CONTEXT: Increased oxidative stress is a significant part of pathogenesis of smoking-related cancer. AIM: The study aims to investigate changes in antioxidant status induced by chronic cigarette smoking in cancer patients and healthy subjects. SETTING AND DESIGN: We examined the venous blood samples of 54 healthy subjects, both smokers (25) and non-smokers and of 50 patients with smoking-related cancer, both smokers (34) and non-smokers. MATERIALS AND METHODS: We measured the activities of five antioxidant (AO) enzymes: glutathione peroxidase, glutathione transferase (GST), glutathione reductase, superoxide dismutase and catalase in the blood of 50 cancer patients and 54 healthy persons. Damage to cellular structures (level of malonic dialdehyde, micro viscosity of erythrocyte membranes, number of leukocyte DNA breaks) was determined. Statistical analysis of results obtained was performed using conventional and multi-factorial statistical methods. RESULTS: Statistically significant increase in GST activity and DNA breaks, but decrease of membranes micro viscosity in cancer patients, compared with healthy subjects were obtained. In the cancer patients, no influence of smoking on studied parameters was found. Correlations of parameters within cancer patients and healthy subjects group did not coincide with each other. CONCLUSIONS: Changes of AO status parameters and oxidative damages in cell structures are related to tumor processes indicating the augmentation of oxidative stress in human blood. This study demonstrated potential applicability of a statistical model based on the evaluated biomarkers of oxidative stress to determine a smoking-induced harm of cancer incidence in healthy subjects.

The effects of melafen (plant growth stimulant) on membrane structure and functions of animal cells were studied. The process of signal transduction from cell surface to intracellular structures and conformation changes in membranes in the presence of this substance were studied by light scatter and differential scanning microcalorimetry. Melafen in a wide range of concentrations (10(-13)-10(-3) M) inhibited Ca(2+) signal system involved in the function of Ca(2+)-dependent K(+) and Cl(-) channels in Ehrlich ascitic carcinoma cells. Being a hydrophilic substance, melafen had little effect on the lipid phase of artificial membranes, but impaired the function state of transformed cell. The importance of studies of transformed cells causes no doubt because of increasing incidence of diseases associated with uncontrolled cell division.