Metabolomics reveals aging-associated attenuation of noninvasive radiation biomarkers in mice: potential role of polyamine catabolism and incoherent DNA damage-repair.

摘要: Development of methods for rapid screening and stratification subjects after exposure is an integral part countermeasures against radiation. The potential demographic history-related heterogeneity exposed populations warrants robust biomarkers that withstand reflect such differences. In this study, the effect aging repeated on metabolic response to sublethal irradiation was examined in mice using UPLC-ESI-QTOF mass spectrometry. Aging attenuated postexposure elevation excretions DNA damage as well N(1)-acetylspermidine. Although N(1)-acetylspermidine 2'-deoxyuridine highly correlated all age groups, xanthine poorly older mice. These results may established decline damage-repair efficiency associated with indicate a novel role polyamine metabolism process. at long intervals did not affect N(1)-acetylspermidine, 2'-deoxyuridine, xanthine, it significantly attenuate 2'-deoxycytidine thymidine compared single exposure. However, these were found identify accuracy ranging from 82% (xanthosine) 98% (2'-deoxyuridine), irrespective their history. This indicates can act noninvasive signatures radiation