Mukadder Serter

Antioxidant status in patients with osteoporosis: A controlled study

OBJECTIVE We aimed to investigate serum antioxidant enzymes and nitric oxide (NO) levels in postmenopausal women with osteoporosis (OP) and in healthy controls; and to determine the relationship between these enzymes, NO and clinical parameters in this present study. METHODS Forty-five postmenopausal women fulfilling OP diagnostic criteria of World Health Organization (WHO) and 42 postmenopausal healthy women without OP were enrolled. Patients in the study population were selected among individuals that were not pre-diagnosed or pre-treated for OP. Patients with metabolic bone diseases, fracture history, which were smokers, alcohol users and taking antioxidant drug treatment, were excluded from the study. Dual Energy X-ray Absorptiometry (DXA) results, body mass indices and demographic data were recorded. Erythrocyte catalases (CAT), glutathione reductase (GR) enzyme activities and erythrocyte glutathione (GSH) levels, plasma malondialdehyde (MDA) levels were measured by spectrophotometer whereas plasma nitrite+nitrate (NOx) levels were measured by ELISA microplate-reader. RESULTS Patients had significantly lower GR (P<0.01) enzyme activity and higher levels of MDA (P<0.01) and NO (P<0.01) than non osteoporotic healthy controls. There was no significant difference between both groups in erythrocyte GSH levels and CAT activities. Total femoral BMD measurements significantly correlated with MDA levels (P=0.001). There was no significant relationship between other antioxidants and lumbar or femoral BMD. CONCLUSION Oxidative stress may play an important role in postmenopausal bone loss and therefore it might be considered when pathogenesis of postmenopausal OP has been investigated.

Adiponectin as a biomarker of systemic inflammatory response in smoker patients with stable and exacerbation phases of chronic obstructive pulmonary disease

Background and objective. Adiponectin is an adipose tissue‐derived specific protein that has a role in energy homeostasis, that has a protective role against the development of insulin resistance and atherosclerosis and that exhibits anti‐inflammatory properties. We investigated serum adiponectin as a biomarker of systemic inflammatory response and its relation with leptin, C‐reactive protein (CRP), erythrocyte sedimentation rate (ESR) and nitric oxide (NO) in chronic obstructive pulmonary disease (COPD) patients. Material and methods. We studied 36 male patients with COPD (15 stable and 21 exacerbated) and 17 age and sex‐matched healthy subjects. The adiponectin and leptin levels were measured by enzyme‐linked immunosorbent assay. Serum CRP levels were measured using the nephelometric method. ESR was determined using the Westergren method and NO by the cadmium reduction method. Results. Adiponectin levels in COPD patients were significantly higher than those in control subjects (p<0.001), whereas there were no differences in leptin or NO levels. Serum levels of CRP, ESR and adiponectin were significantly higher in the exacerbated COPD patients compared to the stable group (p<0.001, p = 0.033 and p = 0.024, respectively), whereas the differences in leptin and NO levels were not significant. Serum levels of adiponectin were not correlated with FEV1, FEV1/FVC, dyspnoea score, BMI or other inflammatory parameters in the stable COPD group. CRP and ESR correlated negatively with FEV1 in the stable COPD group. Conclusions. Adiponectin may be a marker of low‐grade systemic inflammatory response in COPD. A further rise in serum adiponectin in the exacerbation period denotes that this may also be a biomarker of the exacerbation phase as well as CRP and ESR.

Serum antioxidants and nitric oxide levels in fibromyalgia: a controlled study.

We proposed to assess antioxidant status and nitric oxide in fibromyalgia (FM) patients in comparison to healthy controls. Additionally, the association between the serum antioxidant levels and clinical findings in FM patients was also investigated. Thirty-seven FM patients and 37 healthy controls were enrolled in this study. Severity of fatigue and pain were determined by Visual Analogue Scale. Functional capacity in daily living activities was evaluated by fibromyalgia impact questionnaire. Serum NO, catalase and glutathione were measured. Serum glutathione and catalase levels were significantly lower in FM patients than controls. However, no significant difference was seen in serum NO levels between the two groups. A significant correlation was evident between serum NO level and pain. Additionally, the correlation between glutathione level and morning stiffness was found to be significant. These findings support other studies, we assume that these two antioxidants might have impact on the pathogenesis of FM disease.

Protective Effects of Caffeic Acid Phenethyl Ester on Intestinal Ischemia-Reperfusion Injury

Aim Intestinal ischemia reperfusion (IR) causes tissue injury in two ways, starting a pro-inflammatory cascade and oxidative stress. The aim of this study was to investigate the possible protective effects of caffeic acid phenethyl ester (CAPE), which has antioxidant and anti-inflammatory properties, against intestinal IR injury in rats. Materials and Methods Forty male Wistar-Albino rats were divided into five groups: Sham, IR, IR plus ethanol (vehicle), IR plus 10 mg/kg (IR + 10CAPE), and 30 mg/kg CAPE (IR + 30CAPE) at the 30-min ischemic period. Intestines were exteriorized and the superior mesenteric artery was occluded for 45-min ischemia and then the clamp was removed for 120-min reperfusion. After the experiment, the intestines were removed for biochemical and light microscopic examinations. Additionally, blood samples were taken for plasma TNF-α measurement. Results The TBARS levels of the IR and IR + Ethanol groups were higher than the Sham group (P < 0.05). Both CAPE treatments decreased TBARS levels in comparison with the IR group (P < 0.05). In both CAPE-treated groups, while the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were increased compared to all other groups, which was similarly the case for the CAT activity compared to the Sham and IR + Ethanol groups (P < 0.05). There were no significant differences between GSH levels of all study groups. The TNF-α levels of the IR and IR + Ethanol groups were non-significantly increased compared to the Sham group (P > 0.05). The TNF-α levels of 10 and 30 mg/kg CAPE groups were non-significantly decreased compared to the IR group (P > 0.05). The tissue MPO activities of the IR and IR + Ethanol groups were higher than the Sham group (P < 0.05). The MPO activities of the IR + 10CAPE and IR + 30CAPE groups were not significantly different from the Sham group (P > 0.05). There was necrosis of mucosa in the IR and IR + Ethanol groups in light microscopic evaluations. Those changes were significantly reversed by 30 mg/kg CAPE treatment. Conclusion The intestinal IR injury may be reversed by anti-inflammatory and antioxidant actions of the CAPE. However, 30 mg/kg CAPE treatment may be more efficient in preventing intestinal IR injury in rats.

Melatonin ameliorates blood-brain barrier permeability, glutathione, and nitric oxide levels in the choroid plexus of the infantile rats with kaolin-induced hydrocephalus.

Hydrocephalus is a disabling disease for children, but current data concerning the effects of melatonin on ventricular enlargement are still limited. We have investigated the changes in the choroid plexuses (CPs) of ventricles and blood-brain barrier (BBB) of hydrocephalic rats. Forty-five Swiss Albino rats at age 2 weeks were divided into three equal groups: control, hydrocephalus, and melatonin-treated hydrocephalus groups. Hydrocephalus was induced by kaolin injection into the cisterna magna of all pups except control group and melatonin was given at a daily dose of 0.5 mg/100 g body weight for 4 weeks. At the end of the study, one animal from each group was examined using a gamma camera to study the disruption of BBB due to hydrocephalus. All animals were then killed for assay of glutathione (GSH) and nitric oxide (NO), as well as histological study of the CPs during the hydrocephalus. We observed an increased BBB activity was found in hydrocephalus group, while melatonin reversed these changes. It was found that NO concentration was elevated in hydrocephalus group and melatonin partly abolished the increased levels of NO. In contrast, GSH levels were significantly decreased in hydrocephalus group, while melatonin increased the tissue GSH level (p<0.01). Histologically, there was a significant alteration in the CPs of the ventricles of hydrocephalic animals, but it was regressed after melatonin treatment in consistent with the gross morphological changes related to hydrocephalus. In conclusion, our results clearly demonstrated for the first time the neuroprotective effects of melatonin upon hydrocephalus-induced CP changes in infantile rats, but further studies are needed to suggest melatonin as a candidate protective drug in children.

The effect of pioglitazone on antioxidant levels and renal histopathology in streptozotocin-induced diabetic rats.

Objective. Diabetic nephropathy is the most commonly seen cause of chronic renal failure, and oxidative stress is important in etiology. In the present study, favorable effects (if any) of the treatment with a thiazolidinedione group drug, pioglitazone, on antioxidant enzyme levels in the renal tissue, renal histopathology, and inflammatory cytokine levels have been investigated. Method. Forty male Wistar rats were divided into 4 groups as the control, diabetic control, and 10 and 30 mg pioglitazone-administered diabetic groups. After 4 weeks, antioxidant enzyme levels in renal tissues and inflammatory markers were investigated. Results. Blood glucose levels did not differ between the diabetic control and drug-administered groups. In pioglitazone-administered rats, histopathological findings such as tubular dilation, necrotic tubular epithelium, glomerular focal necrosis, and vascular consolidation were observed at a lesser extent than the diabetic control group. Any difference was not detected between the diabetic groups with respect to the levels of malondialdehyde, superoxide dismutase, catalase, glutathione, nitric oxide, interleukin-6, and tumor necrosis factor-alpha. Conclusion. Pioglitazone regressed development of histopathological lesions such as glomerular focal necrosis, tubular epithelial necrosis, tubular dilation, and vascular wall consolidation. However, any favorable effect on antioxidant enzyme levels in renal tissues and inflammation markers was not detected.

Pro-inflammatory cytokine response of the fluid contents of spermatoceles and epididymal cysts.

Summary. The aim of the study was to determine the cellular contents and concentrations of interleukin 6 (IL‐6), interleukin 8 (IL‐8) and tumour necrosis factor alpha (TNF‐α) in fluids of patients with spermatocele or epididymal cyst. Twenty‐five symptomatic patients, 14 with epididymal cysts and 11 with spermatoceles, were included in the study. Fluids were obtained during surgical excision of the cysts and cytological smears were stained with May–Gruenwald–Giemsa to establish cell components. The concentrations of IL‐6, IL‐8 and TNF‐α were measured by chemiluminescent immunometric assay. Cytological analysis of the fluids demonstrated various sperm forms ranging from immature germ cells to degenerated spermatozoa without inflammatory cells such as neutrophils and macrophages. The concentrations (mean± SEM, pg/mg protein) of IL‐6, IL‐8 and TNF‐α were 13.52 ± 1.40, 22.20 ± 2.43, 3.51 ± 1.43 in spermatocele fluids and 5.76 ± 0.48, 11.57 ± 1.89, 2.53 ± 0.41 in epididymal cyst fluids. Both IL‐6 and IL‐8 concentrations in the spermatocele group were higher than in the epididymal cyst group (P < 0.0001). There were no differences in TNF‐α concentrations between the groups (P > 0.05). These findings indicate that local production of pro‐inflammatory cytokines is involved in cyst formation. The presence of immunologic activation in these fluids advocates a policy of selective surgical intervention in patients with spermatocele or epididymal cyst.

The effects of short-interval postconditioning in preventing testicular ischemia-reperfusion injury in rats

AIM Testicular torsion can lead to testicular damage. During reperfusion, tissue damage is more severe. The aim of this study was to investigate the protective effect of short-interval postconditioning and determine the optimal time of reperfusion for postconditioning. MATERIALS AND METHODS Thirty-five adult male rats were divided into 5 subgroups: Sh (sham operated), TD (torsion + detorsion), PC5 (torsion + postconditioning 5 seconds), PC10 (torsion + postconditioning-10 seconds), PC20 (torsion + postconditioning 20 seconds). Torsion was created by rotating the left testis counterclockwise 1080° and the testis fixed to the scrotum with 3 sutures. Torsion was maintained for 4 hours. The testicular artery was visualized, and before detorsion of the testis, an atraumatic vessel clamp was applied to prevent reperfusion in all study groups. Then, detorsion of the testis was performed. In the TD group, the clamp was released just after detorsion; in the PC5 group, the clamp was released for 5 seconds and closed for 10 seconds (10 times); in the PC10 group, the clamp was released for 10 seconds and closed for 10 seconds (10 times); and in the PC20 group, the clamp was released for 20 seconds and closed for 10 seconds (10 times). Then, all testes were reperfused for a 1-hour period in all study groups. After this period, the rats were sacrificed, and the left testes were removed and evaluated histopathologically and biochemically. The Mann-Whitney U test was used for statistical analyses. RESULTS Tissue malondialdehyde levels were 79.3 ± 10.6, 231.7 ± 102.3, 71.3 ± 12.6, 73.8 ± 13.7, and 124.3 ± 48.0 nmol/g tissue in the Sh, TD, PC5, PC10, and PC20 groups, respectively. Tissue malondialdehyde levels were significantly lower in the PC5 and PC10 groups (P < .05) compared to the other groups. However, mean histopathologic grade was lower in all postconditioning groups compared to the control group, but the difference was significant only in the PC5 group (P < .05). CONCLUSION We conclude that short-interval postconditioning can reduce reperfusion injury in ischemic tissue and the optimal mode of short-interval postconditioning is 5 seconds × 10 times. This technique seems easily applicable, and a similar technique may be used during testicular surgery.

Lung Function and IFN-γ Levels in the Sera of Silica-Exposed Workers

Excessive exposure to respirable particles of crystalline silica is an occupational health problem in developing countries and can cause a variety of pulmonary diseases, such as silicosis, chronic obstructive pulmonary disease (COPD), and malignancy, in susceptible hosts. In addition to the well-documented role of pulmonary macrophages, lymphocytes occasionally have been suggested to influence the pneumoconiotic process, but their potential role is not clearly understood. Interferon-gamma (IFN-gamma), a lymphocyte cytokine, is recognized as the most important cytokine in converting macrophages from a resting to an activated state. The aim of the present study was to investigate serum IFN-gamma levels and pulmonary function changes in silica-exposed workers and in silicosis. Twenty-seven silica workers (aged 35.6 +/- 8.2 years with 5.11 +/- 2.98 years exposure duration) and 18 unexposed office workers (aged 33.8 +/- 12 years) were included in the study. Mean spirometry parameters and smoking history were comparable to the values of the office workers, but COPD prevalence was higher in the silica-exposed group, and the age-adjusted ratio was more sensitive than fixed quotient criteria for airway obstruction. We found silicosis in 4 silica workers. The mean serum IFN-gamma level was increased in silica-exposed workers (10.22 +/- 22.68 pg/mL) although it was undetectable in all office workers and even in the workers with silicosis. Evaluating pulmonary function tests (PFT) using an age-adjusted quotient may prevent underestimation of airflow limitation, especially in the young population with risk factors. Although serum IFN-gamma may increase initially in response to silica, low levels of IFN-gamma in later stages may be considered a risk factor for silicosis because this cytokine downregulates the fibroblast responses to transforming growth factor-beta (TGF-beta) and decreases collagen production. Additional research to determine the exact role of this potent cytokine may offer insight into the pathogenesis of silicosis.

Effects of early initiated oestrogen replacement therapy on plasma homocysteine levels in women in surgically induced menopause.

Objective. The aim of this study was to investigate and to compare the effects on serum homocysteine levels of early initiated oral and transdermal oestrogen replacement therapies (ERTs) given to women without a uterus who had undergone surgically induced menopause. Homocysteine levels are considered one of the predictors of cardiovascular disease risk. Methods. This study included 45 women with surgical menopause. Of 45 women, 15 received oral ERT, (oestradiol hemihydrate 2 mg/day, Estrofem®), 15 received transdermal ERT (oestradiol hemihydrate 0.1% gel 1.5 mg/day, Estreva®) and 15 received no hormone therapy. Blood samples were collected from all women to measure homocysteine levels at the mean time of 15 weeks after surgical menopause. Obtained results of the groups were compared. Results. There were no significant differences in age, height, weight, body mass index (BMI), waist circumference and time elapsing since menopause between the three groups. The duration of ERT was not significantly different between the therapy groups. There was no significant difference in homocysteine levels between the groups (p > 0.05). No significant correlation was found between weight, BMI and homocysteine levels (p > 0.05). Conclusion. Considering that homocysteine is a predictor of risk for cardiovascular disease, the results of this study showed that early initiation of ERT in healthy surgically induced menopausal women neither protects nor deteriorates cardiovascular disease.