Cancer of the reproductive tract is an important source of morbidity and mortality among women worldwide. Factors affecting endometrial cancer and endometrial hyperplasia are known to be similar. Endometrial hyperplasia is abnormal proliferation of the glands and the stroma resulting in architectural and cytological modifications. Due to hormonal changes, this condition is most common among women who are nearing the menopause or have reached the menopause. Antioxidant system has a role in preventing cancer initiation and promotion. Since the carcinogenesis occurs in several stages, it is likely that the antioxidant defense depends on the type of cell and tissue. The objective of this study was to investigate whether antioxidant enzymes activities and lipid hydroperoxides concentration in patients with endometrial hyperplasia are influenced by the changes in sex hormones level (estradiol, progesterone, FSH, and LH) during the menstrual cycle and in postmenopause. The material we used consisted of blood and endometrial tissue specimens of women diagnosed with endometrial hyperplasia simplex. Patients were divided in groups depending on the phase of the menstrual cycle: follicular phase, luteal phase and postmenopause. The activities of antioxidant enzymes and the lipid hydroperoxides level were compared among the phases to test the differences and a linear regression model was used to evaluate the associations between hormone levels and antioxidant/oxidant variables. In the blood of examined patients, we observed a phase-related changes of LOOH concentrations. Significant negative correlation between FSH concentration and GR activity (r= -0.42, p<0.05) and significant positive correlation between LH and LOOH concentrations (r= 0.038, p<0.05) was found. In hyperplasia simplex tissue we recorded significant phase-related changes of LOOH level as well as of AO enzyme activities. SOD and CAT had similar activity pattern, which was higher in luteal phase and in postmenopause, compared to follicular phase (p<0.05). GPx and GR activities did not show any statistical difference. Also, negative correlation between progesterone and GR activity (r=-0.036, p<0.05) was observed. Hormonal influence on AO system is of importance in gynecological diseases etiology since they may promote cell proliferation but are also used in conservative therapy, especially for hyperplasia simplex. However, the role of ROS production as a risk factor for endometrial hyperplasia still needs to be clarified as well as the role of AO status in response to gonadotropins and sex steroids.
Part of the book: Basic Principles and Clinical Significance of Oxidative Stress
We examined the effects of daily exercise on the gene expression of catecholamine biosynthetic enzymes (tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DBH), and phenyl ethanolamine N-methyltransferase (PNMT)), vesicular monoamine transporter 2 (VMAT 2), antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)), concentrations of catecholamines (noradrenaline (NA) and adrenaline (A)) and malondialdehyde (MDA), activities of monoamine oxidase (MAO), and antioxidant enzymes in the spleen of chronically psychosocially stressed rats. Exposure of chronically stressed rats to exercise increased the levels of PNMT protein by 19%, VMAT 2 mRNA by 100%, NA by 160%, and A by 140%; decreased/unchanged MAO enzyme activity; returned concentrations of MDA to control level; and increased CAT and GPx mRNA levels (50% and 150%, respectively). Exercise induced the accumulation of the catecholamines and a decrease of stress-induced oxidative stress in the spleen, which may significantly affect the immune-neuroendocrine interactions in stress conditions. Also, exercise induced the catecholaminergic system and antioxidant defense to become more ready to a novel stressor, which indicates that exercise may induce potentially positive physiological adaptations. Our combined model of chronic social isolation and long-term daily treadmill running in rats may be a good animal model in the research of therapeutic role of exercise in human disease caused by chronic stress.
Part of the book: Experimental Animal Models of Human Diseases