The effects of radicals compared with UVB as initiating species for the induction of chronic cutaneous photodamage.

The effects of radicals compared with UVB as initiating species for the induction of chronic cutaneous photodamage.
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DOI:
10.1046/j.1523-1747.1999.00591.x
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发表时间:
1999-06
期刊:
The Journal of investigative dermatology
影响因子:
--
通讯作者:
S. Ibbotson;M. Moran;J. Nash;I. Kochevar
S. Ibbotson;M. Moran;J. Nash;I. Kochevar
中科院分区:
其他
文献类型:
--
作者:
S. Ibbotson;M. Moran;J. Nash;I. Kochevar

文献摘要

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有大量证据表明,紫外线辐射诱导活性氧的形成,而活性氧是光老化发病机制中的有毒中间体。这项研究的目的是确定反复使用过氧化苯甲酰(一种自由基来源)局部治疗是否与慢性紫外线B辐射产生相同的皮肤效应。三种浓度的过氧化苯甲酰(0.1、1.5、5.0% wt/wt)和紫外线B辐射的三种累积影响(0.9、2.2、5.1 J / cm2)单独使用和所有组合以及适当的对照。雌性SKH1 (hr/hr)白化无毛小鼠,每周治疗5 d,连续12周。评估细胞外基质分子和组织学参数。紫外线B辐射诱导皮肤褶皱厚度随影响和时间的增加。在表皮厚度、晒伤细胞数量、真皮厚度、糖胺聚糖含量、肥大细胞数量和皮肤褶皱厚度等方面,观察到Fluence的依赖性。在使用的条件下,与紫外线B相比,单独过氧化苯甲酰处理引起的表皮和真皮测量的显着增加较少。过氧化苯甲酰的浓度依赖于弹性蛋白含量的增加,尽管最高浓度的过氧化苯甲酰增加了表皮厚度和糖胺聚糖含量。紫外线B与过氧化苯甲酰之间没有发现协同作用。这些结果表明,反复施用过氧化苯甲酰在无毛小鼠中产生的皮肤变化在质量上类似于紫外线B产生的变化,并表明可能涉及共同的机制。此外,紫外线B和过氧化苯甲酰的任何潜在协同作用都低于本研究使用的检测水平。
There is substantial evidence that ultraviolet radiation induces the formation of reactive oxygen species which are implicated as toxic intermediates in the pathogenesis of photoaging. The aim of this study was to determine whether repeated topical treatment with benzoyl peroxide, a source of free radicals, produced the same cutaneous effects as chronic ultraviolet B radiation. Three concentrations of benzoyl peroxide (0.1, 1.5, 5.0% wt/wt) and three cumulative fluences of ultraviolet B radiation (0.9, 2.2, 5.1 J per cm2) used alone and in all combinations along with appropriate controls. Female SKH1 (hr/hr) albino hairless mice were treated 5 d per wk for 12 wk. Extracellular matrix molecules and histologic parameters were assessed. Ultraviolet B radiation induced a fluence-dependent and time-dependent increase in skin-fold thickness. Fluence dependence was seen for epidermal thickness, sunburn cell numbers, dermal thickness, glycosaminoglycan content, mast cell numbers, and skin-fold thickness. Benzoyl peroxide treatment alone caused less marked increases in epidermal and dermal measures compared with ultraviolet B under the conditions used. A benzoyl peroxide concentration-dependent increase was only observed for elastin content, although the highest concentration of benzoyl peroxide increased epidermal thickness and glycosaminoglycan content. A synergistic interaction between ultraviolet B and benzoyl peroxide was not found. These results indicate that repeated administration of benzoyl peroxide produces skin changes in the hairless mouse that qualitatively resemble those produced by ultraviolet B and suggest that common mechanisms may be involved. In addition, any potential synergistic effect of ultraviolet B and benzoyl peroxide was below the level of detection used in this study.