Ahmet Belce

Oxidative stress in breast cancer.

The present study was undertaken to evaluate the place of oxidative stress on breast cancer. Lipid peroxidation as evidenced by malondialdehyde (MDA) and the status of the antioxidants superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were estimated in tissues of 10 fibroadenoma and 40 breast cancer patients. Lipid peroxidation in breast cancer tissues was enhanced compared to nonmalignant tissues (p<0.001). Similarly, antioxidants SOD (p<0.001) and GPx (p=0.007) in tumor tissues significantly were increased. On the contrary, CAT activity was found significantly decreased (p<0.001). We found that oxidant/antioxidant status was independent from any prognostic factors concerning breast cancer. The results of our study have shown higher oxygen-free-radical production and decreased CAT activity support the oxidative stress hypothesis in breast carcinogenesis.

The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury.

Study Design: The effect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. Objectives: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective effects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. Setting: Departments of Neurosurgery and Biochemistry, Cerrahpaşa Medical School, Istanbul, Turkey. Methods: Twenty-five female Wistar Albino rats were used. There were five rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining five rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a flow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacrificed and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). Results: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group 1 (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/gww in group 3 (epidural cooling), the differences being statistically significant. Conclusion: The results indicated that epidural cooling of traumatized spinal cord is effective in preventing secondary damage due to the peroxidation of lipid membranes.

Effect of nimodipine and N-acetylcysteine on lipid peroxidation after experimental spinal cord injury.

The effectiveness of nimodipine and N-acetylcysteine in experimental spinal cord injury was evaluated by measuring tissue lipid peroxidation levels of the damaged spinal cords 1 hour after the injury. We used the clip compression method to produce acute spinal cord injury in 40 female Sprague-Dawley rats were used. The rats were divided into four groups of 10 each. Lipid peroxidation was assessed by measuring the tissue content of malonil dialdehyde (MDA). In group 3, nimodipine, and in group 4,n-acetylcysteine, was administered i.p. as a single dose immediately after the injury. The rats were sacrificed 1 hour after clip application. The tissue mean MDA content was 3,992 μmol MDA/gww in group 1 (sham operated), 10,192 μmol MDA/gww in group 2 (trauma), 10,449 μmol MDA/gww in group 3 (nimodipine treatment) and 9,009 μmol MDA/gww in group 4 (n-acetylcysteine treatment). These results demonstrated that a single dose of nimodipine andn-acetylcysteine had no effect on peroxidation of lipid membranes in the early period of experimental spinal cord injury.

Effects of flurbiprofen and tiaprofenic Acid on oxidative stress markers in osteoarthritis: A prospective, randomized, open-label, active- and placebo-controlled trial

BACKGROUND The relationship between oxidative stress and osteoarthritis (OA) has been widely investigated. Serum malondialdehyde (MDA), nitric oxide (NO), and Cu/Zn superoxide dismutase (SOD) levels are useful markers of oxidative stress. Because of the importance of oxidative stress markers in the pathogenesis of OA, treatment might involve modification of these markers to control oxidative stress. OBJECTIVE The aim of this study was to compare the effects of 2 conventionalNSAIDs on markers of oxidative stress in patients with OA of the knee. METHODS This 3-week, prospective, randomized, open-label, active- and placebo-controlled study was conducted at the Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey. Adult patients with clinically and radiographically diagnosed moderate OA of the knee who were previously untreated were enrolled. Patients were randomly assigned to 1 of 3 treatment groups: flurbiprofen 100 mg PO (tablets) BID, tiaprofenic acid 300 mg PO (tablets) BID, or placebo tablets BID. Patients were evaluated using clinical assessment and laboratory testing before treatment (week 0; baseline) and at the end of week 3. The primary end points were the differences in serum MDA, NO, and SOD levels versus placebo. Clinical parameters-pain at rest and on motion-were evaluated using a 10-cm visual analog scale (0 = no pain to 10 = worst pain imaginable). The duration (in minutes) of morning stiffness was recorded by patients, using patient diaries. The differences between treatment groups were assessed using multivariate analysis. RESULTS Thirty-nine patients (20 women, 19 men; mean [SD] age, 59.0 [11.3]years) were included in the study. Mean serum MDA and NO levels were significantly decreased at 3 weeks compared with baseline in the 2 active-treatment groups (all, P < 0.001); these values remained statistically similar to baseline in the placebo group. Serum SOD levels were increased significantly from baseline in the 2 active-treatment groups (both, P < 0.001), but not in the placebo group. No significant differences in serum MDA and NO levels were found between the group receiving flurbiprofen and that receiving tiaprofenic acid. Serum SOD levels were significantly higher in the flurbiprofen group compared with the tiaprofenic acid and placebo groups (both, P < 0.01). The mean (SD) score for pain at rest was significantly lower at 3 weeks compared with baseline with flurbiprofen and tiaprofenic acid (both, P < 0.001), but not with placebo. The mean score for pain on motion was significantly reduced from baseline values only with tiaprofenic acid (P < 0.001). The duration of morning stiffness was significantly shorter at 3 weeks compared with baseline in all 3 study groups (all, P < 0.001). The mean scores for pain on motion and duration of morning stiffness were significantly reduced with tiaprofenic acid compared with placebo (both, P < 0.05). The study had some limitations (ie, small sample size, no blinding, the short duration of the study, and the weak correlation between serum and synovial fluid levels of NO). CONCLUSIONS In this comparison of the effects of 3 weeks of treatment withflurbiprofen 100 mg BID and tiaprofenic acid 300 mg BID in patients with knee OA, both treatments effectively reduced serum MDA and NO levels compared with placebo. Only tiaprofenic acid significantly improved pain at rest and on motion and duration of morning stiffness compared with placebo.

The effects of lipoic acid on redox status in brain regions and systemic circulation in streptozotocin-induced sporadic Alzheimer’s disease model

AbstractWhile the deterioration of insulin-glucose metabolism (IGM), impaired redox homeostasis (IRH), β-amyloid accumulation was reported in Sporadic Alzheimer’s Disease (SAD) model, aforementioned factors related to lipoic acid administration and anthropometric indexes (AIs) are not yet studied with integrative approach. β-amyloid accumulation, redox homeostasis biomarkers and AIs are investigated in SAD model. Streptozotocin-induced inhibition of insulin-signaling cascade but not GLUT-2 and GLUT-3 transporters takes a role in β-amyloid accumulation. Inhibition types are related to IRH in cortex, hippocampus and systemic circulation. Lipoic acid (LA) shows both antioxidant and prooxidant effect according to the anatomical location. LA administration also leads to improved AIs during GLUT-2 inhibition and cortical redox status in GLUT-3 inhibited group. Optimal LA action could be possible if its redox behavior is balanced to antioxidant effect. Diagnostic usage of systemic IRH parameters as biomarkers and their possible correlations with deteriorated IGM should be investigated. Graphical abstractᅟ

Gender and chronological age affect erythrocyte membrane oxidative indices in citrate phosphate dextrose adenine-formula 1 (CPDA-1) blood bank storage condition.

It is well known that in vitro storage lesions lead to membrane dysfunction and decreased number of functional erythrocytes. As erythrocytes get older, in storage media as well as in peripheral circulation, they undergo a variety of biochemical changes. In our study, the erythrocytes with different age groups in citrate phosphate dextrose adenine-formula 1 (CPDA-1) storage solution were used in order to investigate the possible effect of gender factor on oxidative damage. Oxidative damage biomarkers in erythrocyte membranes such as ferric reducing antioxidant power, pro-oxidant-antioxidant balance, protein-bound advance glycation end products, and sialic acid were analyzed. Current study reveals that change in membrane redox status during blood-bank storage condition also depends on both gender depended homeostatic factors and the presence of CPDA-1. During the storage period in CPDA-1, erythrocytes from the male donors are mostly affected by free radical-mediated oxidative stress but erythrocytes obtained from females are severely affected by glyoxidative stress.

Superoxide dismutase, catalase, and guanase in traumatic brain injury

Objectives:Reactive oxygen species generated after brain trauma trigger a cascade of events resulting in neuronal death. Despite numerous defenses, the brain is vulnerable to oxidative damage, mainly because of its high content of unsaturated fatty acids. The goal in this experimental study was to demonstrate the activities of antioxidant enzymes, namely, superoxide dismutase, catalase, and guanase, in plasma and brain tissue at 30 minutes and 60 minutes after brain trauma. Methods:Forty adult male Sprague-Dawley rats were used as subjects. Rats in group 1 were subjected to moderate head injury, whereas rats in group 2 were subjected to severe head injury. Eight rats served as a sham operated (control) group. Results:The results of this study showed that there is, in general, an increase in the activities of these 3 enzymes in plasma; however, in the brain tissue, we observed that guanase activities were decreased during the posttraumatic period. Conclusion:These alterations in enzyme activities suggest that lipid peroxidation ensues in the early period of trauma and that treatment strategies aimed to increase antioxidant enzyme activities may prevent the secondary mechanisms resulting in neuronal death.

Galactose-induced Aging Model In Rat Testicular Tissue

OBJECTIVE To examine whether the D-galactose induced aging model is an appropriate model for further aging research. STUDY DESIGN Experimental study. PLACE AND DURATION OF STUDY Aziz Sancar Institute of Experimental Medicine, Istanbul University, Turkey, June 2015- June 2017. METHODOLOGY The study comprises 3 groups of rats. Group I is young control (YC) 5-month-old rats. Group II is 5-month- old rats, which were mimetically aged (MA) for 6 weeks via intraperitoneal D-galactose (60 mg/kg body weight/day, 0.5 mL) administration. Group III is naturally aged (NA) 24-month-old rats. Group I and III received intraperitoneal saline (0.9% 0.5 mL) for 6 weeks as vehicle. Group I and Group II received injections at 21 weeks age and Group III rats 6 weeks before 24 months age. Tissues were harvested when rats became 6.5-month-old (Group I and Group II) and 24-month-old (Group III). Quantitative biochemical analyses of proteins, lipids, DNA biomarkers and Cu, Zn-SOD were conducted. Statistical analysis of the data was conducted using ANOVA, followed by post-hoc Bonferroni test. RESULTS Higher magnitude of oxidative damage and diminished antioxidant defence capacity were found in both mimetically aged and naturally aged testicular tissues. It is observed that D-galactose aging model group shares significant similarities in terms of impaired redox homeostasis with the naturally aged rats. CONCLUSION D-galactose induced testicular aging model successfully mimics aging process. Therefore, D-galactose induced aging model may be used as an accelerated aging model to study the age related alterations and interventions.