本文選題：羰-氨反應(yīng)　切入點：神經(jīng)退行性疾病　出處：《湖南師范大學》2006年碩士論文　論文類型：學位論文

【摘要】：衰老是先天(遺傳)因素和后天(環(huán)境)因素共同作用的結(jié)果。羰基毒化衰老學說認為在氧自由基引起的脂質(zhì)過氧化和非酶糖基化反應(yīng)中生成的具有反應(yīng)活性的共同中間產(chǎn)物——不飽和醛酮能與生物體內(nèi)的生物大分子發(fā)生羰-氨交聯(lián)反應(yīng),這正是緩慢老化的本質(zhì)。本文討論了衰老的自由基學說、糖基化學說以及在其基礎(chǔ)上根據(jù)老年色素的形成機制發(fā)展而成的羰基毒化衰老學說。在羰基應(yīng)激與神經(jīng)退行性疾病具有相關(guān)性的研究背景下,探討了體內(nèi)常見的神經(jīng)遞質(zhì)/炎癥介質(zhì)——組胺與脂質(zhì)過氧化中間產(chǎn)物之一的丙二醛(MDA)的反應(yīng)機理。同時研究了抗壞血酸與谷氨酰氨反應(yīng)對老年色素生成的影響。 本學位論文研究工作總結(jié)如下: 一、研究組胺(HA)與丙二醛(MDA)的反應(yīng)機理以探討毒性羰基對氨類神經(jīng)遞質(zhì)的毒化作用和HA可能具有潛在的去羰基毒化的作用。HA與MDA在37℃、pH7.4的0.1M磷酸緩沖液中溫浴,反應(yīng)液進行紫外檢測、熒光檢測、色譜分離等分析,其生成的產(chǎn)物用LC/MS鑒定。HA和MDA能在生理條件下發(fā)生反應(yīng),生成兩種穩(wěn)定的產(chǎn)物:無熒光特性的烯胺衍生物和發(fā)熒光的1,4-二氫吡咯產(chǎn)物。熒光產(chǎn)物的熒光特征峰(Ex393/Em430)是典型的老年色素類熒光。反應(yīng)產(chǎn)生的熒光強度與MDA的濃度成正比。本研究結(jié)果揭示了不飽和醛酮對腦的毒化作用并反映了在多種病理應(yīng)激條件下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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