The relationship between the activates of antioxidant enzymes in red blood cells and body mass index in Iranian type 2 diabetes and healthy subjects

Abstract

BackgroundDiabetes mellitus is a metabolic disorder characterized by increased production of free radicals and oxidative stress. The aim of this study was to evaluate the activity of antioxidant enzymes, superoxide dismutase (SOD), glutathione reductase (GR), and glutathione peroxide (GSH-PX) in type 2 diabetic patients compared with healthy subjects.MethodsThis cross-sectional study was conducted on 100 type 2 diabetic patients and 100 healthy controls. Total antioxidant capacity and fasting serum levels of SOD, GR, and GSH-Px were measured. All data were analyzed using SPSS software compatible with Microsoft Windows.ResultsThe activity levels of SOD were lower in diabetic patients (111.93 ± 354.99 U/g Hb) than in healthy controls (1158.53 ± 381.21 U/g Hb), but this was not significant. Activity levels of GSH-PX and GR in diabetics (62.33 ± 36.29 and 7.17 ± 5.51 U/g Hb, respectively) were higher than in controls (24.62 ± 11.2 and 3.16 ± 2.95 U/g Hb, respectively). The statistical difference in enzyme activity of both GSH-Px and GR was significant (P <0.05).ConclusionThe increasing production of free radicals and changes in activity levels of antioxidant enzymes in order to scavenge free radicals and/or the effect of diabetes on the activity levels of antioxidant enzymes has an important effect on diabetic complications and insulin resistance. Evaluation of the levels of antioxidant enzymes and antioxidant factors in patients at different stages of the disease, and pharmaceutical and nutritional interventions, can be helpful in reducing oxidative stress in type 2 diabetic patients. There were positive relationship between BMI and the activity of antioxidant enzymes including SOD, GR and GPX in both groups.

Role of Vitamin D on glycemic control and oxidative stress in type 2 diabetes mellitus

“…[47] There is a considerable body of evidence indicating that hyperglycemia may interfere with natural defense of the antioxidant system, in addition to increasing the production of free radicals. [48] Since SOD enzyme is part of the first line of defense against free radicals, it is expected that the activity of this enzyme may be affected by oxidative stress before the other antioxidant enzymes.…”

“…[49] Taheri et al . [47] indicated that SOD activity was lower in patients with diabetes compared with healthy controls. There is evidence to show that hyperglycemia is accompanied by the loss of Cu 2+ , which is an essential cofactor in SOD activity, and SOD is inactivated by glycosylation in erythrocytes.…”

POTENSI EFEK HIPOGLIKEMIK KOMBINASI EKSTRAK ETANOL UMBI BAWANG HUTAN (Eleutherine bulbosa) DAN KULIT BATANG KAYU MANIS (Cinnamomum burmanii) PADA TIKUS (Rattus norvegicus) DIABETES YANG DIINDUKSI STREPTOZOTOSIN DAN TOLERANSI GLUKOSA

“…Flavonoid diketahui sebagai antioksidan yang baik karena mempunyai sedikitnya dua gugus hidroksil pada posisi orto dan para (Kuntorini, 2013). Antioksidan dapat mengikat radikal bebas (Taheri, 2012), dan membentuk kompleks dengan logam. Kedua mekanisme tersebut membuat flavanoid memiliki beberapa efek, diantaranya menghambat peroksidasi lipid, menekan kerusakan jaringan oleh radikal bebas dan menghambat aktivitas enzim glukokinase yang dapat memproduksi senyawa glukosa (Lukacinova, 2008).…”

“…Kedua mekanisme tersebut membuat flavanoid memiliki beberapa efek, diantaranya menghambat peroksidasi lipid, menekan kerusakan jaringan oleh radikal bebas dan menghambat aktivitas enzim glukokinase yang dapat memproduksi senyawa glukosa (Lukacinova, 2008). Peningkatan enzim antioksidan berperan penting terhadap komplikasi diabetes dan resistensi insulin juga membantu dalammengurangistresoksidatif padapasien diabetes tipe 2 (Taheri, 2012).…”

Anti-Hyperglycemic and in-Vitro Antioxidant Effect of Kigelia Pinnata Fruit.

“…The main pathophysiological defect of type 2 diabetes is insulin resistance, a decrease in cellular response to insulin. Type-2 diabetes is manifested when pancreatic beta cells fail to compensate for chronic elevated blood glucose due to dysregulation of insulin-stimulated glucose uptake in the peripheral tissues (Taheri et al, 2012;Valiathan et al, 1998).…”