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抗坏血酸会导致糖基化,并干扰神经突生长。

Ascorbic acid leads to glycation and interferes with neurite outgrowth.

机构信息

Institut für Physiologische Chemie, Martin-Luther-Universität Halle-Wittenberg, Hollystr. 1, D-06114 Halle/Saale, Germany.

Institut für Physiologische Chemie, Martin-Luther-Universität Halle-Wittenberg, Hollystr. 1, D-06114 Halle/Saale, Germany.

出版信息

Exp Gerontol. 2019 Mar;117:25-30. doi: 10.1016/j.exger.2018.08.005. Epub 2018 Aug 24.

Abstract

Ascorbic acid better known as vitamin C, is a reducing carbohydrate needed for a variety of functions in the human body. The most important characteristic of ascorbic acid is the ability to donate two electrons, predestining it as a major player in balancing the physiological redox state and as a necessary cofactor in multiple enzymatic hydroxylation processes. Ascorbic acid can be reversibly oxidized in two steps, leading to semidehydroascorbic acid and dehydroascorbic acid, respectively. Further degradation is irreversible and generates highly reactive carbonyl-intermediates. These intermediates are able to induce glycation of proteins, a non-enzymatic and unspecific reaction of carbonyls with amino groups involved to several age-related diseases. In this study, we investigated the effect of ascorbic acid- and dehydroascorbic acid-induced glycation on PC12 cells, which represent a model for neuronal plasticity. We found that both applications of ascorbic acid or dehydroascorbic acid leads to glycation of cellular proteins, but that ascorbic acid interferes more with viability and neurite outgrowth compared with dehydroascorbic acid.

摘要

抗坏血酸,又称维生素 C,是人体多种功能所需的还原碳水化合物。抗坏血酸最重要的特性是能够捐赠两个电子,这使它成为平衡生理氧化还原状态的主要参与者,并成为多种酶促羟化过程的必要辅助因子。抗坏血酸可以在两个步骤中可逆地氧化,分别生成半脱氢抗坏血酸和脱氢抗坏血酸。进一步的降解是不可逆的,会产生高反应性的羰基中间产物。这些中间产物能够诱导蛋白质糖化,这是羰基与参与多种与年龄相关疾病的氨基的非酶和非特异性反应。在这项研究中,我们研究了抗坏血酸和脱氢抗坏血酸诱导的糖化对 PC12 细胞的影响,PC12 细胞代表神经元可塑性的模型。我们发现,抗坏血酸或脱氢抗坏血酸的应用都会导致细胞蛋白糖化,但与脱氢抗坏血酸相比,抗坏血酸更会干扰细胞活力和神经突生长。

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