Abstract
Background: The pathogenesis of diabetes mellitus (DM) was affected by oxidative stress. Many inflammatory markers having antioxidant property, among them ceruloplasmin (CP), which is the appropriate candidate to recognize the general insulin resistance in patients suffering from DM- Type II. Objectives: This study aimed to estimate some biochemical parameters (that considered markers of oxidative stress) in patients with DM type II (DM-II) compared to healthy controls and study the correlation between them. Materials and Methods: This study included 75 samples of blood serum divided into (50) samples (26 males and 24 females) as patients with DM-II. The control group included 25 healthy controls (15 males and 10 females). Ceruloplasmin (CP) was isolated from human serum using 60% ammonium sulfate precipitation, then estimated the activity and specific activity of enzyme. The isolated enzyme was characterized by 10% polyacrylamide gel electrophoresis. Some biochemical indicators were also estimated. These included random blood sugar (RBS), total protein, thiol, free amino, and carbonyl. Results: The electrophoresis results for both protein and glycoprotein stain indicated that the bands of CP in patients group have more intensity than the bands of healthy controls. There were nonsignificant increase in total protein, thiol/protein, carbonyl and carbonyl/protein levels, nonsignificant decrease in the free amino and free amino/protein levels, and significant increase in the RBS and thiol levels in patients group compared to healthy controls. The correlation results indicated that there were significant positive correlation between CP and RBS with r = 0.306. Conclusion: The findings may support an association between oxidation proteins and DM-II. The stronger response observed in serum CP and thiol from patients with the change in the concentration of proteins which suggest that these oxidative proteins markers contents may be useful in evaluating the progression of DM-II and in elucidating the mechanisms of disease pathogenesis.
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