Significant differences in the antioxidant systems of the roots of two chickpea (Cicer arietinum L.) cultivars differing in tolerance to drought were observed in under toxic boron (B) conditions. Three-week-old chickpea seedlings were subjected to 0.05 mM (control), 1.6 mM or 6.4 mM B in the form of boric acid (H3BO3) for 7 days. At the end of the treatment period, root length, dry weight, boron concentration, malondialdehyde (MDA) content, and the activities of antioxidant enzymes-superoxide dismutase (SOD), peroxidase (POX), catalase (CAT), ascorbate peroxidase (APOX) and glutathione reductase (GR)-were measured. Root length of the drought-tolerant Gokce cultivar did not change under 1.6 mM B but increased under 6.4 mM B. On the contrary, root length decreased in the drought-sensitive Kusmen cultivar under both B concentrations. While root dry weight was unaffected in Gokce, it decreased in Kusmen under both B concentrations. Boron concentration was significantly higher in Kusmen than in Gokce at both B levels. Significant increases in SOD and POX activities were observed in roots of both cultivars under 1.6 and 6.4 mM B. Root extracts exhibited three SOD and three POX activity bands in both cultivars under B stress when compared to control groups. Although CAT activity in Gokce was increased, it decreased in Kusmen at the highest B concentration as compared to control groups. Roots of both cultivars showed no significant change in APOX activity under B toxicity (except in 1.6 mM B treated roots of Kusmen) when compared to control groups. GR activity in the roots of Kusmen decreased significantly with increasing B concentration. However, a significant increase in GR activity was found in Gokce under 1.6 mM B stress. In addition, lipid peroxidation levels of drought-sensitive Kusmen increased, indicating more damage to membrane lipids due to B toxicity. Lipid peroxidation did not change in the drought-tolerant Gokce cultivar at either B concentration. These results suggest that roots of Gokce are better protected from B-stress-induced oxidative stress due to enhanced SOD, CAT and POX activities under high B levels.