Blood Catalase Activity in Gestational Diabetes is Decreased But Not Associated with Pregnancy Complications (Technical Briefs‪)‬

Gestational diabetes occurs with variable severity in 3%-5% of all pregnancies and may be related to oxidative stress and impaired antioxidant defenses (1). Antioxidant enzymes include superoxide dismutase, which produces hydrogen peroxide, and Catalase, which consumes hydrogen peroxide. Catalase is the main regulator of hydrogen peroxide metabolism (2), which is associated with diabetes mechanisms such as Glut 4 expression, insulin secretion, insulin signaling, protein tyrosine phosphatase regulation, and glucose transport stimulation (3). Hydrogen peroxide has novel insulin-like effects, e.g., inhibition of lipolysis and reactivation of phosphoenolpyruvate carboxy kinase (4,5), and insulin moderates hydrogen peroxide generation (6,7) and Catalase synthesis (8). High concentrations of hydrogen peroxide may damage heme proteins, cause cell death, and together with redox active metal ions, produce highly toxic hydroxyl radicals. High Catalase activity in erythrocytes seems to provide antioxidant defense for tissues with low Catalase activity, particularly pancreatic beta cells. Catalase is important in antioxidant defense against hydrogen peroxide (9,10), but there are conflicting reports of decreases (11,12), increases (13), and no change (14) in catalase activity in diabetes. A high incidence (14%) of diabetes mellitus observed in 63 Hungarian patients with inherited catalase deficiency (1 with type 1 and 7 with type 2 diabetes) could be associated with damage to oxidation-sensitive pancreatic beta cells by exposure to long-term increased hydrogen peroxide concentrations (15), but there have been conflicting reports from small studies of maternal and embryonic catalase in rat (16) and human (17) gestational diabetes.