Background/Aim. Reduced systemic antioxidant defense is considered to play an important mediating role in pathogenesis of diabetic neuropathy. The aim of this study was to evaluate if the total antioxidant blood capacity (TAC) is reduced in patients with type 2 diabetes mellitus (DM) and diabetic distal symmetrical polyneuropathy (DDSP) and to correlate this antioxidant capacity with the degree of peripheral nerve dysfunction. Methods. This study involved 100 patients with type 2 DM and signs of DDSP, as well as the control group of 50 healthy subjects. The evaluation of DDSP was based on physical examination and nerve conduction studies. The degree of peripheral nerve dysfunction was estimated by scoring and analysing sensory and motor nerve conduction parameters (distal latency and amplitude of evoked potential, conduction velocity). Laboratory analyses involved blood glucose and HbA1C levels, as well as plasma TAC. Results. Blood glucose and HbA1C level was significantly higher in the patients than in the control group (p < 0.0001). The TAC was depleted in the diabetic group and the depletion was statistically significant (p < 0.0001). There was no significant correlation between the TAC and the serum glucose level, TAC and HbA1C level as well as between TAC and the duration of DM. There was no significant correlation between TAC and peripheral nerve conduction parameters. Conclusion. Total antioxidant blood capacity is reduced in patients with DDSP, but it does not correlate with blood sugar level, with the duration of DM or with the degree of functional nerve damage. These results show a reduced systemic antioxidant defence in patients with type 2 DM and DDSP. However, it is still unclear to what extent the oxidative stress is a contributing factor or leading cause of diabetic neuropathy, suggesting that further studies are necessary.