非酶分子损伤作为衰老的典型驱动因素。
Non-enzymatic molecular damage as a prototypic driver of aging.
作者信息
Golubev Alexey, Hanson Andrew D, Gladyshev Vadim N
机构信息
From the Department of Biochemistry, Saint-Petersburg State University, Saint Petersburg 199034, Russia,
the Horticultural Sciences Department, University of Florida, Gainesville, Florida 32611, and
出版信息
J Biol Chem. 2017 Apr 14;292(15):6029-6038. doi: 10.1074/jbc.R116.751164. Epub 2017 Mar 6.
The chemical potentialities of metabolites far exceed metabolic requirements. The required potentialities are realized mostly through enzymatic catalysis. The rest are realized spontaneously through organic reactions that (i) occur wherever appropriate reactants come together, (ii) are so typical that many have proper names ( Michael addition, Amadori rearrangement, and Pictet-Spengler reaction), and (iii) often have damaging consequences. There are many more causes of non-enzymatic damage to metabolites than reactive oxygen species and free radical processes (the "usual suspects"). Endogenous damage accumulation in non-renewable macromolecules and spontaneously polymerized material is sufficient to account for aging and differentiates aging from wear-and-tear of inanimate objects by deriving it from metabolism, the essential attribute of life.
代谢物的化学潜能远远超过代谢需求。所需的潜能大多通过酶催化来实现。其余的则通过有机反应自发实现，这些有机反应：（i）在合适的反应物聚集的任何地方都会发生；（ii）非常典型，许多都有专有名称（迈克尔加成反应、阿马多里重排反应和皮克特-施彭格勒反应）；（iii）常常会产生有害后果。对代谢物造成非酶损伤的原因远不止活性氧和自由基过程（那些“常见嫌疑对象”）。不可再生的大分子和自发聚合物质中的内源性损伤积累足以解释衰老现象，并将衰老与无生命物体的磨损区分开来，因为衰老源于新陈代谢，而新陈代谢是生命的基本属性。
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