Effects of periodontal and bisphosphonate treatment on the gingival crevicular levels of sclerostin and dickkopf-1 in postmenopausal osteoporosis with and without periodontitis.

OBJECTIVE AND BACKGROUND: Both periodontitis and osteoporosis are associated with osteoclast-related bone resorption. Bone metabolism is regulated by wingless-type MMTV integration site family (WNT), and WNT/ß-catenin signals are controlled by physiological antagonists including dickkopf-1 (DKK-1) and sclerostin (SOST). This study examined the effects of periodontal and bisphosphonate (BP) treatment on the gingival crevicular fluid (GCF) sclerostin (SOST) and dickkopf-related protein-1 (DKK-1) levels in osteoporotic and systemically healthy postmenopausal women with and without periodontitis. MATERIALS AND METHODS: A total of 48 postmenopausal women were divided into 4 groups (n = 12) according to periodontal health and osteoporosis status, as follows: Group OP/P: subjects with both osteoporosis and periodontitis; Group P: systemically healthy subjects with periodontitis; Group OP: periodontally healthy subjects with osteoporosis; Group H: systemically and periodontally healthy controls. Clinical data and GCF SOST and DKK-1 levels of the participants were collected at baseline and at 6 and 12 months following the initiation of periodontal and/or BP treatment in the experimental groups. GCF SOST and DKK-1 data were obtained by ELISA. RESULTS: Clinical improvements were observed in all experimental groups. GCF SOST and DKK1 baseline levels varied significantly between groups due to periodontal disease (p < .001). Following treatment, significant increases in SOST and DKK-1 concentrations and significant decreases in total amounts of SOST were observed in both periodontitis groups (OP/P, P). However, while total amounts of DKK-1 decreased in Group OP/P, in Group P, these amounts had significantly increased at 12 months post-treatment (p < .05). At both 6 and 12 months post-treatment, SOST and DDK1 total amounts in Groups OP/P, OP, and H were similar (p > .05), whereas significant differences were observed between Groups H and P, indicating a deviation from periodontal health in Group P (p < .01). CONCLUSIONS: Significant changes in GCF SOST and DKK-1 levels were observed among women with osteoporosis who received both periodontal and BP treatment. A more detailed examination of how these treatment protocols can be combined may lead to new therapeutic approaches towards periodontal disease.

Effects of smoking on the gingival crevicular fluid levels of interleukin-17A, interleukin-17E, and oxidative stress following periodontal treatment process.

OBJECTIVE AND BACKGROUND: How smoking affects periodontal inflammation and healing still needs to be revealed with all its mechanisms. In this study, the gingival crevicular fluid (GCF) levels of: (a) interleukin-17A (IL-17A) and interleukin-17E(IL-17E) with their ratios and (b) oxidative stress by means of total oxidative stress (TOS), total anti-oxidant capacity (TAOC), and their ratios as the oxidative stress index (OSI) were evaluated and compared for smoking and non-smoking periodontitis patients after a periodontitis management process including both the non-surgical and surgical treatments. MATERIALS AND METHODS: Fifteen smoker and 15 non-smoker generalized periodontitis patients as 2 distinct groups participated in the study. Conventional clinical and radiographical examinations were utilized for the periodontitis diagnosis. The clinical data and GCF samples were collected at baseline, 4 week after non-surgical periodontal treatment (NSPT), and 4 weeks after surgical periodontal treatment (SPT). IL-17A, IL-17E, TOS, and TAOC were determined by ELISA and Rel Assay. RESULTS: Clinical parameters in both smokers and non-smokers improved following periodontal treatment (P < .001) and their clinical data were similar for all the examination times (baseline, NSPT, and SPT) (P > .05). Following the treatment phases, the IL-17A concentration decreased and the IL-17E concentration increased in both the smokers and non-smokers (P < .01). The total amount of IL-17A decreased while the total amount of IL-17E increased in smokers throughout NSPT and SPT (P < .01). Such an alteration was seen only at SPT compared to NSPT and baseline in non-smokers (P < .01). The concentration and total amount of IL-17A were higher at baseline, and the concentration and total amount of IL-17E were lower at all examination time points in non-smokers as compared to smokers (P < .01). The 17A/E ratio decreased in both groups following the treatment phases and was higher in smokers at all the examination times (P < .01). TOS were higher and TAOC were lower in smokers versus non-smokers at all the time points, but the differences were significant only for TOS levels (P < .01). Throughout the treatment phases, the concentration and total amount of TOS decreased in smokers(P < .01) and only the total amount of TOS decreased in non-smokers (P < .01). The concentration and total amounts of TAOC increased throughout the treatments in both smokers and non-smokers without significant changes (P > .05). The baseline OSI was higher in smokers, and it decreased only in smokers following the treatment phases (P < .01). CONCLUSIONS: Smoking and periodontal inflammation were found to alter IL-17A, IL-17E, and oxidant/anti-oxidant statuses in periodontitis patients. The intra-group assessments in smokers demonstrated more apparent alterations in the oxidant/anti-oxidant statuses and IL-17A and IL-17E levels after periodontitis management.

Antioxidant effect of caffeic acid phenethyl ester in experimentally induced periodontitis.

OBJECTIVES: The aim of the present study was to evaluate the antioxidant effect of systemically administered caffeic acid phenethyl ester (CAPE) in periodontitis. MATERIALS AND METHODS: Forty rats were randomly divided into four groups: control, lipopolysaccharide-induced experimental periodontitis (LPS), CAPE 5: LPS+5 µmol/kg/day CAPE, and CAPE 10: LPS+10 µmol/kg/day CAPE. Following lipopolysaccharide-induced experimental periodontitis, CAPE was administered intraperitoneally for 28 days. Gingival and serumal total antioxidant status (TAS) and total oxidant status (TOS) were analyzed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Gingival tissue TAS was significantly higher with CAPE application compared with the LPS group and was highest in the CAPE 10 group (p<0.05). Gingival tissue TOS was highest in the LPS group, and both of the CAPE dosages decreased the gingival tissue TOS, with the highest decrease in the CAPE 10 group (p<0.05). The differences were not significant for serumal TAS or TOS levels (p>0.05). CONCLUSIONS: The effect of CAPE on increased TAS and decreased TOS levels in inflamed gingival tissue indicates the antioxidant therapeutic potential of CAPE in periodontitis. CLINICAL RELEVANCE: Within the limitations of this study, CAPE may be suggested as an effective host modulator agent for reducing oxidative stress in gingival tissue and might be considered as an adjunctive therapy in periodontitis.

Neurotrophic factors in bipolar disorders patients with manic episode

Background/aim: Neurotrophins are one of the most important molecule groups affecting cerebral neuroplasticity. The amount of evidence about the role of changes in neuroplasticity in the pathophysiology of bipolar disease is growing. Materials and methods: We measured serum levels of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT-3), glial cell-line derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), insulin-like growth factor-1 (IGF-1), fibroblast growth factor (FGF)-2, neuritin 1 (Nrn 1) in bipolar 1 manic episode patients (n = 45) and healthy control group. Results: When controlled for age, BMI and cortisol, it was found that the serum levels of BDNF, NGF, NT-3, VEGF and FGF-2 of bipolar manic episode patients were not statistically different compared to those of the control group. GDNF level and Nrn 1 levels were significantly lower (P = 0.003 and P = 0.025 respectively) while IGF-1 levels were significantly higher than the control group (P = 0.0001). ROC analysis was performed and the area under the the curve was calculated as 0.737, 0.766 for GDNF, IGF-1 respectively. Conclusion: The changes in the levels of GDNF, IGF-1 and Nrn 1 might be involved in pathopysiology of bipolar disorder, and GDNF, IGF-1 may be considered as state markers in bipolar manic episode.

Adipocytokines and ghrelin level of bipolar patients from manic episode to euthymic episode.

PURPOSE: Obesity and metabolic syndrome (MeS) are more frequently observed in bipolar patients than the general population. This may result from the differences of adipocytokines and ghrelin levels in bipolar disorder. MATERIAL AND METHODS: We evaluated the leptin, adiponectin, resistin and ghrelin levels in bipolar patients (n = 30) in manic episode and in a control group (n = 30). After treatment, the same patients were evaluated again during the euthymic episode. We also measured the insulin, glucose, insulin resistance (HOMA), trygliceride (TG), total cholesterol (TCHOL), high density lipoprotein cholesterol (HDL) and low density lipoprotein cholesterol (LDL) in relation to the (MeS). RESULTS: When controlling for age, BMI and glucose, leptin levels were higher in the bipolar disorder manic episode group (BD-ME) and bipolar euthymic episode group (BD-EE) than the control group; resistin levels were higher in the BD-ME compared to the control group and it had a positive correlation with Young Mania Rating Scale (YMRS). After treatment, ghrelin levels were higher in the BD-EE compared to the BD-ME group. There was no difference among the groups with respect to adiponectin. CONCLUSIONS: The present results point that high leptin, resistin and ghrelin levels may be involved in the early pathophysiological process which can lead to later obesity and MeS in patients with bipolar disorder.

An evaluation of vitamin D levels in children with seasonal allergic rhinitis during pollen season.

BACKGROUND: Serum vitamin D levels have not been studied in children with seasonal allergic rhinitis (SAR). The aim of this study was to evaluate the vitamin D levels of children with SAR and to compare them to levels in healthy children during pollen season. METHODS: This study was conducted in 100 children with SAR and 100 healthy controls. Clinical and laboratory evaluations and vitamin D analyses of all the participants were performed between the months of April and July. Pollen sensitization was detected in the patient group using a skin prick test. 25(OH)D3 levels were compared between the patient and control groups. Associations among the patient 25(OH)D3 levels and their demographic, clinical, and laboratory characteristics were analyzed. RESULTS: Overall, 72% of the patients were male, the median age was 12.35 years (range: 6-17.8 years), and the median body mass index value was 19.15 (range: 13.6-27.8). There were no differences between the patients and healthy controls in terms of gender, age, or body mass index. The mean levels of 25(OH)D3 (20.78±6) in patients were higher than those of the controls (17.92±4). In the patient group, no associations were found among 25(OH)D3 levels, demographic characteristics, atopy test results, atopy history, severity of rhinitis, and the total four symptoms score (all P>.05). CONCLUSIONS: During pollen season, children with SAR may have higher vitamin D levels than healthy controls. The presence of asthma and/or atopic dermatitis in addition to SAR did not change this result.

Influence of α-tocopherol and α-lipoic acid on bisphenol-A-induced oxidative damage in liver and ovarian tissue of rats.

Bisphenol A (BPA) is a commonly used material in daily life, and it is argued to cause oxidative stress in liver and ovarian tissue. α-Lipoic acid (ALA) and α-tocopherol (ATF), two of the most effective antioxidants, may play a role in preventing the toxic effect. Therefore, the purpose of this study was to examine the beneficial effects of ALA, ATF, and that of ALA + ATF combination on oxidative damage induced by BPA. Female Wistar rats were divided into five groups (control, BPA, BPA + ALA, BPA + ATF, and BPA + ALA + ATF). BPA (25 mg/kg/day), ALA (100 mg/kg/day), and ATF (20 mg/kg/day) were administered for 30 days. The levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), liver malondialdehyde (L-MDA) and glutathione peroxidase (L-GPx), and ovarian malondialdehyde (Ov-MDA) and nitric oxide (Ov-NO) were significantly higher in the BPA-treated groups compared with the control group. The levels of AST and ALT decreased in the BPA + ALA, BPA + ATF, and BPA + ALA + ATF groups compared with the BPA group. Similarly, BPA + ALA or BPA + ATF led to decreases in L-MDA and Ov-MDA levels compared with the BPA group. However, the BPA + ALA + ATF group showed a significant decrease in L-MDA levels compared with the BPA + ALA group and the BPA + ATF group. The levels of L-GPx decreased in the BPA + ATF and the BPA + ALA + ATF groups compared with the BPA group. The administration of ATF and ALA + ATF significantly decreased the Ov-NO levels. This study demonstrates that BPA causes oxidative damage in liver and ovarian tissues. ALA, ATF, or their combination were found to be beneficial in preventing BPA-induced oxidative stress.

Effect of 900 MHz radiofrequency radiation on oxidative stress in rat brain and serum.

The increasing use of mobile telephones raises the question of possible adverse effects of the electromagnetic fields (EMF) that these phones produce. In this study, we examined the oxidative stress in the brain tissue and serum of rats that resulted from exposure to a 900-MHz EMF at a whole body average specific absorption rate (SAR) of 1.08 W/kg for 1 h/day for 3 weeks. We also examined the antioxidant effect of garlic powder (500 mg/kg/day) given orally to EMF-exposed rats. We found that malondialdehyde (MDA) (p < 0.001) and advanced oxidation protein product (AOPP) (p < 0.05) increased in rat brain tissue exposed to the EMF and that garlic reduced these effects (p < 0.05). There was no significant difference in the nitric oxide (NO) levels in the brain. Paraoxonase (PON) was not detected in the brain. There was a significant increase in the levels of NO (p < 0.001) detected in the serum after EMF exposure, and garlic intake did not affect this increase in NO. Our results suggest that there is a significant increase in brain lipid and protein oxidation after electromagnetic radiation (EMR) exposure and that garlic has a protective effect against this oxidative stress.

Increased levels of lipid and protein oxidation in rat prefrontal cortex after treatment by lithium, valproic acid, and olanzapine.

Oxidative stress is widely accepted to contribute to the pathogenesis of several psychiatric diseases. Many antipsychotic drugs and mood stabilizers act through restoration of the dysregulated oxidative homeostasis in the brain. However, the long-term effect of these drugs per se in terms of their potential to interfere with the oxidative status in the brain remains largely controversial. The present study aimed to investigate the sole effect of three commonly used psychoactive drugs, lithium, valproic acid, and olanzapine, on lipid and protein oxidation status in the prefrontal cortex of healthy rats. A total of 80 adult male albino Wistar rats were used, and groups were treated with saline (control), lithium, valproic acid, or olanzapine daily for 30 days. Following sacrification, right prefrontal cortexes were dissected and homogenized. Lipid peroxidation (LPO) and protein oxidation (AOPP) assays were performed by ELISA. LPO levels were significantly higher in lithium and valproic acid-treated rats by 45% and 40%, respectively. Olanzapine treatment caused a mild 26% increase in LPO levels, but the effect was non-significant. Lithium, valproic acid, and olanzapine treatments significantly increased AOPP levels by 58%, 54%, and 36.5%, respectively. There was a strong positive correlation between the lipid peroxidation and protein oxidation levels. Our results call attention to the need to consider the pro-oxidative capacity of antipsychotic drugs per se and their potential to disturb the oxidative homeostasis in the brain during long-term medication for psychiatric diseases.

Increased growth hormone secretagogue receptor-1a (GHSR-1a) in hypothalamus during olanzapine treatment in rats.

Weight gain is the one of the most important factors which increases global burden of psychiatric disorder. Second-generation antipsychotics, olanzapine (Olz) and valproic acid (Vpa) in particular, are held responsible for weight gain. However, it is still uncertain how these drugs cause this. Thus, the rats selected for the experiment were randomly divided into 3 groups. The 1st group received only 0.5 ml saline solution intraperitoneally (n = 20, control group); the second group was given 200 mg / kg Vpa intraperitoneally (n = 20, Vpa group) and 2 mg / kg Olz was given intraperitoneally to the 3rd group (n = 20, Olz group) between 8 and 10 am for 30 days. We examined serum leptin, adiponectin, resistin, TNF-α, IL-6, ghrelin level and, the amount of ghrelin secreting cells in the stomach and growth hormone secretagogue receptor-1a (GHSR-1a, ghrelin receptor) expression in the hypothalamus. The hypothalamic GHS-1a receptor index was significantly higher in the Olz group compared with the control group and Vpa group (p = 0.036 and p = 0.016 respectively). Ghrelin immune positive cell index in stomach was statistically significantly lower in the Vpa group compared with the control and Olz groups (p = 0.028 and p = 0.013 respectively) There was no difference between the groups in terms of serum leptin, resistin, IL-6 and ghrelin levels. In the Vpa group, a statistically significant increase was found in serum adiponectin level compared with both the control group and the Olz group (p = 0009 and p = 0024 respectively) and, significant decrease was found in serum TNF-α level compared to Olz group (p = 0007). In conclusion, we found that the main cause of weight gain in Olz use was the increase in the number of hypothalamic ghrelin receptors. Investigating the mechanism by which Olz increases the number of ghrelin receptors may help to develop effective treatment strategies in preventing obesity in psychiatric patients.

Is there any association between low level of serum nesfatin-1 and fibromyalgia syndrome?

OBJECTIVES: This study aims to investigate the relationship between serum level of nesfatin-1 and fibromyalgia syndrome (FMS) clinical parameters such as pain severity, disease activity, fatigue, emotional state, and sleep quality. PATIENTS AND METHODS: Forty-six female patients with FMS (median age 40 years; range, 18 to 53 years) and 46 healthy female controls (median age 36 years; range, 19 to 52 years) were included in the study. Severity of pain, disease activity, fatigue, sleep quality, and emotional status were evaluated by visual analog scale, Fibromyalgia Impact Questionnaire, Multidimensional Assessment of Fatigue (MAF), Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory (BDI), and Beck Anxiety Inventory (BAI), respectively. Serum nesfatin-1 concentrations (pg/mL) were measured by enzyme-linked immunosorbent assay method. RESULTS: There was no significant difference with respect to demographic characteristics between the FMS patients and healthy controls. When clinical parameters were compared, MAF, BDI, BAI, and PSQI scores were significantly higher in FMS patients than controls (p<0.05). Serum nesfatin-1 concentration was significantly lower in patients with FMS (p<0.05). When compared to the FMS patients without anxiety, serum nesfatin-1 concentration was significantly increased in FMS patients with anxiety (p<0.05). Serum nesfatin-1 concentration was positively correlated with BAI scores in patients with FMS (p<0.05). CONCLUSION: Low nesfatin-1 serum levels may contribute to pathological changes in FMS. In addition, nesfatin-1 may also be involved in the mediation of anxiety-related responses in FMS.

Assessment of genotoxicity in rats treated with the antidiabetic agent, pioglitazone.

Pioglitazone (PIO), a member of the thiazolidinedione class of antidiabetic agents, specifically targets insulin resistance. Drugs of this class act as ligands for the gamma subtype of the peroxisome proliferator-activated receptor. Although troglitazone, another drug in this class, displayed unacceptable hepatotoxicity, PIO was approved for human use by the U.S. Food and Drug Administration. To our knowledge, there are no published reports on the genotoxicity of PIO; however, the package insert indicates that it has minimal genotoxicity. In this study, we used the comet assay to investigate the DNA damage in the peripheral blood and liver cells of rats treated with PIO. Sixteen male Sprague-Dawley rats were randomly distributed into four groups, and dosed daily for 14 days by oral gavage with 0, 10, 20, and 40 mg/kg/day PIO. A dose-dependent increase in DNA damage, as assessed by % tail DNA, was observed in both hepatocytes and blood lymphocytes of the PIO-treated groups, with significant increases detected between the rats treated with all the doses of PIO and the control, and between the rats treated with different PIO doses (P < 0.005 to P < 0.0001). Treating nuclei from the exposed animals with an enzyme cocktail containing Fpg and Endonuclease III prior to performing the comet assay increased the level of DNA damage, which reflects oxidized purine and pyrimidine. Taken together, our data indicate that PIO is able to dose-dependently induce DNA damage in both the liver and blood lymphocytes of rats, which is partially due to the generation of oxidative lesions.

What is adverse effect of wireless local area network, using 2.45 GHz, on the reproductive system?

AIM: To investigate the inflammatory effect and testicular damage on rats exposed to low level of electromagnetic fields (EMF) at 2.45 GHz microwave radiation. METHODS: Twenty two Wistar rats were divided into two groups. Group 1 was the control group and not exposed to EMF. Group 2 was exposed to low level EMF (average E-field 3.68 ± 0.36 V/m, whole body average SAR, 0.0233 W/kg, in 10 g tissue) at 2.45 GHz for 1 hour/day for 30 consecutive days. At the end of the study, interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-32 (IL-32), C-reactive protein (CRP) were measured in rat serum and IL-6, IL-10, IL-32 were measured in rat testis tissue. Furthermore, testicular tissues were evaluated histopathologically in terms of spermatogenesis and coagulation necrosis. RESULTS: Serum IL-6 and CRP levels were found to be significantly different in the study group compared to the control group (p < .05), but no significant difference was found in serum IL-10, IL-32 levels and testis tissue IL-6, IL-10, IL-32 levels compared to the control group (p > .05). On the other hand, histopathological evaluation of testicular tissue revealed a significant difference in necrosis and spermatogenesis when compared with the control group (p < .05). CONCLUSIONS: It may be concluded that low level EMF at 2.45 GHz increases inflammation and testicular damage and negative impact on male reproductive system function.

Effect of bisphosphonate as an adjunct treatment for chronic periodontitis on gingival crevicuar fluid levels of nuclear factor-κB ligand (RANKL) and osteoprotegerin in postmenopausal osteoporosis.

Osteoporosis and periodontal disease are linked by an altered receptor activator of nuclear factor κB ligand and osteoprotegerin ratio (RANKL/OPG), and medical treatment with bisphosphonate (BP) may help control these molecules. The effect of BP on clinical findings and gingival crevicular fluid (GCF) values of RANKL and OPG using enzyme-linked immunosorbent assays was evaluated in postmenopausal women; 13 patients with both chronic periodontitis and osteoporosis (group A), 12 systemically healthy patients with chronic periodontitis (group B), 12 periodontally healthy patients with osteoporosis (group C), and 10 systemically and periodontally healthy individuals (group D). Recordings were repeated at the end of months 1, 6, and 12 in groups A, B, and C. At the baseline, groups A and B exhibited the lowest OPG values (P < 0.05). After periodontal treatment, OPG values were markedly increased at the end of 6th month in group A and 12th month in group B (P < 0.008). There was no significant difference in GCF RANKL values among groups (P > 0.05) or during the observation period (P > 0.008). The use of BP may be effective in preventing periodontal breakdown by controlling the levels of these markers in osteoporosis as an adjunct to periodontal treatment.

SAA1 alpha/alpha alleles in amyloidosis.

BACKGROUND: Amyloidosis, mainly AA type, is one of the common diseases in nephrology clinics in Turkey. AA type amyloidosis is a complication of various chronic infections or inflammatory diseases such as familial Mediterranean fever (FMF), rheumatoid arthritis (RA), tuberculosis and bronchiectasis. A controversy exists in the literature regarding the relationship between SAA1 genotypes and AA type amyloidosis. This study aimed to investigate SAA1 gene polymorphism in different patient groups: 1) amyloidosis, 2) FMF and 3) healthy controls. METHODS: Eighty-two patients from the three groups were included in the study: 1) amyloidosis, 2) FMF without amyloidosis, and 3) healthy controls. SAA1 genotypes were studied by the polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: The homozygous alpha/alpha genotype is the most common SAA1 genotype among patient groups with amyloidosis, and the alpha/alpha genotype frequency is significantly higher than in healthy controls (68 vs. 38%, p<0.05). CONCLUSIONS: The SAA1 alpha/alpha genotype is a risk factor for AA type amyloidosis in Caucasoid populations and more studies are needed to investigate why the gamma/gamma genotype is associated with AA type amyloidosis in Japan.

Increased Ghrelin Levels and Unchanged Adipocytokine Levels in Major Depressive Disorder.

OBJECTIVE: One of the hypotheses of the pathophysiology of major depressive disorder (MDD) proposes that there is a relationship between adipocytokine and ghrelin levels and depression. METHODS: Patients with major depression with a BMI ≤25 kg/m2 between the ages of 11 and 18 years (n = 30) were compared with a healthy control group (n = 30). Both groups were evaluated across a pretreatment period (MD-PT) and an improved period (MD-I). We measured serum leptin, adiponectin, resistin, and ghrelin levels and other parameters related to metabolic syndrome, such as glucose, insulin, insulin resistance (homeostasis model assessment [HOMA]), triglycerides (TG), and total cholesterol (TCHOL). RESULTS: Leptin, adiponectin, and resistin levels did not differ across groups; however, ghrelin levels were increased in the MD-I group compared with the control and MD-PT groups (p < 0.05). HOMA levels were also higher in the MD-PT group than in the control group (p < 0.05). After treatment, there was no difference in this measurement. CONCLUSIONS: The relationship between adipocytokines and major depression may be dependent on ghrelin levels as a result of antidepressant treatment and subsequent obesity.

Genotoxicity assessment using comet assay in Behcet's disease patients.

Behcet's disease (BD) was originally described by Turkish dermatologist, Hulusi Behcet in 1937. BD is an inflammatory disorder of unknown cause, characterized by recurrent oral aphthous ulcers, genital ulcers, uveitis, and skin lesions. All these common manifestations are self-limiting except for ocular attacks. The aims of this study were to assess whether BD patients have more genotoxicity than healthy controls and whether colchicine (COL) treated BD patients are different from those not using COL in terms of genotoxicity. A few dozens of methods have been developed and used for the assessment of genotoxicity. The most popular method is based on single cell gel electrophoresis (COMET assay) in alkaline condition. After electrophoresis, captured images are subjected to digital image analysis to find the values for percent tail DNA from comet assay parameters consistent with genotoxicity. COMET assay was performed in isolated lymphocytes from 42 COL treated Behcet's disease patients, 9 BD patients not using COL, and 36 healthy controls. In the COL-BD patients and non-COL-BD patients, the mean age (range 14-56 years) and mean disease duration (range 0.5-24 years) did not differ between the two groups. We found statistical differences in percent tail DNA between BD and the healthy controls (13.38+/-9.58 versus 2.77+/-1.45, P<0.0001). No difference in percent tail DNA was observed between users and non-users of COL, whereas it was more different in inactive BD patients than active ones (19.75+/-10.49 versus 11.83+/-8.79, P<0.05, respectively). Genotoxicity, as assessed by COMET assay, is increased in BD patients. These results suggest that genotoxicity is associated with BD itself rather than COL use.

Oxidative stress in bipolar and schizophrenia patients.

Oxidative stress has an important place in studies investigating the pathophysiology of psychiatric diseases. In spite of this fact, longitudinal studies are required to clarify the subject. Therefore, in this study, we examined lipid peroxidation, protein oxidation, total oxidized guanine species, superoxide dismutase (SOD) and total glutathione (GSH) levels in blood collected from adult bipolar patients (n=18) during manic and euthymic episodes, schizophrenic patients (n=18) during acute psychotic attack and remission phases and the control group (n=18). There was a significant increase in the level of lipid peroxidation in the bipolar disorder manic episode group (BD-ME) compared to control group. The level of protein oxidation was significantly higher in the schizophrenia acute psychotic attack group (SZ-APA) compared to the control group. The level of total oxidized guanine species was statistically higher in all psychiatric groups compared to the control group. There was no significant difference among the groups with regard to SOD and GSH. Consequently, we believe that lipid peroxidation may be effective in the pathogenesis of bipolar patients; that protein oxidation may be of importance in the pathogenesis of schizophrenia and that total oxidized guanine species may be crucial in the pathogeneses of both psychiatric disorders.

Increased DNA oxidation (8-OHdG) and protein oxidation (AOPP) by low level electromagnetic field (2.45 GHz) in rat brain and protective effect of garlic.

PURPOSE: To investigate the oxidative damage and protective effect of garlic on rats exposed to low level of electromagnetic fields (EMF) at 2.45 GHz Microwave radiation (MWR). METHODS: Thirty-six Wistar rats were divided into three groups. Group I was the control group and not exposed to EMF. Group II and III were exposed to low level EMF (3.68 ± 0.36 V/m) at 2.45 GHz MWR for 1 hour/day for 30 consecutive days. Daily 500 mg/kg garlic was given to Group III during the study period. At the end of the study, thiobarbituric acid reactive substances (TBARS), advanced oxidation protein products (AOPP) and 8-hydroxydeoxyguanosine (8-OHdG) levels were investigated in brain tissue and blood samples. RESULTS: Exposure to low level of EMF increased 8-OHdG level in both plasma and brain tissue whereas it increased AOPP level only in plasma. Garlic prevented the increase of 8-OHdG level in brain tissue and plasma AOPP levels. CONCLUSIONS: It may be concluded that low level EMF at 2.45 GHz MWR increases the DNA damage in both brain tissues and plasma of the rats whereas it increases protein oxidation only in plasma. It may also be argued that the use of garlic decreases these effects.