EFFECT OF ORAL ADMINISTRATION OF VITAMIN D ON HYDROGEN LEVEL IN DEXTRAN SULPHATE SODIUM INDUCED ULCERATIVE COLITIS IN MICE

Ulcerative colitis (UC) is a chronic inflammatory disorder of the colon associated with oxidative stress and overproduction of reactive oxygen species (ROS), notably hydrogen peroxide (H₂O₂). This study investigated the effect of oral vitamin D administration on hydrogen peroxide levels and oxidative status in dextran sulphate sodium (DSS)-induced ulcerative colitis in mice.Twenty adult male BALB/c mice were randomly assigned into four groups (n = 5 per group): normal control, DSS control, DSS + vitamin D, and DSS + sulfasalazine (standard drug control). Ulcerative colitis was induced in all but the control group by administering 2.5% DSS in drinking water for seven days. Following induction, the treatment groups received either vitamin D (2000 IU/day orally) or sulfasalazine (1000 mg/kg) for 28 days, while the control and DSS groups received normal saline. At the end of treatment, mice were sacrificed, and colon tissues were collected for biochemical analyses. Hydrogen peroxide concentration, antioxidant enzyme activities (catalase, glutathione peroxidase, and glutathione-S-transferase), and oxidative stress biomarkers were assessed spectrophotometrically using standard biochemical methods.Results showed that DSS administration caused a significant elevation (P < 0.05) in hydrogen peroxide generation compared to the normal control, indicating severe oxidative stress in the colonic tissue. Vitamin D administration markedly reduced H₂O₂ concentration to near-control levels, suggesting potent antioxidant activity. Additionally, vitamin D treatment led to a significant increase (P < 0.05) in catalase, glutathione peroxidase, and glutathione-S-transferase activities relative to the DSS group, reflecting restoration of endogenous antioxidant defense mechanisms. The DSS + vitamin D group also exhibited a significant reduction in colon weight and improved body weight gain compared to the DSS group, indicating reduced colonic inflammation and better systemic health.Comparatively, the DSS + sulfasalazine group showed partial improvements, but vitamin D produced a greater reduction in oxidative markers, emphasizing its stronger redox-modulating effect. These findings demonstrate that vitamin D supplementation mitigates DSS-induced oxidative stress, likely through upregulation of antioxidant enzymes and suppression of ROS formation.