Effect of lycopene on As2O3 induced oxidative stress in SH-SY5Y cells.

It is known that oxidative stress may cause neuronal injury and several experimental models showed that As2O3 exposure causes oxidative stress. Lycopene, a carotenoid, has been shown to have protective effect in neurological disease models due to antioxidant activity, but its effect on As2O3-induced neurotoxicity is not identified yet. The aim of this study is to investigate the effects of lycopene on As2O3-induced neuronal damage and the related mechanisms. Cell viability was determined by the MTT assay. Lycopene was administrated with different concentrations (2, 4, 6 and 8 µM) one hour before 2 µM As2O3 exposure in SH-SY5Y human neuroblastoma cells. The anti-oxidant effect of lycopene was determined by measuring superoxide dismutase (SOD), catalase (CAT) hydrogen peroxide (H2O2), malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS). MTT results and LDH cytotoxicity analyses showed that pretreatment with 8 µM lycopene significantly improved the toxicity due to As2O3 exposure in SH­SY5Y neuroblastoma cells. Pretreatment with lycopene significantly increased the activities of anti­oxidative enzymes as well as total antioxidant status and decreased total oxidative status in As2O3 exposed cells. The results of this study indicate that lycopene may be a potent neuroprotective against oxidative stress and could be used to prevent neuronal injury or death in several neurological diseases.

Evaluation of antibiotic use among hospitalised patients in a paediatric department of a training hospital in Turkey.

BACKGROUND: Antibiotics are widely used and inaccurate or inappropriate prescription of antibiotics causes a significant increase in the prevalence of multidrug-resistant bacterial infections among children. This research aimed to study antibiotic prescriptions in hospitalised paediatric patients and to determine the prevalence of inappropriate antimicrobial use and the main types of prescribing errors. METHODS: After obtaining the Ethics Committee approval, screening was conducted among 535 patients admitted to the Department of Pediatrics at Haydarpasa Numune Training and Research Hospital in the period from 01 January 2016 to 31 December 2016 who had been treated with an antibiotic. Patients' demographics, diagnosis and antibiotic therapy details were collected using a standardised case report form and assessed by a clinical pharmacologist and an infectious disease specialist regarding the convenience and accurateness of prescription of antibiotics. RESULTS: Out of 535 antibiotic prescriptions, single antibiotics were used inappropriately in 216 (56.10%) of the patients and there were 39 (26%) unnecessary antibiotic combinations. Most of the errors were made in the dose frequency (55.69%), followed by indication (25.88%), administration route (16.08%) and dosage (2.67%). CONCLUSIONS: The results of our study show that a high level of antibiotics in the paediatric clinic was misprescribed. Inappropriate usage increases the chances of microbial resistance and the cost of treatment. Precautions should be taken in this regard.

Effect of new oral anticoagulants on platelet indices in non-valvular atrial fibrillation patients.

New-generation oral anticoagulants (NOACs) are now preferred as a first-line treatment in the management of atrial fibrillation for prevention of thromboembolic complications. Mean platelet volume (MPV), one of the indicators of increased platelet activity, is also associated with an increased stroke risk in atrial fibrillation patients. The aim of this study was to evaluate changes in MPV, platelet distribution width (PDW) and plateletcrit following use of NOACs. The study included 116 patients with non-valvular atrial fibrillation without previous NOAC use. Complete blood counts, biochemical analyses and echocardiography were performed for all patients. No significant differences were observed in MPV or other platelet indices at 6 months compared to baseline. Our results indicate that MPV and other platelet indices are not affected by NOAC use in non-valvular atrial fibrillation patients.

Polyclonal antibody-based immunoassay of vitellogenin in Van fish (Alburnus tarichi).

Van Lake is the third largest closed lake in the world and the biggest lake in Turkey. An ELISA method has developed with the aim of determining the pollution caused by estrogens and estrogen-like chemicals that have come to the lake Van in recent years. First, the vitellogenin in estrogen-treated male fish plasma was purified by ion exchange chromatography, injected into rats, and the obtained polyclonal antibodies were tested for specificity by Western blot and immunohistochemical methods. Immunohistochemical labeling of the vitellogenin-synthesized liver resulted in the intense marking of the liver of the animals injected with estrogen, while no markings were observed in the control group. The limit of detection of the developed enzyme-linked immunosorbent assay was 4.6 µg L-1, and the working range was 7.8 to 2000 µg L-1. Intra- and inter-assay variations were 13.0 % and 13.3%. The highest level of vitellogenin in male fishes measured was 23.56 µg mL-1.

An In Vitro Model for Conditioning Lesion Effect.

Axons of a peripheral nerve grow faster after an axotomy if it attains a prior injury a few days earlier. This is called conditioning lesion effect (CLE) and very much valued since it may provide new insights into neuron biology and axonal regeneration. There are established in vivo experimental paradigms to study CLE, however, there is a need to have an in vitro conditioning technique where CLE occurs in a maximally controlled environment. Mouse primary sensory neurons were isolated from lumbar 4-5 dorsal root ganglia and incubated at 37 °C on a silicon-coated watch glass that prevents cell attachment. After this conditioning period they were transferred to laminin coated culture dishes. Similar cultures were set up with freshly isolated neurons from control animals and from the animals that received a sciatic nerve cut 3 days earlier. All preparations were placed on a live cell imaging microscopy providing physiological conditions and photographed for 48 h. Axonal regeneration and neuronal survival was assessed. During the conditioning incubation period neurons remained in suspended aggregates and did not grow axons. The regeneration rate of the in vitro conditioned neurons was much higher than the in vivo conditioned and control preparations during the first day of normal incubation. However, higher regeneration rates were compromised by progressive substantial neuronal death in both types of conditioned cultures but not in the control preparations. By using neutralizing antibodies, we demonstrated that activity of endogenous leukemia inhibitory factor is essential for induction of CLE in this model.

Neuronal survival of DRG neurons after neurite transection in vitro promotes by nerve growth factor and brain derived neurotrophic factor.

Neurotrophic factors are growth factors that promote neuronal survival, regulate synaptic function and neurotransmitter release, and promote the plasticity and growth of axons in the peripheral and central nervous systems. This study focused on the roles of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in the survival of adult dorsal root ganglion (DRG) neurons following axotomy. To investigate this, we cultured adult mouse DRG neurons and administered NGF or BDNF to the culture medium at different doses before transection. After determining the optimal doses of NGF and BDNF, these factors were then applied in combination. Axotomy was performed using a precise laser beam and neuronal death was visualized through cell observer microscopy system, by adding propidium iodide to the culture medium. The results demonstrate that the optimal doses of NGF and BDNF for neuronal survival are 150 ng/mL and 50 ng/mL, respectively. The highest level of neuronal survival was observed in the cells treated with a combination of NGF and BDNF. In conclusion, NGF and BDNF have a positive effect, both individually and in combination, on the survival of DRG neurons following neurite transection.

Neuromuscular degenerative effects of Ankaferd Blood Stopper® in mouse sciatic nerve model.

PURPOSE: Ankaferd Blood Stopper® (ABS), a licenced medicinal herbal extract, is commonly used as an effective topical haemostatic agent. This study is designed to investigate whether topical ABS application may cause peripheral nerve degeneration and neuromuscular dysfunction in a mouse sciatic nerve model. METHODS: Twenty mice were randomly divided into two groups; an ABS treated experimental group and a saline-treated control group. Left sciatic nerves were treated with 0.3 ml of ABS in the experimental group and 0.3 ml of sterile saline in the control group for 5 min. Peripheral nerve degeneration and neuromuscular dysfunction were evaluated by behavioural tests, electrophysiological analysis and weight ratio comparison of target muscles. RESULTS: The motor function, assessed by the sciatic function index, was significantly impaired in ABS-treated animals as compared to the animals treated with saline. Motor coordination, evaluated with the rotarod test, was significantly decreased (-42%) in ABS-treated animals compared to the saline-treated animals. The degree of pain, assessed by the reaction latency to thermal stimuli (hot-plate test), was significantly prolonged (313%) in ABS-treated mice when compared to the saline-treated mice. ABS-treated mice showed a significant reduction in motor nerve conduction velocity (MNCV) (-52%) and the compound muscle action potential (CMAP) (-47%); however, it significantly prolonged onset latency (23%). The gastrocnemius muscles weight ratio of the ABS group was considerably lower than that of the control group. CONCLUSIONS: These findings demonstrate that ABS triggers peripheral nerve degeneration and functional impairment and, thus promotes a deterioration of sciatic nerves.

The effects of calcium channel blockers on nephropathy and pigment epithelium-derived factor in the treatment of hypertensive patients with type 2 diabetes mellitus.

The aim of this study was to compare the effects of a dihidropiridin calcium channel blocker amlodipin and a non-dihidropiridin calcium channel blocker verapamil on nephropathy and serum pigment epithelium-derived factor (PEDF) levels of type 2 diabetic patients with hypertension. Forty-one type 2 diabetic patients with uncontrolled hypertension in spite of using angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) were enrolled in the study. The patients were randomized in two groups. First group received amlodipin (5-10 mg/d) and second group verapamil (120-240 mg/d) for 6 weeks. The difference between two calcium channel blocker treatments was investigated by analyzing urinary albumin excretion and plasma PEDF levels of patients at the end of 6 weeks. Urinary microalbumin/creatinine values were decreased in both amlodipin and verapamil groups but it was not statistically significant. Plasma PEDF levels also decreased significantly in both groups at the end of the treatment (p < 0.001 and p < 0.001, respectively). At the end of the treatment there was no significant difference between changes in values of systolic BP, diastolic BP, microalbumin/creatinine and PEDF percentage in both groups (p = 0.788, p = 0.926, p = 0.908, p = 0.140, respectively). PEDF values showed a positive correlation with microalbumin/creatinine, hb A1c, FBS, systolic and diastolic BP levels. It was observed that both of the drugs have similar effects on nefhropathy and PEDF at the end of the treatment. In this study, we suggest that calcium channel blockers may have renoprotective effects by different mechanisms except their antihypertensive effects and this may be important to determine the selection of antihypertensive drug combinations in diabetic nephropathy.

Effects of melatonin on the serum levels of pro-inflammatory cytokines and tissue injury after renal ischemia reperfusion in rats.

We investigated the changes in the serum levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6, the pro-inflammatory cytokines, and the possible effect of melatonin on the modulation of these inflammatory molecules after renal ischemia reperfusion (IR). The study was carried out in the laboratory of Department of Pharmacology. Forty-six male Wistar albino rats were divided into five groups as control (n=6), positive control (n=4), sham (n=12), renal IR (n=12), and renal IR melatonin (n=12). After 1 h renal pedicle occlusion, the blood samples were taken for the measurement of cytokine levels at second hour of the reperfusion. The rats were sacrificed after 24 h of reperfusion for histopathological evaluation. Melatonin or vehicle was administrated to IR rats. Lipopolysaccharide (LPS) was administered to the positive control group and the blood was taken at fourth hour. Serum TNF-α levels increased significantly in renal IR and LPS groups. Serum IL-6 levels were not different from control except the LPS group. There was no significant correlation between the serum TNF-α levels and the histopathological score after renal IR. Melatonin treatment reversed the increase of serum TNF-α levels and histopathological injury in renal tissue after renal IR. Melatonin may have a protective effect by reducing the serum level of TNF-α in renal IR.

Investigation of intercellular adhesion molecules (ICAMs) gene expressions in patients with Barrett's esophagus.

The adhesion molecules play a major role in inflammation as well as in neoplastic diseases. The aim of this study is to evaluate the expressions of the adhesion molecules, intercellular adhesion molecule 1 (ICAM-1), ICAM-2, and ICAM-3, in Barrett's esophagus, recognized as a premalign lesion for esophageal cancer and related to inflammation. Eighteen patients with Barrett's esophagus according to endoscopy and 25 volunteers without Barrett's esophagus disease were included in the study. Tissue samples were supplied by biopsy and used for both gene expression and immunohistochemical analysis. The significance of the differences between the two groups was assessed by Student's t test. The ICAM-1 expression level was fivefold higher in the patient group compared with that of the control. There was an increase in the serum level of ICAM-1 in patients compared to that of the controls, but this increase was not significant. ICAM-2 levels were also increased in the patient group, but it was not significant. There was no difference between controls and patients in ICAM-3 levels. Significantly higher levels of ICAM-1 gene expression make us think that ICAM-1 may play an important role in Barrett's esophagus. We think that more studies, with larger patient groups and preferably detailed histopathological and clinical evaluations, are needed to explain the severity of ICAM-1, ICAM-2, and ICAM-3 molecules in Barrett's esophagus.

Tissue damage in kidney, adrenal glands and diaphragm following extracorporeal shock wave lithotripsy.

This study was designed to investigate whether exposure to short-term extracorporeal shock wave lithotripsy (ESWL) produces histologic changes or induces apoptosis in the kidney, adrenal glands or diaphragm muscle in rats. The effect of shock waves on the kidney of male Wistar rats (n = 12) was investigated in an experimental setting using a special ESWL device. Animals were killed at 72 h after the last ESWL, and the tissues were stained with an in situ Cell Death Detection Kit, Fluorescein. Microscopic examination was performed by fluorescent microscopy. Apoptotic cell deaths in the renal tissue were not observed in the control group under fluorescent microscopy. In the ESWL group, local apoptotic changes were observed in the kidney in the area where the shock wave was focused. The apoptotic cell deaths observed in the adrenal gland of the control group were similar to those observed in the ESWL groups, and apoptosis was occasionally observed around the capsular structure. Apoptotic cell deaths in the diaphragm muscle were infrequently observed in the control group. Apoptosis in the ESWL group was limited to the mesothelial cells. This study demonstrated that serious kidney, adrenal gland and diaphragm muscles damage occurred following ESWL, which necessitated the removal of the organ in the rat model. It is recognized that the ESWL complications related to the kidney, adrenal gland and diaphragm muscles are rare and may be managed conservatively.

Functional and structural neurodegenerative activities of Ankaferd BloodStopper in a mouse sciatic nerve model.

Traumatic and postoperative hemorrhages are life-threatening complications. Ankaferd BloodStopper (ABS) is a potent topical hemostatic agent to stop bleeding. However, ABS is associated with nerve toxicity. The present study aimed to investigate the functional and structural neurodegenerative effects of ABS in a mouse model. A total of 30 male BALB/c mice, aged 6-8 weeks, were randomly divided into control group (no treatment), a sham group (treated with saline) and an experimental group (treated with ABS). In the saline and the ABS groups, the right sciatic nerve was surgically exposed and treated with saline or ABS, respectively. No surgical procedure was performed in the control group. On day 7 post-treatment, functional changes of the sciatic nerve were evaluated by a horizontal ladder rung walking task. Structural changes were assessed with immunohistochemistry. In the horizontal ladder rung walking test, the gait impairment was proportional to the severity of sciatic nerve damage, with the ABS group showing a significantly higher rate of errors than the control and saline groups. Immunohistochemistry demonstrated extensive degeneration and deformation in the axons and myelin sheath of the sciatic nerve in the ABS group. The results provide compelling evidence for the neurotoxicity of ABS.

Investigation of the therapeutic effect of melatonin on deltamethrin applied mouse primary hepatocyte culture.

OBJECTIVE: In recent years, it has been known that the melatonin hormone, secreted from the pineal gland, possesses significant antioxidant activity. This study explores the therapeutic effect of melatonin on the deleterious effects of deltamethrin, a pyrethroid pesticide extensively used worldwide, including in Türkiye, on mouse liver cells. METHODS: Hepatocytes from Balb/C mice were isolated using a two-stage perfusion method, resulting in over 85% live hepatocytes. The isolated cells were cultured with different doses of deltamethrin (1 and 10 µM) and melatonin (100 µM) for 24 and 48 hours. At the conclusion of the culture period, hepatocytes were extracted at the 24th and 48th hours, and Malondialdehyde (MDA), Total Antioxidant Capacity (TAC), Total Oxidation Status (TOS), and DNA damages (8-hydroxy-2'-deoxyguanosine (8-OHdG)) were examined. RESULTS: While an increase in MDA, TOS, and DNA damage was observed in the deltamethrin-administered groups of hepatocytes, a decrease in TAC level was noted. It was determined that the applied deltamethrin had no effect on cell viability throughout the application period. CONCLUSION: Furthermore, it was observed that melatonin, when administered concurrently with deltamethrin, reduced the toxic effect of deltamethrin. This study suggests that melatonin has a protective effect against deltamethrin-induced damage in mouse hepatocyte cells.

Active shrinkage protects neurons following axonal transection.

Trauma, vascular events, or neurodegenerative processes can lead to axonal injury and eventual transection (axotomy). Neurons can survive axotomy, yet the underlying mechanisms are not fully understood. Excessive water entry into injured neurons poses a particular risk due to swelling and subsequent death. Using in vitro and in vivo neurotrauma model systems based on laser transection and surgical nerve cut, we demonstrated that axotomy triggers actomyosin contraction coupled with calpain activity. As a consequence, neurons shrink acutely to force water out through aquaporin channels preventing swelling and bursting. Inhibiting shrinkage increased the probability of neuronal cell death by about 3-fold. These studies reveal a previously unrecognized cytoprotective response mechanism to neurotrauma and offer a fresh perspective on pathophysiological processes in the nervous system.

The short- and long-term effects of a course on rational drug use: A comparative study between prefinal- and final-year undergraduate medical students who attended the course in different clinical years.

BACKGROUND: Rational pharmacology use and appropriate prescribing are among the key learning outcomes in medical education. Some medical faculties include rational pharmacotherapy course in their education programs at different years of education in Turkey. The aims of this study were to investigate the differences in effect of rational pharmacotherapy course on short- and long-terms by comparing two cohorts who attended the course in different clinical years of medical education by identifying which parameters of prescription items are different among groups. MATERIALS AND METHODS: This quasi-experimental study was conducted in School of Medicine. Participants consisted of 157 students who attended the course in Grade 4 (n = 110, Group A) and Grade 5 (n = 47, Group B). Students were asked to complete a prescribing task both upon completion of the course and 1 year after. The performance in prescribing was determined by prescription scoring form. Repeated measures ANOVA was employed to test the intervention effect between two periods. McNemar test was employed to measure the change in each item on the prescription. Point-biserial correlations between each item on the prescription and their scores on the test as a whole were calculated. RESULTS: The mean score of Group A dropped to 59.41 (standard deviation [SD] = 14.06) from 90.43 (SD = 8.90), and the mean score of Group B dropped to 73.37 (SD = 12.56) from 83.91 (SD = 10.03). All the prescription components in the scripts of the Group A students worsened significantly, except the "name of drug," whereas Group B students maintained most of them after 1 year. CONCLUSIONS: This study shows that the long-term retention effect of rational pharmacotherapy course conducted in later years of education is better than the course conducted in earlier years of education, which may be related to the fact that students in later years are more likely to take on responsibility for patient therapy process in clinical education.

Clinical Characteristics, Comorbid Medical Diagnoses, and Causes of Death of Individuals with Severe Mental Illness Who Died During Follow-up in Community Mental Health Centers: A Multicenter, Retrospective Study. / Toplum Ruh Sagligi Merkezlerinde Takipleri Sirasinda Ölen Siddetli Ruhsal Hastaligi Olan Bireylerin Klinik Özellikleri, Ek Tibbi Tanilari ve Ölüm Nedenleri: Çok Merkezli, Geriye Dönük Bir Arastirma.

OBJECTIVE: In this study, it was aimed to define the clinical characteristics, causes of death, disease and treatment of patients who died while being followed for severe mental illness. METHOD: The study was carried out in ten community mental health centers from six provinces. The clinical characteristics, causes of death, course of the illness and treatment characteristics of the patients who had a death report from the date the community mental health centers were opened until the start date of the study were analyzed by retrospective file scanning method. RESULTS: In an average of 52 months, files of 3715 patients were examined. There were death declarations for 106 patients. The diagnosis of most patients with death declarations was schizophrenia (78%), most of them were male (66%), mean age was 57, mean disease duration was 24 years. The rate of multiple antipsychotic medication use was 61%. The most common comorbidities were metabolic syndrome (36%), hypertension (22%), diabetes (18%) and chronic obstructive pulmonary disease (15%). The most frequently reported causes of death were cardiovascular diseases (39%), infectious diseases (14%) and cancer (11%). CONCLUSION: Individuals with severe mental illness followed up in community mental health centers are mostly die due to preventable natural causes of death. Therefore, a sensitive approach should be taken to evaluate psychiatric and other medical conditions together. In our country, there is a need for natural follow-up studies investigating the average age of death and causes of death of individuals with severe mental illness.

Effects of chlorpyrifos on primary gill cell culture of Lake Van fish (Alburnus tarichi Güldenstaadt 1814).

Lake Van fish (Alburnus tarichi Guldenstadt 1814) is the only fish that can adapt to the extreme conditions (pH 9.8 salinity 0.2% and alkalinity 151.2 meq/L) of Lake Van. In this study, it was aimed to determine the cytotoxic and genotoxic effects of chlorpyrifos (CPF) on Lake Van fish primary gill cell culture. Gill epithelium from Lake Van fish was isolated enzymatically and grown in primary culture on Leibovitz's L-15 medium. After different doses (0.01, 0.1, 1, and 10 µM) of CPF were applied to the gill cells, the total oxidant status (TOS), total antioxidant status (TAS), malondialdehyde (MDA), and DNA damage levels (8-hydroxyguanine (8-OHdG)) were examined at the end of 24 and 48 h. It was determined that the TOS, MDA, and 8-OHdG levels increased in the cells exposed to high doses (1 and 10 µM) of CPF and the TAS was decreased (P < 0.05). It was revealed from this study that CPF administered at a dose higher than 1 µM can cause oxidative stress and DNA damage in the primary gill cell culture of Lake Van fish. In addition, the findings showed that Lake Van fish primary gill cell culture was useful in determining the effects of toxic substances likely to be the contaminants of a lake.

Histopathology and immunohistochemistry of gills of Van fish (Alburnus tarichi Güldenstädt, 1814) infected with myxosporean parasites.

The Van fish are a cyprinid species endemic to Turkey's largest soda lake, Lake Van, and have great economic value because they are a food source. Once a year, the fish take part in reproductive migration to the fresh waters flowing into the lake. The fish migrate from an extreme environment with high salinity (2.2%) and high pH (9.8). These fish are unable to reproduce in this alkaline environment and must migrate to fresh water during their breeding season. The aim of the present study is to report the presence of the myxosporean parasites on the gills and the pathological changes. Changes in gill histopathology, mucocytes, mitochondria-rich cells, expression of Heat Shock Protein 70 (Hsp70), and ATPase (NKA) were observed in the gill tissue. As a result of the histopathological changes in gills, infected fish had abundant plasmodia with different sizes. Plasmodia were found on gill filaments inside white ovoid-shaped structures. It was observed that plasmodia were contained on the primary filament which changed the histological structure of the gill tissue to a large extent. It was determined that the density and size of mucocytes in the infected areas of the gill tissue increased, whereas the number of mitochondria-rich cells decreased. Hsp70, an indicator of stress, was not different between normal and infected fish.

Effect of valproic acid on oxidative stress parameters of glutamate-induced excitotoxicity in SH-SY5Y cells.

Glutamate-induced excitotoxicity has been reported to be involved in the pathophysiology of neurodegenerative disorders. It has been proposed that valproic acid (VPA), which is used in epileptic and bipolar disorders, may be protective against excitotoxic insult. The aim of the present study was to investigate the effects of VPA against the glutamate excitotoxicity in the SH-SY5Y human neuroblastoma cell line and determine its anti-oxidant capacity by measuring oxidative and anti-oxidant biochemical parameters. SH-SY5Y human neuroblastoma cells were pre-treated with 1, 5 or 10 mM VPA prior to exposure to 15 mM glutamate. The MTT assay was performed to determine cell viability. To detect oxidative insult in glutamate toxicity and the potential anti-oxidant effect of VPA, the cell catalase (CAT), superoxide dismutase (SOD), malondialdehyde and hydrogen peroxide (H2O2) activity was determined. A progressive decline in cell viability was observed with increasing glutamate concentrations (1-50 mM). Treatment with 1 mM VPA was revealed to be effective in increasing the viability of cells exposed to glutamate for 24 h. Oxidative damage, including an increase in H2O2 and MDA, was observed in SH-SY5Y cells treated with glutamate and was reduced by pre-treatment with VPA. CAT activity was decreased following glutamate exposure, but VPA did not prevent this decrease. SOD activity was increased by treatment with VPA alone and was not affected by glutamate exposure. Overall, the present results confirmed the critical role of oxidative stress in glutamate-induced excitotoxicity. They also suggested that VPA may exert an anti-oxidant effect against glutamate-induced excitotoxicity by decreasing oxidative parameters, including H2O2 and MDA, but only had a slight effect on CAT and SOD activity, which have an anti-oxidant capacity.

Evaluation of potential drug-drug interactions in a pediatric population.

AIM: A large number of medications are prescribed in pediatric clinics and this leads to the development of drug-drug interactions (DDI) that may complicate the course of the disease. The aim of the study was to identify the prevalence of potential drug-drug interactions, to categorize main drug classes involved in severe drug-drug interactions and to highlight clinically relevant DDIs in a pediatric population. MATERIAL AND METHODS: A total of 1500 prescriptions during the 12-month study period were retrospectively reviewed; 510 prescriptions that comprised two or more drugs were included in study. The presence of potential drug-drug interactions was identified by using the Lexi-Interact database and categorized according to severity A (unknown), B (minor), C (moderate), D (major), and X (contraindicated). RESULTS: There were 1498 drugs in 510 prescriptions; 253 of these (49.6%) included 2 drugs, 228 (44.7%) included 3-4 drugs, and 29 (5.6%) included ≥5 drugs. A total of 634 (42%) potential drug-drug interactions were idenfied. Among those, 271 (42.7%) were categorized as A, 284 (44.8%) as B, 53 (8.4%) as C, and 26 (4.1%) as D. There was no potential risk for X interaction. Anti-infectives (36%) were the most commonly prescribed drug classes involved in C and/or D categories. Clarithromycin was the most commonly interacting agent that interfered with budesonide. CONCLUSION: It is noteworthy that a significant number of drugs causing potential drug-drug interactions are prescribed together in pediatric clinics. Increasing the awareness of physicians on this issue will prevent potential complications and ensure patient safety.