Oxidative stress in the pathogenesis of canine zinc-responsive dermatosis.
Oxidative stress in the pathogenesis of canine zinc-responsive dermatosis.
复制标题
犬锌反应性皮肤病发病机制中的氧化应激。
DOI：
10.1111/j.1365-3164.2010.00907.x
复制
发表时间：
2011
影响因子：
1.4
通讯作者：
L. Della Salda
中科院分区：
文献类型：
--
作者：
M. Romanucci;L. Bongiovanni;A. Russo;S. Capuccini;L. Mechelli;L. Ordeix;L. Della Salda
锌缺乏会导致人类和动物的皮肤病。潜在的致病机制尚不清楚，但越来越多的证据表明锌在保护皮肤免受自由基诱导的氧化损伤中的作用。应用免疫组织化学方法检测了热休克蛋白（HSP 27、HSP 72、HSP 73和HSP 90）、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在正常犬皮肤和8只锌反应性皮肤病犬皮肤中的表达。所有研究的热休克蛋白表现出强烈的细胞质免疫染色在受影响的表皮。角质形成细胞中也检测到Hsp 72的灶性核阳性。虽然Cu/Zn SOD的表达与正常皮肤中观察到的相似，但MT免疫反应发生在正常皮肤基底细胞的细胞质和细胞核中，但不存在于受影响的表皮中。Caspase-3活化也不存在于所涉及的表皮，这揭示了高Ki-67指数（与正常皮肤相比增加了3.5至9倍）。这些结果支持了细胞对应激，特别是氧化应激的反应参与了犬锌反应性皮肤病皮肤病变的发病机制的假设。在受影响的表皮MT免疫反应性的缺乏可能是低锌水平的指示，从而导致氧化损伤的脆弱性。相反，锌缺乏时皮肤中热休克蛋白的高表达水平可能会保护皮肤免受各种危险的刺激，有助于抑制细胞凋亡和调节增殖的角质形成细胞的细胞周期。
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.
缺锌引起的大鼠颊粘膜的变化序列。
DOI：
10.1111/j.1600-0714.1991.tb00436.x
发表时间：
1991
期刊：
Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
影响因子：
--
作者：
Hsu,D;Meyer,J;Gerson,S;Daniel,J
通讯作者：
Daniel,J