Instability in circulation, hypoperfusion, hypoxia, and ischemia in pulmonary thromboembolism (PTE) may occur as a result of failure in pulmonary circulation. All these conditions cause inflammation and oxidative stress. We aimed to investigate inflammatory markers, asymmetric dimethylarginine (ADMA) levels, and the oxidant-antioxidant balance in patients with PTE. This study was conducted as a prospective case-control study. Thirty-eight patients with PTE enrolled to the study. Age- and gender-matched 38 healthy subjects without risk factors for pulmonary embolism were selected as control group. Venous blood samples were obtained from the PTE patients during the initial diagnosis and at the first month of treatment and from the control subjects. Interleukine-6 (IL-6), tumor necrosis factor alpha (TNF-α), total antioxidant status (TAS), total oxidant status (TOS), and ADMA levels were measured for all the samples. The results of patients and healthy subjects were compared. The mean age of the control group was 51.81 ± 15.18 years, and the mean age of the patients was 52.90 ± 18.22 years (p = 0.770). Deep venous thrombosis was present in 68 % of the patients. While we found significant differences between the patient and control groups in terms of IL-6, TAS, TNF-α, ADMA and oxidative stress index (OSI) values (p = 0.001, p = 0.011, p = 0.038, p = 0.028, and p = 0.024, respectively), the TOS value was not different between the groups (p = 0.080). The ADMA, TNF-α, TAS, TOS, and OSI values of the patients during the initial diagnosis and at the first month of treatment were not different (p > 0.05). The results of this study indicate an increased inflammation, endothelial damage, and oxidative stress in PTE. No difference at the first month of therapy suggests ongoing processes. We consider that these markers may be useful in the diagnosis and follow up of PTE.
Background: Diabetes mellitus is one of the major health problems for people all over the world today. According to international diabetes federation reports, diabetes affects 382 million people worldwide. Environmental pollutants have deleterious effects on glucose metabolism and cause insulin resistance. We aimed to investigate the effects of the environmental pollutants benzo(a)pyrene, and the therapeutic potential of resveratrol. Methods: 20 µM of benzo(a)pyrene was administered after 48 h of resveratrol (80 µM) application for 24 h in INS-1 (832/13) insulinoma cells. The cells were treated with 20 μM benzo(a)pyrene for 24 hours after 48 hours initial preconditions with 10 μM resveratrol. Oxidative stress status, insulin secretion and apoptosis were analyzed by molecular techniques. Results: Though resveratrol increased the antioxidant status which was decreased by benzo(a)pyrene, interestingly, it increased the oxidative status. Resveratrol increased benzo(a)pyrenedepleted reduced glutathione levels to the control level. The mRNA expression levels of beta-cell functions associated with genes insulin-1, insulin-2 and sirtuin-1 were upregulated by resveratrol. Resveratrol treatment elevated the insulin concentration of culture medium, and the mRNA expression of forkhead box protein-1 gene. Resveratrol upregulated benzo(a)pyrene-downregulated p53 gene expression. On the other hand, benzo(a)pyrene-downregulated mRNA expression of B-cell lymphoma-2 was induced by resveratrol treatment. Conclusion: The data showed that resveratrol could reverse the oxidative alterations, functional impairments and the carcinogenetic effects of benzo(a)pyrene in pancreas beta-cells.
Background/aim: Acetylsalicylic acid (ASA) treatment in diabetic patients is very important owing to the increasing hyperactivity of thrombocytes and atherosclerosis. In several investigations, it was reported that diabetes caused increased coronary artery disease, cerebrovascular disease, and death. In this study, we aimed to investigate the effect of ASA on osmoregulation, glycemic control, and some biochemical parameters in rats induced with experimental diabetes type 2.Materials and methods: Twenty-four rats were randomly divided in four groups: control (I), ASA control (II), diabetic (III), and ASA diabetic (IV). Diabetes was induced by streptozotocin treatment (30 mg/kg, twice, intraperitoneal injection) in obese rats. ASA (150 mg/kg body weight, orally) was administered for 5 weeks in the ASA control and ASA diabetic groups. Serum electrolytes, creatinine, albumin, and total protein levels were analyzed with an autoanalyzer. Arginine vasopressin (AVP) and insulin were analyzed by ELISA techniques.Results: At the end of the study ASA treatments had decreased the fasting blood glucose levels but had interestingly increased the serum AVP levels in diabetics rats. Conclusion:AVP levels were increased 2-fold by ASA treatment in diabetic rats. For the first time in this study, the hypoglycemic effect of ASA was attributed to an increase in blood volume by AVP levels. This explanation may be a new approach to the literature on this topic.
It was assumed that apoptosis is the main factor in beta cell deaths in type II diabetes. Apoptosis is important owing to eradicate the damaged or harmful cells without inflammation in various biological facts. This process is also important for homeostasis of organism. B cells are often exposed to ER stress due to excess insulin secretion. In recent years, it was showed that endoplasmic reticulum was an important organelle in apoptotic signal conduction. Investigations including apoptosis induced ER stress will supply new approaches in to clarify the new mechanisms in diabetic pathogenesis and new treatment strategies in diabetes.
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