Journal of Diabetes & Metabolism

ISSN - 2155-6156



Oxidative Stress in Mongoloids and Caucasians with Type 1 Diabetes

Lubov Ilyinichna Kolesnikova, Marina Alexandrovna Darenskaya, Boris Yakovlevich Vlasov, Lyudmila Anatolievna Grebenkina, Natalya Victorovna Semenova, MariyaIgorevna Dolgikh, Tatyana Prokopievna Bardymova and Svetlana Vasilyevna Gnusina

Objective: It is known that the incidence of type1 diabetes is low among Mongoloid populations. Also, some studies have shown relationship of oxidative stress and this disease. Different parameters of lipid peroxidation and antioxidant defense system, lactate and Fe2+ plasma levels of the same ethnic control groups and groups with type1 diabetes in Mongoloids compared to Caucasians studied in attempt to determine ethnic differences.

Methods: Conjugated dienes, thiobarbituric acid reactants, reduced and oxidized glutathione ratio, total radicaltrapping antioxidant parameter, lactate and Fe2+ levels were evaluated in 65 subjects with type 1 diabetes (38 Mongoloids and 27 Caucasians) and in 82 healthy people (42 Mongoloids and 40 Caucasians). Spectral fluorofotometric methods were used. Statistical analysis was performed by parametric and non-parametric methods.

Results: Lipid peroxidation-antioxidant defense system parameters investigated are not significantly different in ethnic control groups. But, in type 1 diabetes patients mean levels of conjugated dienes, thiobarbituric acid reactants, total radical-trapping antioxidant parameter and ratio of reduced and oxidized glutathione levels were lower in Mongoloids compared to Caucasians. Fe2+ level in Caucasians were higher than of Mongoloids. Plasma lactate level in Mongoloids and in Caucasians was higher than in the control groups and in Caucasians higher than in Mongoloids.

Conclusion: Ethnicity can play a role in development of oxidative stress in non-compensated type1 diabetes. Perhaps, low incidence of type1 diabetes in Mongoloids is partly due to less lipid peroxidation - antioxidative defense, glucose and Fe2+ metabolic imbalance.