| Diabetic retinopathy is one of the most frequent and severe microang ium complications of diabetes mellitus, and the exact mechanism of its development remain selusive. Oxidative stress is defined as a serious imbalance between the production of reactive species and antioxidant defenses, leading to potential tissue damage. Diabetes induced metabolic abnormalities, activation of severecy to kines and cell apoptosis, which are implicated in the development of diabetic retinopathy, appear to be influenced by elevated oxidative stress, which plays a key role in the pathogenes is of diabetic retinopathy. Also, studies have found that blood cell volume change linked with diabetic retinopathy.Oxidative stress is generally defined as active oxygen molecules to reactive oxygen species, groups (ROS) and nitrogen reactive groups (active nitrogen species, etc.) of RNS and/or remove, causing the body of oxygen generation and antioxidant defense functions of the balance between the disorder. ROS include free radicals, such as super oxide anion hydroxyl radicals (O) OH, and the radical groups such as hydrogen peroxide (H2O2) and hydrogen HOCl RNS and iodate (including free radicals) like nitric oxide (NO) and nitrogen dioxide (NO2 -), and the free radicals as peroxide ONOO nitrogen (-).Endogenous antioxidant enzyme system is a system, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (peptide GSH2Px), Another kind is the enzyme system, including vitamin C, vitamin E, carotenoids, coenzyme Q, glutathione (GSH) peptides, homocysteine, copper blue protein, acetone, bilirubin, alpha lipoic acid (2), LA melatonin (MLT), albumin, lactoferrin protein [7]. Its defense mechanism embodied in: on one hand through the formation of free radicals directly removal, protection organization from damage, On the other hand, by albumin, lactoferrin protein hemoglobin protein, combined with ROS produced as the metal ions, thus inhibiting ROS. Pathological conditions, the body produces a large increase of ROS, at the same time with the internal antioxidant defenses, active antioxidants in antioxidant defense system produces beyond its removal and oxidative stress on lipid membranes, and destruction of cells to break down, causing death, Protein, causing damage and loss of function, protein degeneration of enzyme deactivation, The destruction of nucleic acids and chromosome, cause DNA damage fracture of the chain, chromosome aberration and fracture, resulting in tissue injury and disease.Due to the beta cells and retinal cells, make both vulnerable to SOD damage. Oxidative stress in diabetes development process may mechanism of pancreatic islet cells (1): the damage of the performance for the ROS can damage to cells directly within the protein, can also be modified with membrane lipid, sugar, hyaluronic acid, reaction material, can have a direct damage to cells, On the other hand, for through the cell can ROS DNA damage, activate cellsκB NF-islet cell apoptosis mediated factors, in addition, mitochondrial oxidatie stress toxicity is within the direct causes of beta cell apoptosis. (2) increasing insulin resistance, high blood glucose levels of oxidative stress condition, as functional signal molecules in cell activation ROS of stress sensitivity signaling pathways, and studies have shown that these signaling pathways is closely related with IR. While oxidatie stress produce abnormal metabolic pathways as polyols way, amino sugar accumulation and AGEs, the way to influence the way PKC activation of these approaches, DR interaction is created, we see the pathological changes of the diabetic retinopathy.Also, studies have found that patients with diabetes cells with diabetes the abnormal morphology, abnormal RBC volume increases, the structure, and appear erythrocyte deformation caused by increased blood viscosity, reduce blood flow, microcirculation, effective perfusion inadequacy, Large volume, enzyme activity of platelet adhesion and release, and ability to gather ability increases, and promote obviously thrombosis, eventually led to the development of capillaries.Patients with type 2 diabetes as the research objects, which is divided into diabetic retinopathy (DM2) and no concurrent diabetic retinopathy group (DM1), select age-matched healthy people as control group. Record gender, age, body mass index commonly material, measurement of TG, TC, HbA1C, MCV, MPV and MDA and SOD TAOC serum concentrations. Results show that, the CN group, DM1 group and DM2 group, three groups of serum level of MDA have remarkable significance (P<0.05), with rising trend. Serum level of TAOC SOD, in three groups have remarkable significance (P<0.05), with gradually drop tendency. In three groups MCV have remarkable significance (P<0.05). MPV between the DM1, DM2 groups have remarkable significance (P< 0.05). In patients with DR, do MDA , SOD, TAOC, with the MCV, MPV correlation analysis, MDA positively correlated with the MCV, MPV, remarkable significance (P<0.05), and SOD positively correlated with the MCV, has the remarkable significance (P<0.05). SOD has no correlation with MPV (P > 0.05), TAOC has no correlation with MCV and MPV (P> 0.05).Experimental results suggest that oxidatie stress is in the occurrence and development of T2DM and DR, and plays an important role in the blood volume changes in patients with DR. Therefore application of effective antioxidant therapy, early intervention oxidatie stress, from many link, may delay diabetes complications, actively looking for effective antioxidant therapy appears especially important in patients. In DR, oxidatie stress due to the change of blood cell volume, and the process of concrete mechanism is unclear, deserves further study. |
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