Potential therapeutic effect of pomegranate seed oil on ovarian ischemia/reperfusion injury in rats

Objective(s): The aim of this study is to determine the therapeutic effects of pomegranate seed oil, which is a powerful antioxidant and anti-inflammatory agent, on ovarian-ischemia and reperfusion injury in rats.Materials and Methods: Fifty-six  female albino Wistar rats were divided into 7 equal groups. Group 1; Sham Operation, Group 2; Ischemia, Group 3; Ischemia + Reperfusion, Group 4; Ischemia + Pomegranate 0,32 ml / kg (IP), Group 5; Ischemia + Pomegranate 0.64 ml / kg, Group 6; Ischemia + Pomegranate 0,32 ml / kg + reperfusion, Group 7; Ischemia + Pomegranate 0,64 ml / kg + reperfusion. Three hours after ischemia and 3 hours after reperfusion, the study was terminated. Results: While NADPH oxidase activity, MDA and TNF-α levels were significantly increased, SOD activity and GSH levels were reduced in ischemia and I/R groups. Low dose pomegranate seed oil  application reduced significantly oxidative stress and NADPH oxidase activity in both ischemic and ischemic/reperfusion groups. At the same time, low-dose pomegranate seed oil extract reduced TNF-α levels and significantly increased antioxidant activity.Conclusion: PSO demonstrated an important therapeutic effect in the treatment of ovarian ischemia and reperfusion injury

Continuous Glucose Monitoring and Hypoglycemia Unawareness in Children and Adolescents with Type 1 Diabetes

WOS: 00038416680049

EFFECTIVENESS OF CONTINUOUS SUBCUTANEOUS INSULIN INFUSION PUMP THERAPY DURING FIVE YEARS OF TREATMENT ON METABOLIC CONTROL IN CHILDREN AND ADOLESCENTS WITH TYPE 1 DIABETES MELLITUS

WOS: 00041259540538

Transcriptome profiles associated with selenium-deficiency-dependent oxidative stress identify potential diagnostic and therapeutic targets in liver cancer cells

Hepatocellular carcinoma (HCC) is one of the most common cancer types with high mortality rates and displays increased resistance to various stress conditions such as oxidative stress. Conventional therapies have low efficacies due to resistance and off-target effects in HCC. Here we aimed to analyze oxidative stress-related gene expression profiles of HCC cells and identify genes that could be crucial for novel diagnostic and therapeutic strategies. To identify important genes that cause resistance to reactive oxygen species (ROS), a model of oxidative stress upon selenium (Se) deficiency was utilized. The results of transcriptome-wide gene expression data were analyzed in which the differentially expressed genes (DEGs) were identified between HCC cell lines that are either resistant or sensitive to Se-deficiency-dependent oxidative stress. These DEGs were further investigated for their importance in oxidative stress resistance by network analysis methods, and 27 genes were defined to have key roles; 16 of which were previously shown to have impact on liver cancer patient survival. These genes might have Se-deficiency-dependent roles in hepatocarcinogenesis and could be further exploited for their potentials as novel targets for diagnostic and therapeutic approaches. Key words: Hepatocellular carcinoma, selenium, oxidative stress, transcriptome-wid

Is Plasma C-Type Natriuretic Peptide Level Available for Typing and Diagnosis of Skeletal Dysplasia Cases?

WOS: 00044520410110

Effectiveness of Continuous Subcutaneous Insulin Infusion Pump Therapy During Five Years of Treatment on Metabolic Control in Children and Adolescents with Type 1 Diabetes Mellitus

WOS: 000432911500009PubMed ID: 29537377Objective: To compare continuous subcutaneous insulin infusion (CSII) therapy with multiple daily insulin (MDI) therapy on metabolic control in children and adolescents with type I diabetes mellitus (T1DM) over the long term. Methods: Fifty-two T1DM patients treated with CSII and monitored for at least one year prior to and at least five years following CSII were included. Thirty-eight age and sex-matched MDI controls with a 5-year follow up were recruited. Results: Mean age of the subjects, duration of diabetes and CSII therapy were 17.0 +/- 4.8 years, 10.7 +/- 2.8 years and 7.7 +/- 1.5 years respectively. Mean hemoglobin A1c (HbA I c) in the year prior to CSII, during the first year of treatment and after 5 years of CSII were 7.3 +/- 1 % (56 mmol/mol), 7.0 +/- 0.7% (53 mmol/mol) and 7.8 +/- 1.3 % (62 mmol/mol) respectively. Initial and 5-year mean HbA1C levels of controls were 7.9 +/- 1.08 % and 8.6 +/- 1.8 %. Mean HbA1c values were significantly lower in those receiving CSII therapy throughout follow-up. Basal and total insulin doses were significantly lower in the CSII group at all times. HbA1c was compared between subjects by age (0-5, 6-11 and 12-18 years) with no significant difference between them. Conclusion: Although CSII mean HbA1c values exceeded accepted good metabolic control limits after 5 years, CSII produces better HbA1c control at all times and in all age groups compared to MDI

CYTOTOXICITY AND GENOTOXICITY OF IRON OXIDE NANOPARTICLES: AN IN VITRO BIOSAFETY STUDY

With the development of nanotechnology and the wide use of iron oxide nanoparticles, it has become necessary to assess the potential adverse biological effects of magnetite. This study investigated the cytotoxicity, genotoxicity and oxidative damage of different concentrations of magnetite (0 to 1000 mg/L) in human whole blood cultures. After supplementation of magnetite, the blood samples were incubated for 72 h. Cell viability was assessed by the 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) release assays. The total antioxidant capacity (TAC) and total oxidant status (TOS) were determined to evaluate the dose-dependent effects of magnetite on the oxidant/antioxidant balance and to evaluate the potential oxidative injury due to increased oxidative stress. Genotoxicity was estimated by by the sister chromatid exchange (SCE), micronuclei (MN) and chromosome aberration (CA) assays and determination of 8-oxo-2-deoxyguanosine (8-OH-dG) levels. The results of MTT and LDH assays showed that the higher concentrations of magnetite (100, 150, 300, 500 and 1000 mg/L) decreased cell viability. Concentrations of magnetite higher than 10 mg/L increased TOS levels and decreased TAC levels in human blood cells. Increasing concentrations of magnetite caused significant increases in MN, SCE and CA rates and 8-OH-dG levels. The obtained results showed that magnetite exerted dose-dependent effects on oxidative damage, genotoxicity and cytotoxicity in human blood cells