧基磷酰基）-5-甲基-1-吡咯啉-N-氧化物（DEPMPO）作为自旋捕获剂时，没有观察到OH的加合物.当在DMPO存在下用DEPMPO进行自旋捕获时，出现DMPO和DEPMPO的OH加合物。结果表明，DMPO介导的OH的产生发生在光动力学反应的自旋捕获过程中。因此，在体内ESR光谱与硝酰基自旋探针检测活性氧在皮肤中产生。氨基甲酰基-PROXYL的水溶液静脉注射到麻醉的脱毛ddY小鼠或无毛小鼠，并记录探针的L-带ESR光谱在小鼠的背部区域。使用表面线圈型谐振器来检测皮肤中的氨甲酰基-PROXYL。ESR信号的衰减速率通过用UV光（UVA+B）照射而增加。预先给予自旋捕获剂N-叔丁基-α-苯基硝酮（PBN）可抑制信号衰减的增强，而PBN对未照射小鼠的衰减率无影响。过氧自由基在体外引起氨甲酰-PROXYL信号衰减，PBN可抑制这种衰减。这些结果表明，在紫外线照射下，小鼠皮肤产生过氧化氢自由基。

项目成果

Application of in vivo ESR spectroscopy to in vivo detection of radicals produced in skin during irradiation of ultraviolet light.

体内ESR光谱法在体内检测紫外线照射期间皮肤产生的自由基中的应用。

• 发表时间: 2001
• 期刊: Magn.Reson.Med.Jpn. 12
• 作者: J.Ueda et al.;Y.Miura et al.;S.Ueno et al.;J.-Y.Han et al.;K.Takeshita et al.
• 通讯作者: K.Takeshita et al.

Detection of dichromate (VI)-induced DNA strand breaks and formation of paramagnetic chromium in multiple mouse organs

• DOI: 10.1006/taap.2000.9081
• 发表时间: 2001-01-01
• 期刊: TOXICOLOGY AND APPLIED PHARMACOLOGY
• 影响因子: 3.8
• 作者: Ueno, S;Kashimoto, T;Sugiyama, M
• 通讯作者: Sugiyama, M

Jin-Yi Han: "Noninvasive detection of hydroxyl radical generation in lung by diesel exhaust particles"Free Radic.Biol.Med.. 30. 516-525 (2001)

Jin-Yi Han：“柴油机尾气颗粒物在肺部产生羟基自由基的无创检测”Free Radic.Biol.Med.. 30. 516-525 (2001)

Yuri Miura: "Pathophysiological significance of in vivo ESR signal decay in brain damage caused by X-irradiation"Biochim.Biophys.Acta.. 1525. 167-172 (2001)

Yuri Miura：“X 辐射引起的脑损伤中体内 ESR 信号衰减的病理生理学意义”Biochim.Biophys.Acta.. 1525. 167-172 (2001)

Autoxidation of ascorbic acid catalyzed by the copper(II) bound to L-histidine oligopeptide, (His)iGly an acetyl-(His)iGly (i=9,19,and 29). Relationship between catalytic activity and coordination mode.

由与 L-组氨酸寡肽、(His)iGly 和乙酰基-(His)iGly (i=9,19 和 29) 结合的铜 (II) 催化的抗坏血酸自氧化。

• 发表时间: 2000
• 期刊: Chem.Pharm.Bull. 48
• 作者: J.Ueda et al.;Y.Miura et al.;S.Ueno et al.;J.-Y.Han et al.;K.Takeshita et al.;J.Ueda et al.;J.Ueda et al.;Y.Miura et al.;S.Ueno et al.;K.Takeshita et al.;J.Ueda et al.
• 通讯作者: J.Ueda et al.