Ionizing radiation exposure can cause damage to diverse tissues and organs, with the hematopoietic system being the most sensitive. However, limited information is available regarding the radiosensitivity of various hematopoietic cell populations in the bone marrow due to the high heterogeneity of the hematopoietic system. In this study, we observed that granulocyte–macrophage progenitors, hematopoietic stem/progenitor cells, and B cells within the bone marrow showed the highest sensitivity, exhibiting a rapid decrease in cell numbers following irradiation. Nonetheless, neutrophils, natural killer (NK) cells, T cells, and dendritic cells demonstrated a certain degree of radioresistance, with neutrophils exhibiting the most pronounced resistance. By employing single-cell transcriptome sequencing, we investigated the early responsive genes in various cell types following irradiation, revealing that distinct gene expression profiles emerged between radiosensitive and radioresistant cells. In B cells, radiation exposure led to a specific upregulation of genes associated with mitochondrial respiratory chain complexes, suggesting a connection between these complexes and cell radiosensitivity. In neutrophils, radiation exposure resulted in fewer gene alterations, indicating their potential for distinct mechanisms in radiation resistance. Collectively, this study provides insights into the molecular mechanism for the heterogeneity of radiosensitivity among the various bone marrow hematopoietic cell populations.

With the ubiquitous and prolonged nature of human exposure to S-band electromagnetic fields (EMF, 2.45 GHz), concerns regarding its potential health impacts are growing. However, existing preclinical evidence is inconsistent, and a comprehensive assessment of its effects across multiple physiological systems is lacking. This study aimed to perform an integrated evaluation of the biological consequences of prolonged 2.45 GHz EMF exposure in mice, focusing on the reproductive, immune, metabolic, and hematopoietic systems. We established a murine model of prolonged EMF exposure, wherein mice were subjected to 2.45 GHz radiation (whole-body average specific absorption rate, SAR 15 W/kg) for 5 months. A combination of physiological monitoring, functional sperm analysis, comprehensive flow cytometry, hematopoietic stem cell functional assays, and metabolic challenge tests insulin tolerance test (ITT) and pyruvate tolerance test (PTT) was employed to assess systemic impacts. Our findings revealed a system-specific pattern of responses. Notably, prolonged EMF exposure did not induce measurable adverse effects on core physiological parameters, sperm functional integrity (kinematics and morphology), immune cell populations and distribution, or hematopoietic competence. In stark contrast, it significantly disrupted systemic glucose homeostasis, leading to elevated fasting blood glucose and impaired insulin sensitivity. This study demonstrates that biological effects of prolonged 2.45 GHz EMF exposure are not monolithic but exhibit distinct organ susceptibility. We identified a selective vulnerability in metabolic regulation, while reproductive, immune, and hematopoietic systems remained resilient under our specific exposure conditions. These findings challenge the universality of generalized toxicity claims, underscore the critical role of exposure parameters, and highlight metabolic dysfunction as a potential risk for prolonged EMF exposure, providing crucial insights for future risk assessment.

Ionizing radiation exposure can cause damage to diverse tissues and organs, with the hematopoietic system being the most sensitive. However, limited information is available regarding the radiosensitivity of various hematopoietic cell populations in the bone marrow due to the high heterogeneity of the hematopoietic system. In this study, we observed that granulocyte-macrophage progenitors, hematopoietic stem/progenitor cells and B cells within the bone marrow showed the highest sensitivity, exhibiting a rapid decrease in cell numbers following irradiation. Nonetheless, neutrophils, natural killer (NK) cells, T cells, and dendritic cells demonstrated a certain degree of radioresistance, with neutrophils exhibiting the most pronounced resistance. By employing single-cell transcriptome sequencing, we investigated the early responsive genes in various cell types following irradiation, revealing that distinct gene expression profiles emerged between radiosensitive and radioresistant cells. In B cells, radiation exposure led to a specific upregulation of genes associated with mitochondrial respiratory chain complexes, suggesting a connection between these complexes and cell radiosensitivity. In neutrophils, radiation exposure resulted in fewer gene alterations, indicating their potential for distinct mechanisms in radiation resistance. Collectively, this study provides insights into the molecular mechanism for the heterogeneity of radiosensitivity among the various bone marrow hematopoietic cell populations.