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Names | |
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IUPAC name
5,6-Dihydroxy-5-methyldihydro-2,4(1H,3H)-pyrimidinedione
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Other names
5,6-Dihydroxy-5,6-dihydrothymine
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Identifiers | |
3D model (JSmol)
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ChEBI | |
ChemSpider | |
PubChem CID
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CompTox Dashboard (EPA)
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Properties | |
C5H8N2O4 | |
Molar mass | 160.129 g·mol−1 |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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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]
The 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]