Browsing by Author "Engin, A"

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    Thyroid hormones-mediated effects of insulin on antioxidant enzymes from diabetic rat hearts
    Kosova, F; Altan, N; Sepici, A; Engin, A; Kocamanoglu, N
    Free radicals, oxidative stress, and antioxidants have become commonly used terms in modern discussion of disease mechanisms. Accumulation of evidence suggests that toxic oxygen-derived reactive free radicals (superoxide, peroxide and hydroxyl radicals) play a crucial role in etiology of diabetes and its complication. Thus, it was aimed to determine the role of thyroid hormones in reversal of antioxidatant enzyme activities and lipid peroxidation alterations observed in experimentally induced diabetic rat hearts. The present study investigates the antioxidant enzyme activities such as SOD, CAT, GSH-Px and lipid peroxidation products in cardiac tissues of streptozotosin (STZ)-induced diabetic rats before and after thyroidectomy. Our results showed that CAT, GPx enzyme activities and FOX, MDA levels were increased (p<0.05) and SOD, Mn-SOD, Cu-SOD activities were decreased (p<0.05) during diabetes, hypothyroidism and hypothyroidism with diabetes, which can be regulated in different percentages with treatment of insulin and various doses of thyroid hormone (p<0.05). In conclusion, in this study, the possible contribution of thyroid hormones to the insulin effect of normalizing the induced diabetic changes in cardiac tissue and serum of rat has been seen (Tab. 5, Ref. 32). Full Text in PDF www.elis.sk.
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    Oxidative DNA damage: the thyroid hormone-mediated effects of insulin on liver tissue
    Altan, N; Sepici-Dinçel, A; Sahin, D; Kocamanoglu, N; Kosova, F; Engin, A
    Thyroid hormone affects glucose homeostasis with its actions between the skeletal muscle and liver and the altered oxidative and non-oxidative glucose metabolism. In our study three chemicals are considered biomarkers associated with oxidative stress for protein modifications were measured; 8-hydroxy-2-deoxyyguanosine (8-OHdG), a major lesion that can be generated by reactive oxygen species for DNA damage, protein carbonyl content (PCO), products of protein oxidation and advanced oxidation protein products (AOPPs) a dithyrosine containing cross-linked protein products. The purpose of the recent study was to determine the effects of insulin and T4 or their combination in diabetic, thyroidectomized, or diabetic-thyroidectomized rats and possible relations with oxidative DNA and protein damages. For this purpose, rats were assigned to eight groups: Group 1; control, Group 2; diabetes, Group 3; diabetes + insulin, Group 4; surgically thyroidectomized control, Group 5; thyroidectomized + diabetes, Group 6; thyroidectomized + diabetes + insulin, Group 7; thyroidectomized + diabetes + insulin + thyroid hormone, levothyroxin sodium, 2.5 mu g/kg and Group 8; thyroidectomized + diabetes + insulin + thyroid hormone, levothyroxin sodium, 5.0 mu g/kg for 5 weeks. After the genomic DNA of liver tissues was extracted, the ratio of 8-OHdG to deoxyguanosine and liver tissue protein oxidation markers was determined. The main findings of our recent study were the increased 8-OHdG levels during the diabetes, hypothyroidism, and hypothyroidism with diabetes, which can be regulated in different percentages with the treatment of 2.5 and 5.0 mu g/kg doses of thyroid hormone and the altered protein carbonyl and AOPP levels of liver tissue. Consequently, it was observed that the DNA and protein damage induced by oxidative stress in diabetes could be regulated by dose-dependent thyroid hormone-mediated effects to insulin treatment.