New Insights for Oxidative Stress and Diabetes Mellitus
Contributions of polyol pathway to oxidative stress in diabetic cataract. .. Epidemiologic relationships between A1C and all-cause mortality during a median. Oxidative stress is the outcome of an imbalance between the production and response relationship between hyperglycemia and overall oxidative stress in DM. Oxidative Stress: A Link between Diabetes Mellitus and Periodontal as a correlation between periodontal disease incidence and T2D.
Oxidative stress in type 2 diabetes: the role of fasting and postprandial glycaemia
Overexpression of superoxide dismutase in transgenic diabetic mice prevents diabetic retinopathy, nephropathy, and cardiomyopathy.
The aim of this review is to highlight advances in understanding the role of metabolite-generated ROS in the development of diabetic complications. Hyperglycemia, Mitochondria, Metabolic Memory, Epigenetic modifications, insulin resistance Introduction All forms of diabetes are characterized by hyperglycemia, a relative or absolute lack of insulin action, pathway-selective insulin resistance, and the development of diabetes-specific pathology in the retina, renal glomerulus, and peripheral nerve.
Diabetes is also associated with accelerated atherosclerotic disease affecting arteries that supply the heart, brain, and lower extremities. In addition, diabetic cardiomyopathy is a major diabetic complication. Diabetes and impaired glucose tolerance increase cardiovascular disease risk three to eight-fold.Oxidative Stress, Antioxidants and Complications of Diabetes
Finally, new blood vessel growth in response to ischemia is impaired in diabetes, resulting in decreased collateral vessel formation in ischemic hearts, and in non-healing foot ulcers [ 3 ]. Also, periodontal disease was stated the 6th complication of diabetes mellitus.
Oxidative Stress: A Link between Diabetes Mellitus and Periodontal Disease
Reactive oxygen species ROS or free oxygen radicals are products of normal cellular metabolism and are produced in case of oxidative processes. Many biochemical pathways strictly associated with hyperglycemia, such as glucose autooxidation, polyol pathway, prostanoid synthesis, and protein glycation, can increase ROS production.
Furthermore, endothelial cell exposure to elevated levels of glucose can lead to ROS production [ 3 ]. This might be one of the reasons why alterations of periodontal tissues occur in type 2 diabetes subjects T2Deven in the absence of dental plaque and calculus which are the main etiologic factors of periodontal disease.
Objective The aim of this study was to investigate oxidative stress that occurs in the periodontium of subjects with type 2 diabetes mellitus without signs of periodontal disease and to establish a possible link between this systemic condition and the morphologic changes in periodontal structures.
Material and Methods The present study was conducted on two groups of patients; one consisted of ten diabetic patients without signs of periodontal disease and the other one consisted of eight systemically and periodontally healthy subjects as controls.
All diabetic subjects included in the present study had records of at least 4 to 5 years of diagnosed T2D, were on medication with oral antidiabetic drugs, and all had well-controlled T2D; none was insulin treated and none used any antioxidant agent. Subjects aged 30 to 58, nonsmokers, without any inflammatory disease or use of anti-inflammatory drugs in the last three months prior to the study.
This study was approved by the Ethical Committee of UMF Tg-Mures, and all the patients included in the study signed for informed consent. From each subject biopsy specimens were obtained during the extraction of irrecoverable teeth.
Biopsy specimens were harvested from a dental-periodontal unit in the posterior region of dental arches. Histopathological examination was performed using formalin-fixed, paraffin-embedded tissue fragments following standard protocols. The micron thick tissue sections were stained with hematoxylin-eosin stain and also digitally archived using Zeiss MiraxScan system. From conserved tissue biopsies we determined the levels of malondialdehyde MDA as a marker for OS and glutathione GSH as a marker of defense antioxidant mechanism, using the fluorometric methods according to Conti et al.
Mean age of patients in study group was and in controls, with a nonsignificant difference between groups. The mean MDA value in diabetic tissues was 3.
Statistical comparison between the two groups yielded a Figure 1.
Comparison between MDA tissue levels in diabetics versus controls. The mean GSH value in diabetic subjects was 2.
- International Journal of Endocrinology
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- Oxidative stress in type 2 diabetes: the role of fasting and postprandial glycaemia
Comparison between GSH tissue levels in diabetics versus controls. Histological alterations in tissue sections obtained from diabetic patients were present in both the epithelium and the lamina propria of the gingival mucosa.
The Role of Oxidative Stress and Antioxidants in Diabetic Complications
The epithelium displayed variable amounts of acanthosis and parakeratosis, with reduced quantities of acute inflammatory infiltrate composed mostly of polymorphonuclear leucocytes segmented granulocytes throughout its thickness and in superficially located microabscesses. A diffuse polymorphous inflammatory infiltrate consisting of lymphocytes, plasma cells, and, to a lesser extent, granulocytes was present in the mildly fibrotic lamina propria, displacing collagen fibers and surrounding ectatic blood vessels and exteriorized erythrocytes Figures 3 and 4.
The causes of the development of cardiorenal syndrome in T1DM are poorly understood. Previous studies suggest that endothelial dysfunction and the concomitant atherosclerotic process may lead to simultaneous development and progression of renal and cardiac pathology, since endothelial dysfunction is already present at the early stages of T1DM.
Due to electron spin constraints, the oxygen molecule cannot readily react with organic substrates. The first mechanism of activation is absorption of sufficient energy to reverse the spin on one of the unpaired electrons, called a monovalent reduction. The biradical form of oxygen is in a triplet ground state because the electrons have parallel spins.
If triplet oxygen absorbs sufficient energy to reverse the spin of one of its unpaired electrons, it will become singlet oxygen, in which the two electrons have opposite spins [ Figure 1 ]. This activation overcomes the spin restriction and singlet oxygen can consequently participate in reactions involving the simultaneous transfer of two electrons divalent reduction.
The second mechanism of activation is by the stepwise monovalent reduction of oxygen to form superoxide O2H2O2, hydroxyl radical OH and finally water according to the scheme shown in Figure 2.