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首页> 外文期刊>Journal of dermatological science >Differentiation-specific localization of catalase and hydrogen peroxide, and their alterations in rat skin exposed to ultraviolet B rays.
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Differentiation-specific localization of catalase and hydrogen peroxide, and their alterations in rat skin exposed to ultraviolet B rays.

机译：过氧化氢酶和过氧化氢的分化特异性定位及其在暴露于紫外线B射线的大鼠皮肤中的变化。

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BACKGROUND: It is now well known that to counteract oxidative stress and maintain a redox balance within the cells, the skin is equipped with a network of antioxidant enzymes. Among these enzymes, SOD and CAT are the major antioxidant enzymes protecting the epidermis. OBJECTIVE: In the present study, we have attempted to demonstrate the distribution of endogenous H(2)O(2) and the expression of CAT in the epidermis of newborn rats, in relation to epidermal differentiation, and alterations after UVB irradiation. METHODS: We have localized the antioxidant enzyme catalase (CAT) using immunohistochemical analysis, and hydrogen peroxide (H(2)O(2)) using in situ H(2)O(2) assay. RESULTS: We demonstrated that keratinocytes in the stratum granulosum produced H(2)O(2), and CAT was mainly expressed in the cytoplasm of cells from the stratum granulosum to the lower corneum, and in the cell periphery in the stratum granulosum of newborn rat skin. The results suggested that generation of H(2)O(2) and expression of CAT were coordinated and were indicative of epidermal differentiation as well as of the role of CAT in repairing redox damage by discomposing H(2)O(2). When rat skin was exposed to 50 mJ/cm(2) of ultraviolet B (UVB) rays, the accumulation of H(2)O(2) in the upper epidermis increased twenty-four hours later, while CAT immunoreactivity decreased. CONCLUSION: The results suggested that generation of H(2)O(2) and expression of CAT were coordinated and were indicative of epidermal differentiation as well as of the role of CAT in repairing redox damage by discomposing H(2)O(2). In addition, UVB-induced oxidative stress in the present study seemed to alter the endogenous and differentiation-specific redox balance between H(2)O(2) and CAT.
机译：背景技术：众所周知，为了抵消氧化应激并维持细胞内的氧化还原平衡，皮肤配备了抗氧化酶网络。在这些酶中，SOD和CAT是保护表皮的主要抗氧化酶。目的：在本研究中，我们试图证明新生大鼠表皮中内源性H（2）O（2）的分布和CAT的表达与表皮分化和UVB照射后的变化有关。方法：我们已经使用免疫组织化学分析定位了抗氧化酶过氧化氢酶（CAT），并使用了原位H（2）O（2）分析法检测了过氧化氢（H（2）O（2））。结果：我们证明颗粒层中的角质形成细胞产生H（2）O（2），并且CAT主要在从颗粒层到角质层的细胞的细胞质中以及新生颗粒层中的细胞外围表达大鼠皮肤。结果表明，H（2）O（2）的产生和CAT的表达是协调的，并指示表皮分化以及CAT通过分解H（2）O（2）修复氧化还原损伤的作用。当大鼠皮肤暴露于50 mJ / cm（2）的紫外线B（UVB）射线时，二十四小时后，上表皮中H（2）O（2）的积累增加，而CAT免疫反应性降低。结论：结果表明，H（2）O（2）的产生和CAT的表达是协调的，并且指示表皮分化以及CAT通过分解H（2）O（2）修复氧化还原损伤的作用。 。此外，在本研究中，UVB诱导的氧化应激似乎改变了H（2）O（2）和CAT之间的内源性和分化特异性氧化还原平衡。

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