Odebunmi, Oluwaseun2020-04-232020-04-232020-04-23http://hdl.handle.net/10393/40413http://dx.doi.org/10.20381/ruor-24646There is substantial evidence on the carcinogenic properties of high doses of Ionizing Radiation (IR), however, whether such risks exist following exposure to low doses of radiation (LDR) (below 100mGy) remains controversial. The longevity of skeletal muscle stem cells in the body as a “satellite pool” increases their chances of accumulating genotoxic damage from stressors including IR. LDR has been reported to reduce these threats and salvage the health and survival of the skeletal muscle and that of the whole body. Previous studies suggested that muscle myoblasts exposed to LDR (10 and 100mGy) retain their myogenic capacity over a prolonged period of time better than non-irradiated control cells. Therefore, the aim of this study was to determine whether the observed LDR-triggered delay in ageing and functional decline was associated with enhanced genomic stability and error-free Homologous Recombination (HR) repair. To achieve this, mouse (C2C12) and human (HSKM) myoblasts were exposed to 10 or 100mGy of gamma-radiation and grown under optimal conditions for up to 12 (C2C12) or 2 weeks (HSKM). These cells were examined at time points 0, 4, 8 and 12 weeks for function, double-strand breaks (DSB) formation and repair and genomic instability. The results showed the suppression of genomic instability following exposure to LDR and a slight enhancement of HR repair in aged mouse myoblasts. On the other hand, LDR did not affect the generic DSB repair capacity. The unpronounced changes in the human model suggest that responses to LDR vary between species. The variability in the results still leaves a gap as to whether the improved function induced by LDR is associated with better HR activity and may imply alternative DNA repair mechanisms.enIonizing RadiationMyoblastsMyogenicityDNA damageDNA repairDouble-strand BreaksLDR primingHomologous RecombinationNon-Homologous End JoiningGenomic InstabilityThesis