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Objective: The aim of the study was to investigate whether oxidative stress resulting from enhanced free-radical formation, inflammation and higher total oxidation status plays a role in the initiation, progression and pathology of type 2 diabetes (T2D). Materials and methods: A total of 207 participants were enrolled, which comprised of 157 T2D patients (experimental group), and 50 people without diabetes (control group). Any subject suffering from cardiovascular diseases, impaired renal or liver functions has been excluded. The activities of certain oxidase enzymes, total oxidative stress and inflammatory leukocyte markers were investigated and compared between the studied groups. Results: Of the patients, 29.3% had HbA1c level < 7% and 28.0% had FPG level ≤ 7 mmol/L. The NADPH oxidase and myeloperoxidase, both of which are major contributors to reactive oxygen species (ROS) production, showed significantly higher activities in patients than in controls (p < 0.0001 and p < 0.001 respectively). Malondialdehyde (MDA), one of the end products of lipid peroxidation, was significantly higher in the patients (p < 0.0001). The total oxidative stress that estimates the overall oxidation status, was also significantly higher in the patients. The inflammatory leukocyte markers including total white blood cell count, percentage of neutrophils, and the neutrophil to lymphocyte ratio (NLR) were significantly higher in the patients (p < 0.0001). Further, the NADPH oxidase activity showed significant positive correlations with MDA, and NLR in T2D patients. Conclusions: These findings suggest that excessive productions of ROS by the oxidase enzymes, NADPH oxidase and myeloperoxidase, cause increased oxidative stress which in turn led to cellular inflammatory responses in patients with T2D.