| 词条 | Thymine glycol |
| 释义 |
| ImageFile = Thymine glycol.svg | ImageSize = 180px | ImageAlt = | IUPACName = 5,6-Dihydroxy-5-methyldihydro-2,4(1H,3H)-pyrimidinedione | OtherNames = 5,6-Dihydroxy-5,6-dihydrothymine | Section1 = {{Chembox Identifiers | CASNo = 2943-56-8 | PubChem = | ChemSpiderID = 17061 | SMILES = CC1(C(NC(=O)NC1=O)O)O | Section2 = {{Chembox Properties | C=5|H=8|N=2|O=4 | Appearance = | Density = | MeltingPt = | BoilingPt = | Solubility = | Section3 = {{Chembox Hazards | MainHazards = | FlashPt = | AutoignitionPt = }}Thymine glycol (5,6-dihydroxy-5,6-dihydrothymine) is one of the principal DNA lesions that can be induced by oxidation and ionizing radiation.[1] Aging, strokeThe rate at which oxidative reactions generate thymine glycol and thymidine glycol in the DNA of humans is estimated to be about 300 per cell per day.[2] Oxidized DNA bases that are excised by DNA repair processes are excreted in urine. On a body weight basis, mice excrete 18 times more thymine glycol plus thymidine glycol than humans, and monkeys four times more than humans.[2] It was proposed that rate of occurrence of oxidative DNA damages correlates with metabolic rate, and that a higher rate of oxidative damage might cause a higher rate of cellular aging.[2] Base excision repair is a major DNA repair pathway for removal of oxidative DNA damages. The rate of repair of thymine glycol damage in human fibroblasts was found to decrease with age.[3] Brain samples from humans who died of stroke were found to be deficient in base excision repair of thymine glycol as well as other types of oxidative damages.[4] It was suggested that impaired base excision repair is a risk factor for ischemic brain injury.[4]References1. ^{{cite journal |title=Genetic effects of thymine glycol: site-specific mutagenesis and molecular modeling studies. |doi=10.1073/pnas.86.20.7677 |pmc=298133 | pmid=2682618 |volume=86 |year=1989 |journal=Proc. Natl. Acad. Sci. U.S.A. |pages=7677–81 | last1 = Basu | first1 = AK | last2 = Loechler | first2 = EL | last3 = Leadon | first3 = SA | last4 = Essigmann | first4 = JM}} 2. ^1 2 {{cite journal |vauthors=Adelman R, Saul RL, Ames BN |title=Oxidative damage to DNA: relation to species metabolic rate and life span |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=85 |issue=8 |pages=2706–8 |year=1988 |pmid=3128794 |pmc=280067 |doi= 10.1073/pnas.85.8.2706|url=}} 3. ^{{cite journal |vauthors=Pons B, Belmont AS, Masson-Genteuil G, Chapuis V, Oddos T, Sauvaigo S |title=Age-associated modifications of Base Excision Repair activities in human skin fibroblast extracts |journal=Mech. Ageing Dev. |volume=131 |issue=11-12 |pages=661–5 |year=2010 |pmid=20854835 |doi=10.1016/j.mad.2010.09.002 |url=}} 4. ^1 {{cite journal |vauthors=Ghosh S, Canugovi C, Yoon JS, Wilson DM, Croteau DL, Mattson MP, Bohr VA |title=Partial loss of the DNA repair scaffolding protein, Xrcc1, results in increased brain damage and reduced recovery from ischemic stroke in mice |journal=Neurobiol. Aging |volume=36 |issue=7 |pages=2319–30 |year=2015 |pmid=25971543 |doi=10.1016/j.neurobiolaging.2015.04.004 |url=}} 2 : Pyrimidinediones|Vicinal diols |
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