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首页> 外文期刊>Veterinary Dermatology >Oxidative stress in the pathogenesis of canine zinc-responsive dermatosis.
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Oxidative stress in the pathogenesis of canine zinc-responsive dermatosis.

机译：犬锌反应性皮肤病发病机理中的氧化应激。

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摘要

Zinc deficiency causes skin diseases both in humans and in animals. The underlying pathogenic mechanisms remain unclear, but a growing body of evidence indicates a role for zinc in skin protection against free radical-induced oxidative damage. The immunohistochemical expression of heat shock proteins (HSPs; Hsp27, Hsp72, Hsp73 and Hsp90), Cu/Zn superoxide dismutase (SOD), metallothionein (MT), Ki-67 antigen and active caspase-3 were evaluated in normal canine skin and in samples from eight dogs with zinc-responsive dermatosis. All investigated HSPs showed intense cytoplasmic immunostaining in the affected epidermis. Focal nuclear positivity of Hsp72 was also detected in keratinocytes. Although Cu/Zn SOD expression was similar to that observed in normal skin, MT immunoreactivity occurred in both the cytoplasm and the nucleus of basal cells in normal skin but was absent from the affected epidermis. Caspase-3 activation was also absent in the involved epidermis, which revealed a high Ki-67 index (a 3.5- to 9-fold increase compared with normal skin). These results support the hypothesis that cellular response to stress, particularly oxidative stress, is involved in the pathogenesis of skin lesions in canine zinc-responsive dermatosis. The lack of MT immunoreactivity in the affected epidermis may be indicative of low zinc levels, thus resulting in vulnerability to oxidative damage. In contrast, high expression levels of HSPs in skin during zinc deficiency may confer protection against a variety of dangerous stimuli, contributing to inhibition of apoptosis and to cell cycle regulation of proliferating keratinocytes.
机译：缺锌会导致人类和动物皮肤疾病。潜在的致病机理尚不清楚，但是越来越多的证据表明锌在保护皮肤免受自由基引起的氧化损伤中起作用。在正常犬的皮肤和皮肤中评估了热休克蛋白（HSPs; Hsp27，Hsp72，Hsp73和Hsp90），Cu / Zn超氧化物歧化酶（SOD），金属硫蛋白（MT），Ki-67抗原和活性caspase-3的免疫组织化学表达从八只具有锌反应性皮肤病的狗的样本。所有调查的HSPs在受影响的表皮中均显示出强烈的细胞质免疫染色。在角质形成细胞中也检测到了Hsp72的局部核阳性。尽管Cu / Zn SOD的表达与正常皮肤相似，但MT免疫反应性在正常皮肤的细胞质和基底细胞核中均发生，但在受影响的表皮中却没有。所涉及的表皮中也不存在Caspase-3激活，这揭示了高的Ki-67指数（与正常皮肤相比增加了3.5到9倍）。这些结果支持这样的假说：对犬，特别是氧化应激的细胞应答参与犬锌应答性皮肤病的皮肤病变的发病机理。在受影响的表皮中缺乏MT免疫反应性可能表明锌水平低，从而导致易受氧化损伤。相反，锌缺乏时皮肤中HSP的高表达水平可能赋予针对各种危险刺激的保护作用，从而有助于抑制细胞凋亡和促进增殖性角质形成细胞的细胞周期调控。

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