Effects of selenium on endothelial dysfunction and metabolic profile in low dose streptozotocin induced diabetic rats fed a high fat diet.

Endothelial dysfunction develops as a result of oxidative stress and is responsible for diabetic vascular complications. We investigated the effects of selenium on endothelial dysfunction and oxidative stress in type 2 diabetic rats. Male Wistar rats were divided into five groups: controls, untreated diabetics, and diabetics treated with 180, 300, 500 mcg/kg selenium each day. Diabetes was induced by a single intraperitoneal injection of low dose streptozotocin to rats fed a high fat diet. Endothelium-dependent and -independent relaxations were measured in the thoracic aorta. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and endothelial nitric oxide synthase (eNOS) mRNA expressions were analyzed using real-time polymerase chain reaction (RT-PCR). Fasting blood glucose, lipid profile, lipid oxidation, insulin and nitric oxide were measured in blood samples. Malondialdehyde, superoxide dismutase, catalase and glutathione peroxidase levels were measured in liver samples. RT-PCR showed that selenium reversed increased NADPH oxidase expression and decreased eNOS expression to control levels. Selenium also improved the impairment of endothelium-dependent vasorelaxation in the diabetic aorta. Selenium treatment significantly decreased blood glucose, cholesterol and triglyceride levels, and enhanced the antioxidant status in diabetic rats. Our findings suggest that selenium restores a normal metabolic profile and ameliorates vascular responses and endothelial dysfunction in diabetes by regulating antioxidant enzyme and nitric oxide release.

Measurement of radioactivity levels and assessment of radioactivity hazards of soil samples in Karaman, Turkey.

In this study, the levels of the natural and artificial radioactivity in soil samples collected from surrounding of Karaman in Turkey were measured. Activity concentrations of the concerned radionuclides were determined by gamma-ray spectrometry using a high-purity germanium detector with a relative efficiency of 40 % at 1.332 MeV. The results obtained for the (238)U series ((226)Ra, (214)Pb and (214)Bi), (232)Th series ((228)Ac), (40)K and fission product (137)Cs are discussed. To evaluate the radiological hazard of radioactivity in samples, the radium equivalent activity (Raeq), the absorbed dose rate (D), the annual effective dose and the external (Hex) and internal hazard index (Hin) were calculated and presented in comparison with the data collected from different areas in the world and Turkey.

Radioprotective effect of montelukast sodium in rat lacrimal glands after radioiodine treatment.

PURPOSE: The aim of this study was to evaluate the morphological changes of rat lacrimal glands at the third month following radioiodine (RAI) treatment and the radioprotective effect of montelukast (ML) sodium against RAI-related lacrimal gland damage. METHODS: Fifty female Wistar Albino rats were divided into three groups. The control group (n=10) consisted of rats with no intervention. RAI group (n=20) consisted of rats treated with oral (131)I (111 MBq). The ML group (n=20) consisted of rats treated with intraperitoneal 10mg/kg/day ML sodium, starting three days before and continuing for one week after oral RAI administration. Intraorbital (IG), extraorbital (EG) and Harderian glands (HG) were removed bilaterally after three months. RESULTS: The existence of acinar atrophy, acinar fibrosis, abnormal cell lines, peripheral basophilia, cell size variation and decrease in amount of cytoplasm was significantly more common in the RAI-rat treated group than in the ML group, in each of the glands. The ML-treated group had less-frequent cell shape variation in EG (P=0.001) and HG (P=0.027), cell size variation in IG (P<0.001) and HG (P=0.01), ductal pathology in EG (P<0.001) and HG (P<0.001) and lipofuscin accumulation in EG (P=0.001) and in HG (P=0.01) than the RAI-treated group. CONCLUSIONS: RAI treatment seems to cause morphological damage to rat lacrimal glands, and ML sodium effectively protects against damage to lacrimal glands.