TBI causes persistent increases in ROS production and cell cycling in HSCs without induction of telomere shortening. BMCs were harvested from control (CTL) and irradiated (TBI) mice 2 months after 6 Gy TBI as described. (A) Fold increases in ROS production in BM HPCs, LSK cells, MPPs, HSCs, ST-HSCs, and LT-HSCs after TBI are presented as mean ± SD (CTL: n = 4 ; TBI: n = 6). *P < .05, TBI vs CTL. (B-C) Percentages of G₀ (B) and BrdU-positive cells (C) in BM HPCs, LSK cells, MPPs, HSCs, ST-HSCs, and LT-HSCs from control (CTL) and irradiated (TBI) mice are presented as mean ± SD (CTL: n = 4 ; TBI: n = 6). *P < .05, **P < .01, and ***P < .001, TBI vs CTL. (D) Representative flow plots for telomere length measurement in T cells and myeloid cells (M cells) by flow FISH. (E) The relative telomere lengths of these cells from 3 independent experiments using sorted T and M cells pooled from 3 to 4 TBI or control (CTL) mice per group are presented as mean ± SD of relative MFI of telomere fluorescent staining. (F) Relative telomere lengths of HSCs, LSK cells, T cells, and myeloid cells (M cells) from control (CTL) and irradiated (TBI) mice analyzed by qPCR-based telomere length assays. Data from 3 independent experiments using sorted HSC, LSK cells, T cells, and M cells pooled from 3 to 4 mice per group are presented as mean ± SD of the ratios of telomere vs the 36B4 single-copy gene.