Allergic asthma is a chronic inflammatory airway disease concomitant with oxidative stress. The aim of this study was to evaluate the effects of betaine against asthma-induced oxidative stress in experimentally animal model. 32 BALB/C mice were divided into four equal groups as: control, asthma, prednisolone and betaine groups. 100 μl of the solution (Ova albumin (OVA, 400 μg and AL(OH)3 gel in 1 ml of phosphate buffer) was injected intraperitoneally to each mouse on days 0, 7, 14 and 21 and sensitized with OVA drop, three times a week from days 27 until 84 in asthma, prednisolone and betaine groups. Prednisolone (3 mg/kg) and betaine (1% of the total diet) were administered at day 27 to 84 as orally once daily and vehicle to controls and asthma group. Sera were collected for IgE detection and lung tissue was taken for histopathology assessment. Glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD) activities, and glutathione content (GSH) as well as malondialdehyde (MDA) concentration as lipid peroxidation marker were also measured in the liver and kidney tissues. Pathological changes of the lung tissue were observed in the asthma and prednisolone groups. Prednisolone also caused significant increase level of anti-OVA IgE. The GPx activity increased significantly in the liver and kidney of asthmatic group when compared to the control and prednisolone groups. Liver MDA as lipid peroxidation marker was also significantly higher in the prednisolone-treated mice when compared to the other groups. Although the CAT and SOD activities as well as GSH content increased in the betaine and prednisolone-treated mice, these enhancements were not statically significant. Predinsolone as first choice in asthma treatment showed some oxidative properties. In contrast, betaine improved airway inflammation of lung tissue which may be associated with the antioxidant properties of betaine. This study provides a potential promising effect of betaine for treatment of asthma in future studies.