Sub-acute Exposure to Benzene Accelerates the Aging Process of Red Blood Cells; an In vivo Study

Background: The well-known toxic effects of benzene toxicity are bone marrow depression, reduction in blood cell counts, and induction of leukemia and aplastic anemia. This study was designed to evaluate biomarkers of aging in red blood cells (RBCs). Methods: Mice were exposed to benzene (50, 100, and 200 mg/kg/day) orally for 28 days. A group of benzene-exposed mice were injected intraperitoneally with N-acetylcysteine (NAC, 150 mg/kg/day). Hematological factors, erythrocyte morphology, and sialic acid content of RBCs along with oxidative stress biomarkers were investigated.  Results: Benzene dose-dependently reduced RBCs count, hemoglobin level, RBCs membrane sialic acid levels, the total antioxidant capacity of plasma, and G6PD activity of RBCs. The activity of antioxidant enzymes and lactate dehydrogenase, oxidative damage end-products and bilirubin levels, reticulocyte count, and RDW and MCV ranges increased in a dose-dependent manner. Poikilocytosis (spherocyte, burr cell, schistocyte and blister cell) and anisocytosis were observed in high doses of benzene.  Conclusion: Our results support the acceleration of RBCs aging and hemolytic anemia in mice exposed to benzene. Co-administration of NAC as an antioxidant effectively alleviated hematotoxicity of benzene.