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Aim: Breast cancer is the most common malignancy in women. This disease is a critical public health problem and further research at the molecular level would define its prognosis and specific treatment. Phenformin is an antidiabetic agent. Recent studies showed that it should be considered as a potential agent for the prevention and treatment of cancer cell lines. This study aimed to investigate the antiproliferative effect of phenformin on MDA-MB-231 and MCF-7 breast cancer cell lines. Materials and Methods: MDA-MB-231 and MCF-7 breast cancer cell lines were used in the study. Experimental groups; control group, 1 μM, 2.5 μM, and 5 μM phenformin administered groups were planned. WST-1 analysis was performed to evaluate the viability of cells 24 h after the treatments. Statistical analysis was carried out using the SPSS 17.0 statistical program. p<0.05 was considered to indicate a statistically significant difference. Results: In the MDA-MB-231 breast cancer cell line, there were statistically significant differences among all groups (p<0.05, for all), except between the 1 μM phenformin-treated and control groups (p>0.05). In the MCF-7 breast cancer cell line; there were statistically significant differences between the control group and 5 μM phenformin-treated, and between 1 μM phenformin-treated and 5 μM phenformin-treated (p<0.05, for all) groups. Conclusion: Phenformin seems to exert antiproliferative effects on MDA-MB-231 and MCF-7 breast cancer cell lines. It was observed that the antiproliferative effect was stronger in the MDA-MB-231 cell line. It showed a stronger antiproliferative effect in the MDAMB-231 cell line of antiproliferative effect. [ABSTRACT FROM AUTHOR]

Ranolazine is beneficial when given as an adjunct to treatment in symptomatic angina pectoris. Therefore, it may be useful to evaluate the effect of ranolazine on cardiovascular endothelial cells in hypoxic conditions that may resemble decreased oxygen delivery during angina pectoris. In this study, chemical hypoxia caused by exposure of Human Umbilical Vein Endothelial Cells (HUVECs) to different concentrations of cobalt chloride (CoCl2) (100 µM - 1000 µM) for 24 and 48 h was evaluated. In this chemical hypoxia model, HIF-1alpha and eNOS were measured semi-quantitatively by immunocytochemistry. Activation of the intracellular MAPK and PI3K pathways was evaluated by flow cytometry. During chemical hypoxia, HIF-1alpha was increased in a CoCl2 concentration-dependent manner; however, eNOS did not change significantly. In the presence of 10 µM ranolazine, HIF-1alpha increased in cells exposed to 1000 µM CoCl2 for 24 h, whereas HIF-1alpha decreased in cells exposed to 1000 µM CoCl2 for 48 h. Endothelial cell viability decreased with a high concentration of CoCl2. Ranolazine (1 µM, 10 µM) added to the medium failed to restore cell viability as measured by WST-1. The proportional percentage of cells in which only the MAP kinase pathway was activated increased during chemical hypoxia. Although ranolazine could reduce HIF-1alpha levels in the 48hour group, it had no beneficial effect on CoCl2 toxicity. [ABSTRACT FROM AUTHOR]

The present study was planned to investigate the protective effect of 10 % and 20 % apricot-containing feed on carbon tetrachloride (CCl4)-induced hepatic steatosis and damage. Adult male Wistar rats (n 42) were divided into six groups of seven each, as follows: control group; CCl4 group; CCl4+10 % apricot group; CCl4+20 % apricot group; 10 % apricot group; 20 % apricot group. All apricot groups were fed with 10 % or 20 % apricot-containing feed for 5 months. CCl4 injections were applied to the CCl4 groups at the dose of 1 mg/kg for 3 d at the end of 5 months. In the CCl4 group, vacuolated hepatocytes and hepatic necrosis were seen, especially in the centrilobular area. Hepatocytes showed an oedematous cytoplasmic matrix, large lipid globules and degenerated organelles. The area of liver injury was found significantly decreased with apricot feeding. Malondialdehyde and total glutathione levels and catalase, superoxide dismutase and glutathione peroxidase activities were significantly changed in the CCl4 group and indicated increased oxidative stress. Apricot feeding decreased this oxidative stress and ameliorated histological damage. We concluded that apricot feeding had beneficial effects on CCl4-induced liver steatosis and damage probably due to its antioxidant nutrient (β-carotene and vitamin) contents and high radical-scavenging capacity. Dietary intake of apricot can reduce the risk of liver steatosis and damage caused by free radicals. [ABSTRACT FROM PUBLISHER]

The aims of this study were to observe the changes in antioxidative defense enzymes and renal morphology after 7,12-dimethyl-benz[ a]anthracene (7,12-DMBA) administration in mice and to investigate the possible protective effects of melatonin against 7,12-DMBA-induced renal damage in comparison with vitamin E + selenium (vit E + Se). Forty female mice were divided into four groups: control, DMBA, DMBA + vit E + Se and DMBA + melatonin. In the DMBA group, mice were given injections of 7,12-DMBA (20 mg/kg). DMBA + vit E + Se group mice received injections of 7,12-DMBA + vit E + Se (20 mg/kg + 90 mg/kg + 1.8 μg/kg). In the melatonin group, mice were given injections of 7,12-DMBA + melatonin (20 mg/kg + 4.2 mg/kg). The experiment lasted for 21 days. Mice were killed and the kidneys were taken for enzyme analyses and histologic examination. Catalase (CAT) and glutathione peroxidase (GSH-Px) activities were found significantly decreased in the DMBA group and in the DMBA + vit E + Se group when compared with the control group ( P < 0.05), whereas CAT and GSH-Px activities were found significantly elevated in the DMBA + melatonin group when compared with the control ( P < 0.05) and the DMBA group ( P < 0.01). Exposure to DMBA resulted in tubular alterations in renal cortex. Morphometric analysis revealed proximal and distal tubular damage ( P < 0.05). These alterations were found to be prevented by melatonin but not with vit E + Se administration. These results reveal that melatonin stimulates CAT and GSH-Px activities and prevents renal injury better than vit E + Se combination in mice kidneys. [ABSTRACT FROM AUTHOR]

Presents a study that determined the morphological effects of chronic nitric oxide inhibition on the thoracic aorta of Wistar rats. Cannulation of the carotid arteries; Measurement of the blood pressure; Detection of irregular luminal layers of endothelial cell linings.