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Relation of Redox and Structural Alterations of Rat Skin in the Function of Chronological Aging

机译:氧化还原与大鼠皮肤结构改变的关系

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摘要

Accumulation of oxidative insults on molecular and supramolecular levels could compromise renewal potency and architecture in the aging skin. To examine and compare morphological and ultrastructural changes with redox alterations during chronological skin aging, activities of antioxidant defense (AD) enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), thioredoxin reductase (TR), and methionine sulfoxide reductase A (MsrA), and the markers of oxidative damage of biomolecules—4-hydroxynonenal (HNE) and 8-oxoguanine (8-oxoG)—were examined in the rat skin during life (from 3 days to 21 months). As compared to adult 3-month-old skin, higher activities of CAT, GSH-Px, and GR and a decline in expression of MsrA are found in 21-month-old skin. These changes correspond to degenerative changes at structural and ultrastructural levels in epidermal and dermal compartments, low proliferation capacity, and higher levels of HNE-modified protein aldehydes (particularly in basal lamina) and 8-oxoG positivity in nuclei and mitochondria in the sebaceous glands and root sheath. In 3-day-old skin, higher activities of AD enzymes (SOD, CAT, GR, and TR) and MsrA expression correspond to intensive postnatal development and proliferation. In contrast to 21-month-old skin, a high level of HNE in young skin is not accompanied by 8-oxoG positivity or any morphological disturbances. Observed results indicate that increased activity of AD enzymes in elderly rat skin represents the compensatory response to accumulated oxidative damage of DNA and proteins, accompanied by attenuated repair and proliferative capacity, but in young rats the redox changes are necessary and inherent with processes which occur during postnatal skin development. Мorphological and ultrastructurаl changes are in line with the redox profile in the skin of young and old rats.
机译:分子和超分子水平的氧化损伤的积累可能会损害衰老皮肤的更新能力和结构。要检查并比较按时间顺序在皮肤老化过程中氧化还原改变的形态和超微结构变化,抗氧化剂防御(AD)酶,超氧化物歧化酶(SOD),过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GSH-Px),谷胱甘肽还原酶(GR)的活性,在大鼠的一生中,对其一生中的皮肤进行了检测,包括硫氧还蛋白还原酶(TR)和蛋氨酸亚砜还原酶A(MsrA)以及生物分子的氧化损伤标记物(4-羟基壬烯醛(HNE)和8-氧鸟嘌呤(8-oxoG)(来自3天到21个月)。与成人的3个月大的皮肤相比,在21个月大的皮肤中发现CAT,GSH-Px和GR的活性更高,MsrA的表达下降。这些变化对应于表皮和真皮区室的结构和超微结构水平的退化性变化,低增殖能力和较高水平的HNE修饰的蛋白醛(特别是在基底层)和皮脂腺和核和线粒体的8-oxoG阳性。根鞘。在3天大的皮肤中,AD酶(SOD,CAT,GR和TR)和MsrA表达的较高活性对应于出生后的密集发育和增殖。与21个月大的皮肤相比,年轻皮肤中高水平的HNE并没有伴随8-oxoG阳性或任何形态异常。观察到的结果表明,老年大鼠皮肤中AD酶的活性增加表示对DNA和蛋白质累积氧化损伤的代偿性反应,伴随着修复和增殖能力的减弱,但在幼鼠中,氧化还原变化是必需的,并且是氧化还原变化的固有过程。产后皮肤发育。形态和超微结构的变化与年轻和老年大鼠皮肤中的氧化还原谱一致。

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