Oxidative stress responses of virtual reality use in refugee children undergoing elective surgery: A randomized controlled trial.

BACKGROUND: With the Virtual Reality (VR) technique, 3D movies can be made for refugee children for pre-operative stress. The study aims to reveal the oxidative responses of the VR technique in pre-operative anxiety in elective surgery in children aged 5-12 years. METHODS: The Study was designed according to the CONSORT checklist with a randomized controlled parallel design. The whole sample (n = 23), VR experimental group (n = 12), and control group (n = 11) were determined according to the total count method prospectively in 6 months. Oxidative stress parameters (Cortisol, Malondialdehyde, Nitric oxide, Glutathione) were measured in blood samples from the first hospitalization (beginning) and before the intervention (pre-operative) in the experimental and control groups. FINDINGS: MDA, NO, and cortisol levels (p < 0.05), which indicate the stress level, are high in all groups. In pre-operative measurements, oxidative parameters were lower in the VR experimental group than in the control group. At the same time, the anti-stress antioxidant factor Glutathione was higher in the VR experimental group in pre-operative measurements. DISCUSSION: The application of 3D film as a VR technique reduces stress parameters in pre-operative stress, and its antioxidant system activating effect has been determined. APPLICATION TO PRACTICE: It can be applied to refugee child groups for pre-operative stress by shooting 3D movies in different languages.

Antioxidant Effects of Oleuropein on Hydrogen Peroxide-Induced Neuronal Stress- An In Vitro Study.

BACKGROUND: Persistent oxidative stress can lead to chronic inflammation and mediate most chronic diseases including neurological disorders. Oleuropein has been shown to be a potent antioxidant molecule in olive oil leaf having antioxidative properties. OBJECTIVE: The aim of this study was to investigate the protective effects of oleuropein against oxidative stress in human glioblastoma cells. METHODS: Human glioblastoma cells (U87) were pretreated with oleuropein (OP) essential oil 10 µM. After 30 minutes, 100 µM H2O2 was added to the cells for three hours. Cell survival was quantified by colorimetric MTT assay. Glutathione level, total oxidant capacity, total antioxidant capacity and nitric oxide levels were determined by using specific spectrophotometric methods. The relative gene expression level of iNOS was performed by qRT-PCR method. RESULTS: According to viability results, the effective concentration of H2O2 (100µM) significantly decreased cell viability and oleuropein pretreatment significantly prevented the cell losses. Oleuropein regenerated total antioxidant capacity and glutathione levels decreased by H2O2 exposure. In addition, nitric oxide and total oxidant capacity levels were also decreased after administration of oleuropein in treated cells. CONCLUSION: Oleuropein was found to have potent antioxidative properties in human glioblastoma cells. However, further studies and validations are needed in order to understand the exact neuroprotective mechanism of oleuropein.

Silencing of PrP C (prion protein) expression does not affect Brucella melitensis infection in human derived microglia cells.

Cellular prion proteins (PrP(C)) are mainly expressed in the central nervous system where they have antioxidant effects and a role in the endocytosis of bacteria within cells. These proteins also have some crucial biological functions including roles in neurotransmission, signal transduction and programmed cell death. However, the role of prion proteins in neuronal Brucella infection, specifically in the interaction of the pathogen and the host cell is controversial. In the present study, the silencing of PrP(C) mRNA by small interfering RNA (siRNA) transfection was investigated in human microglia cells infected with Brucella melitensis. More than 70% of prion proteins were down-regulated in microglia by siRNA transfection and this caused a slight decrease in the cellular viability of the control cells. Silencing of PrP(C) suppressed the antioxidant systems, though it led to an up-regulation of pro-inflammatory cytokines such as IL-12 and TNF-α as demonstrated by qRT-PCR analysis. B. melitensis infection of prion protein-silenced cells led to increase host viability, but had no effect on bacterial phagocytosis. According to the present study, there is no significant effect of prion proteins on phagocytosis and intracellular killing of B. melitensis in microglia cells.

Cisplatin reduces Brucella melitensis-infected cell number by inducing apoptosis, oxidant and pro-inflammatory cytokine production.

Brucella species are able to survive and replicate within the phagocytic cells and cause chronic infections in domestic animals and humans. Modulation of programmed cell death by Brucella spp. may be one of the reasons of the chronicity of the infection. In this study, whether cisplatin treatment, an apoptotic anticancer agent, would enhance the host resistance against Brucella melitensis-infected human macrophage-like cells was investigated. The infection neither induced inflammation nor oxidative stress. But, Brucella caused a decrease in infected macrophage viability of 36% at 48 h postinfection (p.i.) as compared with uninfected cells. Treatment of infected macrophages with 20 microM cisplatin for 48 h caused a large increase in nitric oxide (NO) levels in a time-dependent manner via induction of iNOS transcription. Cisplatin also enhanced glutathione peroxidase, myeloperoxidase and xanthine oxidase activities, providing evidence of generation of reactive free radicals. N-acetylcysteine was able to decrease cisplatin-induced NO, and prevented the agent-induced apoptosis, similar to effects found in l-NAME (N(G)-nitro-l-arginine methyl ester) treatment. Cisplatin stimulated inflammation through the induction of TNF-alpha and IL-12 secretion, and down-regulated Brucella-stimulated IL-10 transcription. The number of infected cells and their viability were decreased by 80% at 48 h p.i. by cisplatin in comparison with infected cells. Similar to this result, cisplatin treatment resulted in reduced intracellular CFU of B. melitensis being reduced by 80% at 48 h p.i. These findings demonstrate that pharmacological agents such as cisplatin may be considered to influence immune responses and apoptosis to help decrease Brucella-infected cell number.

Effect of zinc on the lipid peroxidation and the antioxidant defense systems of the alloxan-induced diabetic rabbits.

The effects of oral zinc supplementation on lipid peroxidation and the antioxidant defense system of alloxan (80-90 mg/kg)-induced diabetic rabbits were examined. Forty-five New Zealand male rabbits, 1 year old, weighing approximately 2.5 kg, were allocated randomly and equally as control, diabetic, and zinc-supplemented diabetic groups. After diabetes was induced, zinc-supplemented diabetic rabbits had 150 mg/L of zinc as zinc sulfate (ZnSO(4)) in their drinking tap water for 3 months. The feed and water consumption was higher in diabetic groups than (P<0.01) healthy rabbits. The body weight was lower in diabetic rabbits compared to control. The blood glucose levels were higher in diabetic groups than controls. The elevated plasma malondialdehyde (MDA) levels were determined in the diabetic group (P<0.01). The glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), and ceruloplasmin levels in the diabetic group were decreased by the effect of diabetes but there was no difference between zinc-supplemented diabetic and control rabbits. Serum zinc concentrations were lower in diabetic rabbits but iron (Fe) and copper (Cu) levels in sera were not different among the groups. As a result, it was concluded that daily zinc supplementation could reduce the harmful effects of oxidative stress in diabetics.