This article investigates the responses of Brassica campestris seedlings to an acute level of nitrogen dioxide (NO2) exposure in a plant growth chamber, and examines whether pretreating plants with hydrogen peroxide (H2O2) will alleviate NO2-caused injury. Twenty-eight-day-old B. campestris plants sprayed with 10 mmol L-1 H2O2 aqueous solution (corresponding to approximate 1.0 mg H2O2 per single plant) were exposed to different concentrations of NO2 (0.25, 0.5, 1.0, and 2.0 μL L-1, respectively) for 24 h under controlled environment. To measure the plant biomass, the plants were fumigated with the same NO2 concentrations as mentioned above for 7 h per day (8.00-15.00) for 7 days. As a control, charcoal filtered air alone was applied. Data were collected on plant biomass, total chlorophyll, photosynthetic rate, stomatal conductance, nitrate and nitrate reductase (NR), antioxidative enzymes, ascorbate (ASA), and malondialdehyde (MDA), immediately after exposure. The results showed that exposure to a moderate dose of NO2 (e.g., 0.25 μL L-1) had a favorable effect on plants, and the dry weight of the above-ground part increased, whereas the exposure to high NO2 concentrations (e.g., 0.5 μL L-1 or higher) caused a reduction in the plant biomass and the total chlorophyll, when compared with the control. In addition, at 0.5 μL L-1 or higher NO2 concentrations, prominent increases in the MDA level and superoxide dismutase (SOD) and NR activities were observed. Exposure to 1 μL L-1 and higher NO2 resulted in necroses appearing on older leaves, and an increase in catalase (CAT) activity, decrease in ASA content, increased accumulation of NO3-, and reduction in photosynthesis, when compared with the controls. No changes were detected in stomatal conductance under NO2 fumigation. The pretreatment with 10 mmol L-1 H2O2 alleviated significantly NO2- caused biomass decrease and photosynthetic inhibition when compared with H2O2-untreated plants. Under NO2 fumigation, further induction in SOD and CAT activities occurred in H2O2 treated plants when compared with H2O2- untreated plants. The effect of NO2 on the ASA and MDA contents was also absent in H2O2-treated plants. However, the H2O2 treatment did not alter the nitrate content and NR activity in plants under NO2 fumigation. The H2O2 treatment caused a lower rate of stomatal conductance. Taken together, these data suggest that fumigation with an acute level of NO2 causes oxidative damage to B. campestris seedlings. The H2O2 pretreatment markedly protects plants against NO2 stress and this may be associated with inducible antioxidative level. NO2 fumigation contributes, at least in part, to the enhanced levels of nitrate in B. campestris leaves. This article investigates the responses of Brassica campestris seedlings to an acute level of nitrogen dioxide (NO2) exposure in a plant growth chamber, and examines whether pretreating plants with hydrogen peroxide (H2O2) will alleviate NO2-caused injury. Twenty-eight-day- old B. campestris plants sprayed with 10 mmol L -1 H2O2 aqueous solution (corresponding to approximate 1.0 mg H2O2 per single plant) were exposed to different concentrations of NO2 (0.25, 0.5, 1.0, and 2.0 μL L-1, respectively) for 24 h under controlled environment. To measure the plant biomass, the plants were fumigated with the same NO2 concentrations as mentioned above for 7 h per day (8.00-15.00) for 7 days. As a control, charcoal filtered air alone was applied. Data were collected on plant biomass, total chlorophyll, photosynthetic rate, stomatal conductance, nitrate and nitrate reductase (NR), antioxidative enzymes, ascorbate (ASA), and malondialdehyde (MDA) exposure to a moderate dose of NO2 (eg, 0.25 μL L-1) had a favorable effect on plants, and dry weight of the above-ground part increased, but the exposure to high NO2 concentrations (eg, 0.5 μL L- at higher than 0.5 μL L-1 or higher NO2 concentrations, prominent increases in the MDA level and superoxide dismutase (SOD) and NR activities Exposure to 1 μL L-1 and higher NO2 resulted in necroses appearing on older leaves, and an increase in catalase (CAT) activity, decrease in ASA content, increased accumulation of NO3-, and reduction in photosynthesis, when compared with the controls. No changes were detected in stomatal conductance under NO2 fumigation. The pretreatment with 10 mmol L-1 H2O2 alleviated significantly NO2- caused biomass decrease and photosynthetic inhibition when compared with H2O2-untreated plants. Under NO2 fumigation, further i nduction in SOD and CAT activities occurred in H2O2 treated plants when compared with H2O2-untreated plants. However, the effect of NO2 on the ASA and MDA contents was also absent in H2O2-treated plants. However, the H2O2 treatment did not alter the nitrate content and NR activity in plants under NO2 fumigation. The H2O2 treatment caused a lower rate of stomatal conductance. Taken together, these data suggest that fumigation with an acute level of NO2 causes oxidative damage to B. campestris seedlings. The H2O2 pretreatment markedly protects plants against NO2 stress and this may be associated with inducible antioxidative level. NO2 fumigation contributes, at least in part, to the enhanced levels of nitrate in B. campestris leaves.