Chemistry:Thymine glycol
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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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PubChem CID
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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). | |
| Infobox references | |
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, stroke
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]
References
- ↑ Basu, AK; Loechler, EL; Leadon, SA; Essigmann, JM (1989). "Genetic effects of thymine glycol: site-specific mutagenesis and molecular modeling studies.". Proc. Natl. Acad. Sci. U.S.A. 86 (20): 7677–81. doi:10.1073/pnas.86.20.7677. PMID 2682618. Bibcode: 1989PNAS...86.7677B.
- ↑ 2.0 2.1 2.2 "Oxidative damage to DNA: relation to species metabolic rate and life span". Proc. Natl. Acad. Sci. U.S.A. 85 (8): 2706–8. 1988. doi:10.1073/pnas.85.8.2706. PMID 3128794. Bibcode: 1988PNAS...85.2706A.
- ↑ "Age-associated modifications of Base Excision Repair activities in human skin fibroblast extracts". Mech. Ageing Dev. 131 (11–12): 661–5. 2010. doi:10.1016/j.mad.2010.09.002. PMID 20854835.
- ↑ 4.0 4.1 "Partial loss of the DNA repair scaffolding protein, Xrcc1, results in increased brain damage and reduced recovery from ischemic stroke in mice". Neurobiol. Aging 36 (7): 2319–30. 2015. doi:10.1016/j.neurobiolaging.2015.04.004. PMID 25971543.
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