羰—氨反应在老年色素形成中的重要作用

发布时间：2018-03-20 15:56

  本文选题：羰-氨反应　切入点：神经退行性疾病　出处：《湖南师范大学》2006年硕士论文　论文类型：学位论文

【摘要】：衰老是先天(遗传)因素和后天(环境)因素共同作用的结果。羰基毒化衰老学说认为在氧自由基引起的脂质过氧化和非酶糖基化反应中生成的具有反应活性的共同中间产物——不饱和醛酮能与生物体内的生物大分子发生羰-氨交联反应,这正是缓慢老化的本质。本文讨论了衰老的自由基学说、糖基化学说以及在其基础上根据老年色素的形成机制发展而成的羰基毒化衰老学说。在羰基应激与神经退行性疾病具有相关性的研究背景下,探讨了体内常见的神经递质/炎症介质——组胺与脂质过氧化中间产物之一的丙二醛(MDA)的反应机理。同时研究了抗坏血酸与谷氨酰氨反应对老年色素生成的影响。 本学位论文研究工作总结如下: 一、研究组胺(HA)与丙二醛(MDA)的反应机理以探讨毒性羰基对氨类神经递质的毒化作用和HA可能具有潜在的去羰基毒化的作用。HA与MDA在37℃、pH7.4的0.1M磷酸缓冲液中温浴,反应液进行紫外检测、荧光检测、色谱分离等分析,其生成的产物用LC/MS鉴定。HA和MDA能在生理条件下发生反应,生成两种稳定的产物:无荧光特性的烯胺衍生物和发荧光的1,4-二氢吡咯产物。荧光产物的荧光特征峰(Ex393/Em430)是典型的老年色素类荧光。反应产生的荧光强度与MDA的浓度成正比。本研究结果揭示了不饱和醛酮对脑的毒化作用并反映了在多种病理应激条件下HA可能具有的去羰基毒化的作用。
[Abstract]:Senescence is the result of both innate (genetic) and acquired (environmental) factors. Carbonyl toxic senescence theory suggests that it is reactive in lipid peroxidation and non-enzymatic glycosylation induced by oxygen free radicals. The common intermediate product, unsaturated aldehydes and ketones, can be crosslinked with biological macromolecules in vivo. This is the essence of slow aging. The free radical theory of aging is discussed in this paper. The theory of glycosyl chemistry and the theory of carbonyl poisoning and senescence developed on the basis of the formation mechanism of senile pigments. In the context of the study of the correlation between carbonyl stress and neurodegenerative diseases, The reaction mechanism of histamine, a common neurotransmitter / inflammatory mediator, and malondialdehyde (MDA), one of the intermediate products of lipid peroxidation, was studied. The effects of ascorbic acid and glutamine on the formation of senile pigments were also studied. The research work of this thesis is summarized as follows:. Firstly, the reaction mechanism between histamine (HA) and malondialdehyde (MDA) was studied to investigate the toxic effect of carbonyl group on ammonia neurotransmitters and the potential decarbonyl toxicity of HA. Ha and MDA were incubated in 0.1M phosphoric acid buffer solution at 37 鈩，

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