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    Effect of exercise on blood antioxidant status and erythrocyte lipid perodixation: Role of dietary supplementation of vitamin E
    (1999) Kelle M.; Diken H.; Sermet A.; Atmaca M.; Tumer C.
    We tested the effects of moderate physical exercise on the blood antioxidant capacity and erythrocyte lipid peroxidation in 21 Wistar albino rats. Erythrocyte superoxide dismutase (SOD) activity increased significantly (p<0.05) in control exercised animals (C-Ex), but catalase activity did not change. SOD activity was decreased by dietary supplementation of vitamin E (p<0.05). In vitamin E supplemented group (E-Ex), catalase activity was reduced in comparison to C-Ex group. Total glutathione (total GSH) level was unaffected by the exercise. However, significant reduction was observed in reduced glutathione (GSH), whereas oxidized glutathione (GSSG) increased (p<0.01 and p<0.001, respectively). In E-Ex animals, total GSH and GSH were increased in comparison to C-Ex group. GSH/GSSG ratio decreased abnormally in both exercised groups (p<0.001). Serum cholesterol and uric acid levels increased significantly after exercise (p<0.05). The susceptibility of erythrocytes to in vitro peroxidation increased in C-Ex and E-Ex animals (p<0.001 and p<0.01, respectively). Elevated malondialdehyde (MDA) concentration in serum attained statistical significance after exercise. However, this elevation was prevented by vitamin E supplementation. Our results indicated that moderate intensive treadmill running exercise was sufficient to result in muscle damage and increases in the susceptibility of erythrocytes to in vitro peroxidation. In addition, dietary supplementation of vitamin E is able to minimize oxidative damage caused by exercise.
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    Time-dependent changes in plasma ghrelin and angiotensin II levels in the diabetic nephropathy model
    (Parlar Scientific Publications, 2021) Gul C.; Kelle M.; Baylan M.; Yokus B.; Tasdemir E.
    Ghrelin is an appetite-enhancing anabolic hormone secreted from the stomach. Angiotensin II maintains sodium and potassium levels in body fluids and plays a very important role in the regulation of arterial blood pressure. Although their relationship with Type 2 diabetes and complications have been reported, their role in diabetic nephropathy is not fully understood. We investigated time dependent possible changes in plasma ghrelin and angiotensin II levels during the development and progression of diabetic nephropathy in experimental diabetic rat model. Adult 63 male Wistar Albino rats were randomly divided into 9 groups as 4 control (C1-C4), 4 diabetic (D1-D4) and one treatment (T) group. Group D1, sacrificed by cardiac puncture one week after diabetes, group D2 three weeks later, group D3 six weeks later, and groups D4 and T eight weeks later. Antidiabetic treatment was not administered to the D1-D4 group diabetic rats. Group T diabetic rats were treated with antidiabetic metformin (100 mg / kg / day) for 8 weeks. A single dose of 35 mg / kg intraperitoneal streptozotocin was administered to the rats to induce diabetes. Significant differences were found between the D4 and C4 groups in body weight, plasma glucose, ghrelin and angiotensin II, serum and urine creatinine levels. While there was a linear (positive) relationship between plasma ghrelin levels of all rats and urinary creatinine and creatinine clearance and body weight, negative correlations were found between plasma ghrelin and angiotensin II levels and fasting blood glucose levels of all rats. During the progression of diabetes and the development of diabetes-related nephropathy, plasma angiotensin and serum creatinine levels increased, while plasma ghrelin levels decreased over time. Therefore, it was concluded that changes in plasma ghrelin and angiotensin II levels in diabetic rats may be associated with the pathogenesis of diabetic nephropathy. © 2021 Parlar Scientific Publications. All rights reserved.