Oxidative stress-induced alterations in bone marrow cytomorphology in BALB/c mice

Background: Bone marrow (medulla ossium) is the principal hematopoietic organ in mammals, accounting for 1.5–2% of body weight in mice. Oxidative stress, defined as an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense, is not only a physiological byproduct of metabolism but also a key pathological factor when excessive. Elevated ROS can disrupt bone marrow homeostasis, impair hematopoietic balance, and promote inflammatory responses. Aim: To investigate in vivo the cytomorphological alterations of bone marrow under oxidative stress in BALB/c mice. Methods: Male BALB/c mice were randomly allocated into two groups: (1) control (physiological saline) and (2) oxidative stress (AlCl₃ solution). Oxidative stress symptoms appeared within 30 minutes of AlCl₃ administration. Bone marrow smears were prepared from femurs. For each specimen, 500 cells were counted and classified into myeloid and erythroid lineages. Megakaryocytes were quantified across 10 high-power fields (HPF). The myeloid-to-erythroid (M:E) ratio was calculated for comparative evaluation. Results: Control animals showed a physiologically balanced hematopoietic profile, with segmented neutrophils predominating and active erythropoiesis represented by rubricytes and metarubricytes. The mean M:E ratio was 1.69, consistent with reported physiological values (1.6–1.9). In the oxidative stress group, a significant increase in segmented neutrophils and their precursors (promyelocytes, metamyelocytes, myeloblasts) indicated enhanced granulopoiesis. Megakaryocytes averaged 15/10 HPF, a 1.9-fold increase compared to controls. The M:E ratio rose to 2.96, demonstrating hematopoietic imbalance and an inflammatory marrow environment. Conclusion: AlCl₃-induced oxidative stress significantly alters bone marrow cytomorphology in BALB/c mice, characterized by increased granulopoiesis, elevated megakaryocyte density, and a pathologically high M:E ratio. These findings confirm that oxidative stress profoundly disrupts hematopoietic homeostasis and highlight the suitability of this in vivo model for studying ROS-mediated hematological alterations.