It is known that there is a strong association between oxidative stress and insulin resistance in type 2 diabetes mellitus (T2DM). Although the role of glibenclamide in diabetes treatment has been evaluated, there is only limited evidence about its antioxidant effects in diabetic patients. Moreover, previous studies showed discrepant results regarding the effects of metformin on antioxidant/ oxidant parameters in type 2 diabetic patients. The present study aimed to evaluate the effects of metformin versus glibenclamide on oxidative stress biomarkers, represented by serum malondialdehyde (MDA), nonenzymatic, and enzymatic antioxidants in type 2 diabetic patients. Forty-six patients with T2DM participated in this study and categorized into 3 groups, Group A included 17 newly diagnosed diabetic patients, group B included 15 diabetic patients received metformin monotherapy (1000 mg/day) for up to 1 year and group C included 14 diabetic patients received glibenclamide monotherapy (5 mg/day) for up to 1 year. Serum MDA, catalase (CAT), vitamin C, E, and reduced glutathione (GSH) were measured. We found significantly lower concentrations of MDA and significantly higher antioxidant levels (CAT, GSH, vitamin C, and E) in the metformin-treated group compared to the glibenclamide counterpart. Our data confirmed that metformin has a more beneficial effect on oxidant/antioxidant status compared to glibenclamide, therefore, provides protection against reactive oxygen species (ROS) induced oxidative damage during diabetes.
Metformin and glibenclamide may have beneficial effects on the levels of trace elements in diabetic patients. The aim of the current study was to assess the effects of metformin and glibenclamide on the concentrations of copper (Cu), zinc (Zn) and magnesium (Mg) in patients with type 2 diabetes mellitus. The metformin-treated patients showed significantly lower serum Cu levels compared with the untreated and glibenclamide groups. In addition, treatment with metformin was associated with a significant increase in serum concentrations of Zn compared to the newly diagnosed patients, whereas it did not show a noticeable alteration in the serum level of Mg. In contrast, the glibenclamide treated group revealed significantly higher Zn and Mg levels compared with the newly diagnosed group, while the serum level of Cu was not significantly modified. In conclusion, treatment with metformin led to a reduction in serum Cu and an increase in serum Zn concentrations, whereas glibenclamide treatment displayed enhancement in serum Zn and Mg levels.
Background: oxidative stress(OS) happens when harmful reactive oxygen species (ROS) exceed antioxidants leading to damage of lipid, protein and DNA. OS was documented to participate in pathogenesis and complication of polycystic ovary syndrome(PCOS). PCOS is a common endocrine disorder, with incidence 4-12% between female at fertility period that leads to anovulation and infertility. This syndrome is accompanied with over production of androgen and dysfunction of ovaries which are associated by classical signs and/or symptoms and biochemical characteristics comprising hirsutism, acne, ultrasonic feature of polycystic ovaries, irregular menstrual period, adiposity, dyslipidemia, decrease insulin sensitivity and prediabetes. Aim of the Study: to evaluate biomarkers levels of oxidative stress in women with PCOS and in healthy control women. This evaluation is necessary to show the effect of oxidative stress on sex hormonal profile of women with PCOS. Participants and Methods: thirty women (16-38 year) with PCOS and thirty matched age women were enrolled to evaluate oxidative status by measuring serum levels of malondialdehyde(MDA) concentration and total antioxidant capacity(TAC) in all participants. Results: Women with Polycystic ovary exhibited significantly increased means of MDA levels and significantly decreased mean of TAC levels when compared to healthy participants. Conclusion: it concluded from this study there is a disturbance of oxidant and antioxidant profile in PCO women supposes a status of oxidative stress, guided by high level of oxidative stress biomarker of lipid peroxidation (MDA) and decreased antioxidant defense mechanism which indicated by TAC. Moreover, the oxidative stress biomarkers can be employed as indicator in early diagnosis of PCOS and utilization of them in monitoring and preventing further complication of it.
The sympathetic response to rigid bronchoscopy, laryngoscopy and esophagoscopy, performed under general anesthesia with isoflurane, was examined in patients who either received 5 ml of 2 % lidocaine (n = 7) or 5 ml of saline (n = 7), sprayed on larynx and upper trachea under direct laryngoscopy, 2 min before the introduction of the rigid bronchoscope. Blood pressure, heart rate and plasma catecholamine and lidocaine levels were measured at specific time points of the study. Topical lidocaine led to a rapid and prolonged increase in plasma lidocaine levels. Patients treated with lidocaine showed a small but significant decrease in plasma epinephrine levels from baseline following endotracheal intubation and extubation, as compared to the saline control group. Blood pressure and heart rate response during rigid panendoscopy, isoflurane requirements and time interval from termination of panendoscopy to extubation were not different between the two groups. However, in contrast to the control group, patients who had received lidocaine had no significant rise in blood pressure and heart rate from baseline following the introduction of the rigid bronchoscope. The benefit of this moderate hemodynamic stabilizing effect of lidocaine has to be weighed against the risk of decreased protective airway reflexes due to topical laryngeal lidocaine during recovery from anesthesia.
Thyroid cancer is a rare type of malignancy. However, thyroid cancer constitutes more than 90 % of endocrine tumors. Metformin (N', N'-dimethybiguanide) is the most commonly prescribed drug in the world, and the annual number of prescriptions for this drug exceeds 120 million. Metformin is the first-line oral treatment for patients with type II diabetes. Metformin has recently been investigated for potential anti-cancer activity in patients with thyroid cancer by stimulating the Adenosine Mono-Phosphate-Activated Protein Kinase (AMPK) pathway in some types of tumors. In general, the anti-cancer mechanism of metformin acts directly by blocking mitochondrial oxidative phosphorylation through down-regulation of mitochondrial complex I and mitochondrial glycerophosphate dehydrogenase. This leads to a state of metabolic stress that in turn stimulates the AMPK pathway due to ATP reduction, and leads to inhibition of the mechanical (mammalian) target of the rapamycin (mTOR) pathway, which subsequently inhibits cancer cell proliferation and stimulates apoptosis and autophagy with cell cycle perturbation. Metformin also acts in an independent manner, in addition to its indirect actions that target insulin resistance. In this review, we reviewed 21 studies on the use of metformin in thyroid cancer, which showed that administration of metformin in diabetic patients is associated with a reduced incidence of thyroid cancer. On the other hand, the use of metformin enhances the response to anticancer drugs in thyroid cancer. Overall, we need further prospective studies to elucidate the synergistic mechanism of metformin when it is used to treat thyroid cancer as adjuvant therapy with anticancer drugs.
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