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首页> 美国卫生研究院文献>Cardiovascular Diabetology >Asymmetric dimethylarginine (ADMA) symmetric dimethylarginine (SDMA) and homoarginine (hArg): the ADMA SDMA and hArg paradoxes
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Asymmetric dimethylarginine (ADMA) symmetric dimethylarginine (SDMA) and homoarginine (hArg): the ADMA SDMA and hArg paradoxes

机译：不对称二甲基精氨酸（ADMA）对称二甲基精氨酸（SDMA）和高精氨酸（hArg）：ADMASDMA和hArg悖论

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摘要

NG-Methylation of l-arginine (Arg) residues in certain proteins by protein arginine methyltransferases and subsequent proteolysis yields NG-monomethyl-l-arginine (MMA), NG,NG-dimethyl-l-arginine (asymmetric dimethylarginine, ADMA) and NG,N′G-dimethyl-l-arginine (symmetric dimethylarginine, SDMA). Biological MMA, ADMA and SDMA occur as free acids in the nM-range and as residues of proteins of largely unknown quantity. Arginine:glycine amidinotransferase (AGAT) catalyzes the synthesis of L-homoarginine (hArg) from free Arg and l-lysine. Biological hArg is considered to occur exclusively as free acid in the lower µM-range. Nitric oxide synthase (NOS) catalyzes the conversion of Arg (high affinity) and hArg (low affinity) to nitric oxide (NO) which is a pleiotropic signaling molecule. MMA, ADMA and SDMA are inhibitors (MMA > ADMA ≫ SDMA) of NOS activity. Slightly elevated ADMA and SDMA concentrations and slightly reduced hArg concentrations in the circulation are associated with many diseases including diabetes mellitus. Yet, this is paradox: (1) free ADMA and SDMA are weak inhibitors of endothelial NOS (eNOS) which is primarily responsible for NO-related effects in the cardiovascular system, with free hArg being a poor substrate for eNOS; (2) free ADMA, SDMA and hArg are not associated with oxidative stress which is considered to induce NO-related endothelial dysfunction. This ADMA/SDMA/hArg paradox may be solved by the assumption that not the free acids but their precursor proteins exert biological effects in the vasculature, with hArg antagonizing the effects of NG-methylated proteins.
机译：N G -某些蛋白质中的L-精氨酸（Arg）残基被蛋白质精氨酸甲基转移酶甲基化，随后蛋白水解产生N G -单甲基-1-精氨酸（MMA），N G ，N G -二甲基-1-精氨酸（不对称二甲基精氨酸，ADMA）和N G ，N' G -二甲基-1-精氨酸（对称的二甲基精氨酸，SDMA）。生物MMA，ADMA和SDMA以nM范围内的游离酸形式存在，并以数量未知的蛋白质残基形式存在。精氨酸：甘氨酸酰胺基转移酶（AGAT）催化由游离Arg和L-赖氨酸合成L-高精氨酸（hArg）。人们认为，生物hArg仅以较低的µM范围内的游离酸形式存在。一氧化氮合酶（NOS）催化Arg（高亲和力）和hArg（低亲和力）转化为一氧化氮（NO），后者是一种多效信号分子。 MMA，ADMA和SDMA是NOS活性的抑制剂（MMA> ADMA≫SDMA）。血液中ADMA和SDMA浓度的略微升高以及hArg浓度的略微降低与包括糖尿病在内的许多疾病有关。然而，这是自相矛盾的：（1）游离的ADMA和SDMA是内皮NOS（eNOS）的弱抑制剂，其主要负责心血管系统中与NO相关的作用，而游离的hArg是eNOS的不良底物； （2）游离的ADMA，SDMA和hArg与氧化应激无关，氧化应激可诱导NO相关的内皮功能障碍。这种ADMA / SDMA / hArg悖论可以通过以下假设来解决：假想不是游离酸而是其前体蛋白在脉管系统中发挥了生物作用，而hArg拮抗了N G -甲基化蛋白的作用。

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