Neuroprotective effect of quercetin against oxidative damage and neuronal apoptosis caused by cadmium in hippocampus.

The purpose of the present investigation was to evaluate cadmium (Cd)-induced neurotoxicity in hippocampal tissues and beneficial effect of quercetin (QE) against neuronal damage. A total of 30 male rats were divided into 3 groups: control, Cd-treated, and Cd + QE-treated groups. After the treatment, the animals were killed and hippocampal tissues were removed for biochemical and histopathological investigation. Cd significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in hippocampal tissue compared with the control. Administration of QE with Cd significantly decreased the levels of MDA and PC and significantly elevated the levels of antioxidant enzymes in hippocampal tissue. In the Cd-treated group, the neurons of both tissues became extensively dark and degenerated with pyknotic nuclei. The morphology of neurons in Cd + QE group was well protected, but not as neurons of the control group. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd-treated group. Treatment of QE markedly reduced the immunoreactivity of degenerating neurons. The results of the present study show that QE therapy causes morphologic improvement in neurodegeneration of hippocampus after Cd exposure in rats.

Neuroprotective effect of ebselen against intracerebroventricular streptozotocin-induced neuronal apoptosis and oxidative stress in rats.

The goal of this study was to examine the neuroprotective effect of ebselen against intracerebroventricular streptozotocin (ICV-STZ)-induced oxidative stress and neuronal apoptosis in rat brain. A total of 30 adult male Sprague-Dawley rats were randomly divided into 3 groups of 10 animals each: control, ICV-STZ, and ICV-STZ treated with ebselen. The ICV-STZ group rats were injected bilaterally with ICV-STZ (3 mg/kg) on days 1 and 3, and ebselen (10 mg/kg/day) was administered for 14 days starting from 1st day of ICV-STZ injection to day 14. Rats were killed at the end of the study and brain tissues were removed for biochemical and histopathological investigation. Our results demonstrated, for the first time, the neuroprotective effect of ebselen on Alzheimer's disease (AD) model in rats. Our present study, in ICV-STZ group, showed significant increase in tissue malondialdehyde levels and significant decrease in enzymatic antioxidants superoxide dismutase and glutathione peroxidase in the frontal cortex tissue. The histopathological studies in the brain of rats also supported that ebselen markedly reduced the ICV-STZ-induced histopathological changes and well preserved the normal histological architecture of the frontal cortex tissue. The number of apoptotic neurons was increased in frontal cortex tissue after ICV-STZ administration. Treatment of ebselen markedly reduced the number of degenerating apoptotic neurons. The study demonstrates the effectiveness of ebselen, as a powerful antioxidant, in preventing the oxidative damage and morphological changes caused by ICV-STZ in rats. Thus, ebselen may have a therapeutic value for the treatment of AD.

Role of quercetin in cadmium-induced oxidative stress, neuronal damage, and apoptosis in rats.

The present study was carried out to evaluate the neuroprotective effect of quercetin (QE) in protecting the cadmium (Cd)-induced neuronal injury in frontal cortex of rats. A total of 30 adult male Sprague-Dawley rats were randomly divided into three groups of 10 animals each: control, Cd treated and Cd treated with QE. The Cd-treated group was injected subcutaneously with cadmium chloride (CdCl2) dissolved in saline at a dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in QE-treated groups were given QE (15 mg/kg body weight) once a day intraperitoneally starting 2 days prior to Cd injection, during the study period. Rats were sacrificed at the end of the study and the frontal cortex tissues were removed for biochemical and histopathological investigation. To date, there is no available information on the effect of QE on neuronal injury after Cd exposure. Rats intoxicated with Cd for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants superoxide dismutase, glutathione peroxidase and catalase in the frontal cortex tissue. Administration of QE with Cd significantly diminished the levels of MDA and significantly elevated the levels of enzymatic antioxidants in the frontal cortex tissue. The histopathological studies in the brain of rats also supported that QE markedly reduced the Cd-induced histopathological changes and well preserved the normal histological architecture of the frontal cortex tissue. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd group. Treatment with QE markedly reduced the immunoreactivity of degenerating neurons. In conclusion, the results of the current study suggest that QE may be beneficial in combating the Cd-induced neurotoxicity in the brain of rats. We believe that further preclinical research into the utility of QE may indicate its usefulness as a potential treatment for neurodegeneration after Cd exposure in rats.

The change in plasma GABA, glutamine and glutamate levels in fluoxetine- or S-citalopram-treated female patients with major depression.

OBJECTIVE: The aim of this study was to investigate the relationship between plasma glutamate, glutamine and gamma-aminobutyric acid (GABA) levels in female patients with major depression treated with S-citalopram or fluoxetine. METHODS: The patients were assigned into S-citalopram (10 mg/day) or fluoxetine (20 mg/day) groups (n = 15 per group). The Hamilton and Beck Depression Inventory Scales were performed on all study participants, and blood samples were collected. The same procedures were repeated 10 days following the onset of therapy. Fifteen female healthy volunteers were also included in the study for the evaluation of normal plasma levels. RESULTS: The plasma GABA levels of the healthy volunteers were higher whereas those for glutamate and glutamine were lower than the day zero samples of the patients. An increase in plasma GABA levels and a decrease in glutamate and glutamine levels were observed on the 10th day of treatment. No difference was detected between the drug treatments. CONCLUSION: Our findings may suggest that GABA, glutamate and glutamine play a role in depression and that plasma GABA may be used as a biomarker for treatment control.

Increased serum levels of apoptosis in deficit syndrome schizophrenia patients: a preliminary study.

BACKGROUND: Schizophrenia is a chronic and debilitating disorder, the etiology of which remains unclear. Apoptosis is a programmed cell death mechanism that might be implicated in neuropsychiatric disorders, including schizophrenia. In this study, we aimed to compare the serum levels of apoptosis among deficit schizophrenia (DS) syndrome patients, nondeficit schizophrenia (NDS) patients, and healthy controls (HCs). PATIENTS AND METHODS: After the inclusion and exclusion criteria were applied, 23 DS patients, 46 NDS patients, and 33 HCs were included in the study. The serum apoptosis levels were measured using a quantitative sandwich enzyme immunoassay with human monoclonal antibodies directed against DNA and histones. RESULTS: There was a significant difference among the three groups in terms of the levels of apoptosis (F 2,96=16.58; P<0.001). The serum apoptosis levels in the DS and NDS groups were significantly higher than those in the HC group. Furthermore, the serum apoptosis levels in the DS group were significantly higher than the levels in the NDS group. CONCLUSION: This study suggests that increased levels of apoptosis may be implicated in the pathophysiology of DS syndrome. However, further studies are needed to support the role of apoptosis in DS.

Increased serum dehydroepiandrosterone sulfate in the first episode but not in subsequent episodes in male patients with schizophrenia.

BACKGROUND: Many studies have investigated the relationship between blood levels of dehydroepiandrosterone (DHEA) and its sulfate ester (DHEA-S), cortisol, progesterone, and testosterone and the onset, prognosis, symptom severity, and treatment response of schizophrenia. In the present study, we assessed potential differences in blood levels of neurosteroids between drug-naïve first-episode patients with schizophrenia (FES), and drug-free patients with schizophrenia who were not in the first episode but were in a phase of acute exacerbation (DFP). MATERIALS AND METHODS: The present study included 32 male FES, 28 male DFP, and 24 male healthy controls (HC). Groups were compared in terms of blood levels of adrenocorticotropic hormone (ACTH), cortisol, testosterone, progesterone, and DHEA-S. RESULTS: Blood levels of ACTH, cortisol, testosterone, and progesterone were similar among the groups. The mean value of serum DHEA-S was significantly different among the groups (P<0.001). The value of serum DHEA-S was higher in the FES group than in the DFP and HC groups (both P<0.001). The mean values of serum DHEA-S in the HC and DFP groups were found to be similar (P=0.33). CONCLUSION: We suggest that higher values of DHEA-S in the FES group compared with both the DFP and HC groups indicate that this neurosteroid response is unique to first-episode schizophrenia patients. Further studies are needed to investigate the difference in blood levels of neurosteroids in different groups in terms of age of diagnosis.

Effect of standard versus patient-targeted in-patient education on patients' anxiety about self-care after discharge from cardiovascular surgery clinics.

We compared standard and patient-targeted in-patient education in terms of their effect on patients' anxiety. One hundred and ninety-eight patients who were hospitalised for coronary artery bypass surgery were given standard education (group 1) or individualised education (group 2) on the management of their healthcare after discharge. Patients in group 2 were assessed on the patient learning needs scale and were given education according to their individual needs. The level of anxiety was measured by the state-trait anxiety inventory. Anxiety scores were significantly lower in group 2 than group 1 after education (p < 0.001). While state anxiety did not change after education in group 1 (p = 0272), it decreased significantly in group 2 (p < 0.001). For cardiovascular surgery patients, patient-targeted in-patient education was more effective than standard education in decreasing anxiety levels, therefore the content of the education should be individualised according to the patient's particular needs.

Is there a new finding added to the fibromyalgia syndrome?

OBJECTIVE: The aim of this study is to examine depression and anxiety related arrhytmia risk in fibromyalgia syndrome (FMS). METHODS: Fifty-nine patients with the diagnosis of FMS and 20 control participants were included in the study. Fibromyalgia Impact Questionnaire (FIQ), Visual Pain Scale (VPS) surveys were applied to determine the severity of the disease. Beck Anxiety (BAS) and Beck Depression scales (BDS) were applied to all participants. Electrocardiograms were obtained from all participants. P-wave dispersions (Pd) were estimated to determine the risk of the atrial arrhythmia, and QT wave dispersion (QTd) and corrected QT(QTdd) values were used to predict the risk of ventricular arrhythmia. RESULTS: BAS and BDS results were significantly higher in the patient group compared to the control group (p˂0001). In the patient group, Pd was significantly longer (p=0.034). Other clinical, and demographic data did not differ significantly between groups. CONCLUSION: In this study, the risk of arrhythmia in FMS was evaluated and increased Pd in patients with FMS compared to the control group was detected. This finding shows increased risk of atrial fibrilation (AF) in patients with FMS. If we consider that patients with fibromyalgia consist relatively of young patients together with the increased risk of AF with age, it is important to follow-up these patients in later ages for AF risk.

Distinct temperament and character profiles in first onset vitiligo but not in alopecia areata.

Alopecia areata (AA) and vitiligo (V) are diseases that are correlated with psychiatric disorders before, during and after diagnosis. The Temperament and Character Inventory (TCI) is a well-established approach for investigating personality traits in various psychosomatic diseases. The aim of this study is to compare and investigate the differences in the TCI between patients with first onset AA, patients with V and healthy controls (HC). Participants in the study included 42 patients with first onset AA, 50 adult patients with V and 60 HC who had no history or diagnoses of psychiatric or dermatological disorders. All participants were assessed with the TCI and the Dermatology Life Quality Index (DLQI). Among the temperament traits, the extravagance, disorderliness and total novelty-seeking scores were lower, and the worry and pessimism scores were higher in patients with V compared with patients with AA and the HC. The mean score of the enlightened second nature and the total self-directedness score of the character traits were higher in patients with V compared with patients with AA and the HC group. In the AA group, there was a negative correlation only between the reward dependence total score and the DLQI score. This study suggests that patients with first onset V have a distinct temperament, such as being unenthusiastic and unemotional, and character profiles, such as worry and pessimism, independent of their psychiatric comorbidities, and patients with AA do not have a different personality from the non-affected population.

Possible association between vitamin D deficiency and restless legs syndrome.

BACKGROUND AND AIM: Restless legs syndrome (RLS) is a distressing sleep disorder that occurs worldwide. Although there have been recent developments in understanding the pathophysiology of RLS, the exact mechanism of the disease has not been well elucidated. An increased prevalence of neurologic and psychiatric diseases involving dopaminergic dysfunction in vitamin D-deficient patients led us to hypothesize that vitamin D deficiency might result in dopaminergic dysfunction and consequently, the development of RLS (in which dopaminergic dysfunction plays a pivotal role). Thus, the aim of this study was to evaluate the relationship between vitamin D deficiency and RLS. METHODS: One hundred and fifty-five consecutive patients, 18-65 years of age, who were admitted to the Department of Internal Medicine with musculoskeletal symptoms and who subsequently underwent neurological and electromyography (EMG) examination by the same senior neurologist, were included in this study. The patients were divided into two groups according to serum 25-hydroxyvitamin D (25(OH)D) (a vitamin D metabolite used as a measure of vitamin D status) level: 36 patients with serum 25(OH)D levels ≥20 ng/mL comprised the normal vitamin D group, and 119 patients with serum 25(OH)D levels <20 ng/mL comprised the vitamin D deficiency group. The two groups were compared for the presence of RLS and associated factors. RESULTS: The two groups were similar in terms of mean age, sex, mean body mass index (BMI), and serum levels of calcium, phosphate, alkaline phosphatase (ALP), and ferritin. The presence of RLS was significantly higher in the vitamin D deficiency group (χ (2)=12.87, P<0.001). Regression analysis showed vitamin D deficiency and serum 25(OH)D level to be significantly associated with the presence of RLS (odds ratio [OR] 5.085, P<0.001 and OR 1.047, P=0.006, respectively). CONCLUSION: The present study demonstrated a possible association between vitamin D deficiency and RLS. Given the dopaminergic effects of vitamin D, 25(OH)D depletion may lead to dopaminergic dysfunction and may have a place in the etiology of RLS. Prospective vitamin D treatment studies are needed to confirm this relationship and to evaluate the efficacy of vitamin D as a treatment for RLS patients.