The level of endogenous DNA damage in lymphocytes isolated from blood is associated with the fluctuation of 17β-estradiol concentration in the follicular phase of healthy young women
نویسندگان
چکیده
al., 1999), caused by environmental toxins or drug administration (Abd-Allah et al., 1999; Puhakka et al., 2002) and some nutritional deficiencies (Giovannelli et al., 2002; Szete et al., 2002; White et al., 2002; Kapiszewska et al., 2005a). It was shown that the comet assay used to study single/double strand breaks and oxidative modifications in the DNA bases was sensitive enough to detect also alterations in the antioxidant status in the body induced by nutritional supplements or vitamins (Betancourt et al., 1995; Anderson et al., 1997; Anderson, 2001; Beani, 2001). The endogenous DNA damage analyzed in lymphocytes is very o en used as a biomarker of the oxidative stress in the human body (Porrini et al., 2002; Szeto et al., 2002; Wolf et al., 2002; Mayne, 2003). Constant exposure of lymphocytes to substances transported by circulation make them very useful and reliable as a diagnostic tool. Taking all of the above into account, it is reasonable to expect that if circulating estrogens and their metabolites enhance free radical production, then their detrimental effect can be manifested in DNA modification also in lymphocytes. We showed recently that Communication
منابع مشابه
The level of endogenous DNA damage in lymphocytes isolated from blood is associated with the fluctuation of 17beta-estradiol concentration in the follicular phase of healthy young women.
The aim of this study was to evaluate whether the differences in plasma 17beta-estradiol concentration in early and late follicular phases of the menstrual cycle can affect the level of endogenous DNA damage in lymphocytes assessed by comet assay, and whether the extent of this damage in the follicular phase is associated with the genotype of catechol-O-methyltransferase (COMT). The level of DN...
متن کاملRelationships between Body Mass Index, Serum Leptin Levels, and 17β-Estradiol in Postmenopausal Women with Breast Cancer: A Case-Control Study
Introduction: There is a close relationship between the incidence of breast cancer and fat intake in different populations. Overweight and obesity during menopause can increase the risk of breast cancer in women. Hormones like estrogen and leptin are factors that affect the growth and proliferation of breast cells. The main purpose of this study was to evaluate the relationships between body ma...
متن کاملSerum Liver proteins and 17β-estradiol in Postmenopausal Women with Breast Cancer
Background: Breast cancer is a hormone-dependent malignancy that is associated with estrogen and progesterone interactions. The liver is the most important organ to be affected by the metastasis of breast cancer, which causes functional impairment. We compared levels of obesity, 17β-estradiol, and secreted proteins in postmenopausal women with breast cancer but without hepatic symptoms to those...
متن کاملThe effect of 17β-estradiol on gene expression of calcitonin gene-related peptide and some pro-inflammatory mediators in peripheral blood mononuclear cells from patients with pure menstrual migraine
Objective(s):The neuropeptide calcitonin gene-related peptide (CGRP) has long been postulated to play an integral role in the pathophysiology of migraine. Earlier studies showed that CGRP can stimulate the synthesis and release of nitric oxide (NO) and cytokines from trigeminal ganglion glial cells. The purpose of this study was to determine the effect of 17β-estradiol in regulation of CGRP exp...
متن کاملCombined Effects of 528 Hz Sound and X-ray in Peripheral Blood Lymphocytes
Introduction: Radiotherapy is still one of the main options for cancer treatment but it is in association with damage to normal cells as well as the tumor cells. To reduce the injury in normal cells we have evaluated the effect of 528 hertz sound after X irradiation in peripheral blood lymphocytes. Materials and Methods: in this study, peripheral blood was o...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2005