Abstract

Chronic exposure to sodium arsenite (SA), a common environmental pollutant, induces systemic toxicity characterized by hematological dysregulation and organ-specific inflammation, primarily through oxidative stress pathways. Vitamin E (α-tocopherol) is a potent lipid-soluble antioxidant with potential protective effects against such toxicity. This study investigated the ameliorative impact of Vitamin E on SA-induced hematological alterations and inflammatory indices in Wistar rats. Thirty-five male Wistar rats (150-180g) were randomly divided into five groups (n=7). Group A (Control) received corn oil (2ml/kg), Group B received Vitamin E (50 mg/kg), Group C received SA (10 mg/kg), Group D received SA (10 mg/kg) + Vitamin E (25 mg/kg), and Group E received SA (10 mg/kg) + Vitamin E (50 mg/kg). All treatments were administered orally for 14 days. Animals were sacrificed, and blood and organs (heart, kidney) were collected for analysis of hematological indices, nitrite levels, myeloperoxidase (MPO) activity, and reactive oxygen and nitrogen species (RONS). SA exposure caused significant (p<0.05) hematotoxicity (anemia, leukocytosis, neutrophilia, lymphopenia) and elevated inflammatory markers (nitrite, MPO, RONS) in the heart and kidney. Co-administration of Vitamin E, particularly at 50 mg/kg, dose-dependently and significantly (p<0.05) reversed these SA-induced alterations, restoring hematological parameters and attenuating inflammatory and oxidative stress markers. The findings demonstrate that Vitamin E exerts a potent protective effect against sodium arsenite-induced toxicity by ameliorating hematological abnormalities and mitigating inflammation and oxidative stress.

Keywords: Sodium arsenite, Vitamin E, Hematology, Inflammation, Oxidative stress, Wistar rats