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Obesity is associated with an increased risk of certain types of cancer, including colon cancer. Adipose tissue is an endocrine organ that produces biologically active substances, such as leptin and ghrelin. Recent research has suggested that adipose-derived hormones may be associated with mechanisms linked to tumorigenesis and cancer progression. Furthermore, previous studies have demonstrated that pineal gland-derived melatonin possesses important oncostatic and antioxidant properties. The present study aimed to determine the effects of the adipokines ghrelin and leptin, and the melatonin on intracellular levels of reactive oxygen species (ROS) and the activity of selected antioxidant enzymes, such as superoxide dismutase, catalase (CAT) and glutathione peroxidase. The effects of these compounds were also determined on the viability of HCT 116 human colorectal carcinoma cells in vitro. The pro-oxidant and growth inhibitory effects of melatonin resulted in an accumulation of ROS and decreased antioxidant capacity in melatonin-treated cells. Ghrelin administration alone caused a significant decrease in the levels of ROS, due to an increased activity of CAT in the HCT 116 cells. In addition, the present study observed increased lipid peroxidation following melatonin treatment, and decreased levels of malondialdehyde following ghrelin or leptin treatment. In conclusion, ghrelin, leptin and melatonin have various influences on the antioxidant capacity of HCT 116 cells. Compared with the adipokines, treatment with melatonin increased ROS levels and decreased cellular viability.

Antioxidant enzymes (AOEs), including superoxide dismutase isoenzymes (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) along with glutathione reductase (GR), reduced glutathione (GSH) and glutathione transferase (GST), are thought to be necessary for life process in all oxygen-metabolizing cells by removing reactive oxygen species (ROS). The biological significance of AOEs in transformed cells is still unclear, but their capacity to survive may be affected by changes in cellular process such as proliferation, invasiveness, migration, apoptosis and drug resistance. This review summaries the significance of antioxidant enzymes in cancer cell progression mainly in an in vitro context.

Introduction. GLP-1 receptor agonists (e.g., exenatide) are novel drugs used in the treatment of diabetes. These drugs, working with other mechanisms of action, improve glycemic control by increasing secretion of insulin and improving survival of pancreatic islet beta cells. Alterations in the oxidative stress level or the expression of proteins associated with cholesterol uptake might be responsible for those findings. Currently, there are few in vitro studies on the impact of exenatide antioxidant capacity in human islet beta cell lines and none that assess the influence of exenatide on LDL receptors and PCSK9 under hyperglycemia and oxidative stress. Therefore, we evaluated the impact of exenatide on antioxidant capacity, insulin secretion, and proteins involved in cholesterol metabolism. Materials and Method. An in vitro culture of insulin-secreting cells 1.1E7 was subjected to hyperglycemia and oxidative stress. Assessment was made of the expression of enzymes associated with oxidative stress (NADPH oxidase, catalase, glutathione peroxidase, superoxide dismutase, iNOS) and cholesterol uptake (LDL receptors, PCSK9). Additionally, insulin and nitrite levels in culture media were quantified. Results. We showed that exenatide improves expression of catalase and reduces the amount of nitrite in cell cultures in a protein kinase A-dependent manner. Those results were accompanied by a drop in the expression of LDL receptors and PCSK9. Insulin secretion was modestly increased in the culture condition. Conclusions. Our findings show potential protective mechanisms exerted by exenatide in human insulin-secreting pancreatic beta cell line (1.1E7), which may be exerted through increased antioxidant capacity and reduced accumulation of cholesterol. [ABSTRACT FROM AUTHOR]

This study examines the effects of vitamin E and an extremey low frequency electromagnetic field (ELF-EMF) and their combination in different time intervals of exposure of vitamin E (tocopherol) on the AT478 murine squamous cell carcinoma line. This study provides insight into the influence of correlations between ELF-EMF and vitamin E supplementation on antioxidant enzyme activity in malignant cells in vitro. Following vitamin E treatment, activity of the antioxidant enzymes is increased in an exposure-dependent manner compared with the untreated group. Application of ELF-EMF alone or with vitamin E increases both superoxide dismutase isoenzymes and glutathione peroxidase activities in comparison to the control group. The results suggest that ELF-EMF alters antioxidative activities of vitamin E in AT478 tumor cells. This study confirms the role of vitamin E in decreasing susceptibility to lipid peroxidation in AT478 tumor cells. [ABSTRACT FROM AUTHOR]