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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.

The treatment of diabetes and its complications is a key challenge for healthcare professionals. Accelerated atherosclerosis is associated with progressive diabetes, and it has been indicated that macrophages serve a crucial function in this process. Currently, the first-line treatment of diabetes is based on metformin, which is an inducer of AMP-activated protein kinase (AMPK) and belongs to the biguanide class of pharmaceuticals. It has been previously demonstrated that metformin exhibits more than just hypoglycemic effects. Therefore, the aim of the present study was to investigate the in vitro impact of metformin on cell viability and the expression levels of nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase (p22phox), a major enzyme in reactive oxygen species generation, and the three antioxidative enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) in monocytes/macrophages derived from 10 healthy volunteers. The effects of metformin were observed in the presence or absence of lipopolysaccharide (LPS), which was administered to induce oxidative stress. Furthermore, certain cells were treated with compound C, an inhibitor of AMPK, in order to determine the mechanistic role played by AMPK in the oxidative changes in the macrophages. Cell viability was evaluated using trypan blue and MTT assays. The mRNA and protein expression levels of p22phox and the various antioxidative enzymes were determined using polymerase chain reaction and western blot analysis, respectively. The results indicated that metformin, predominantly in LPS-pretreated monocytes/macrophages, reduced the expression levels of p22phox and increased those of SOD and GPx, but had only a minor effect on CAT levels. Therefore, metformin appears to alter the oxidative status of macrophages toward increasingly antioxidative activity, which may account for the pleiotropic effects observed during metformin treatment. [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]