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The objective of this study was to analyse the response of hepatocytes on various concentrations of 17ß-oestradiol (17ß-E) under iron-induced oxidative stress in vitro. Isolated by in situ collagenase perfusion hepatocytes were cultured in DMEM/HAMS-12 (v/v) medium without any additional agents (control), with Fe³⁺ alone, and with Fe³⁺ aild 0.2%, 0.02%, and 0.002% solution of 17ß-E (17ß-EI, 17ß-EII, and 17ß-EIII, respectively). After 24, 48, and 72 h, medium malonylodialdehyde (MDA), haptoglobin (Hpt) concentration and proliferative activity were determined. In comparison to control samples, and samples collected at 24 and 72 h, hepatocytes exposition to Fe³⁺, caused a significant increase in MDA (0.056 ±0.011 nM/mL) only after 48 h of incubation. Each of 17ß-E concentrations resulted in a decrease in MDA in samples obtained after 24 and 48 h. In comparison to the first 24 h, Fe³⁺ alone and together with 17ß-EI, 17ß-EII, and 17ß-EIII caused a significant augmentation of Hpt level in 48 h and 72 h of the experiment. Each of the 17ß-E concentrations added to the culture medium resulted in inhibition of hepatic proliferative activity, especially in the 72 h of cell culture.
The presence and location of specific binding sites for progesterone and 17β-estradiol in cells of wheat were estimated using radioligand binding assay. Membrane and cytosolic fractions of non-vernalized and vernalized plants were tested using tritium-labelled ligands. Specific binding of [3H]progesterone and [3H]17β-estradiol occurs in wheat cells. The binding sites are located in membranes and in the cytosol. Specific binding of [3H]17β-estradiol is higher in the membranes than in the cytosol. Specific binding of both ligands in the cytosolic fraction is higher in vernalized plants than in non-vernalized ones. The possibility of the occurrence of steroid binding proteins specific for progesterone and 17β-estradiol, putative steroid receptors for these steroids in Triticum aestivum L., is discussed.
In the present study, we evaluated the transduction pathways involved in the cardiac effects elicited by 17ß-estradiol (E2) on the isolated, Langendorff perfused male Wistar rat heart. E2 and selective agonists for ER and ERß induced a dose-dependent reduction of contractility which was blocked by the ER inhibitor ICI 182,780. Moreover, the potential involvement of the novel membrane estrogen receptor GPR30 in mediating estrogen activity was determined using the selective GPR30 ligand G-1. Notably, specific inhibitors of ERK, PI3K, PKA, and eNOS transduction pathways abolished the cardiac responses to E2. Taken together, our data suggest that ER and ERß along with several signaling cascades are involved in the action of E2 on the male rat heart. Our results also point to a potential role of GPR30, however further evaluation is required in order to fully understand the contribution of the different estrogen receptors in mediating estrogen activity on cardiac performance.
The extent of oxidative DNA damage in lymphocytes can be used as a biomarker of the level of oxidative stress in the body. The comet assay has been widely used to measure such damage. The aim of our study was to evaluate: i) the extent of the oxidative DNA damage in lymphocytes isolated from blood of female donors taken in early and late follicular phases [low (LE) and high (HE) concentration of 17bestradiol, respectively], ii) the susceptibility of these lymphocytes to hydrogen peroxide exposure, and iii) the protective ability of five plant extracts against the hydrogen peroxide-induced DNA damage. The effect of the catechol-Omethytransferase genotype (wild COMT H/H and mutated homozygote COMT L/L) of female donors was also analyzed. The amount of endogenous DNA damage was higher in HE lymphocytes as compared with LE ones, independently of the genotype. When lymphocytes were stratified by COMT genotype, the level of DNA damage was higher in L/L donors. The protective effect of pretreatment with plant extracts (1 and 10 µg/ml for 1 h) against the H2O2 (25 µM, 5 min. at 4°C)-induced oxidative DNA damage was observed only in H/H HE lymphocytes. In contrary, the plant extract pre-incubation enhanced the DNA damage in L/L HE lymphocytes. The plant extracts alone did not induce the DNA damage. The results showed that concentration of the circulating 17b-estradiol influenced the extent of endogenous oxidative DNA damage while the beneficial or hazardous effects of the plant extracts might depend on the COMT genotype and the estrogen level.
The experiment was carried out on nine sexually mature, aged 1-3 years, clinically healthy bitches being in anoestrus. The animals were divided into two experimental groups and one control group. The bitches from the experimental groups were receiving zearalenone per os at the doses of 25 µg/kg b.w. and 50 µg/kg b.w., respectively for 100 d. The concentrations of zearalenone, progesterone, and 17β- oestradiol were analysed in weekly intervals. Zearalenone was noted as early as minute 30 and then during the whole experiment. High concentration of zearalenone (9.34 - 124.33 ng/mL.) was observed in weeks 6-9. The intoxication was accompanied by hormonal disturbances due to progesterone concentration (to 25-30 ng/mL) depending on zearalenone dose and by the increasing in 17β-oestradiol concentration (to 33 pg/ml). Hormonal disturbances of this kind are similar to those noted in different pathological conditions in the genital tract in bitches.
Retinoic acid and transforming growth factor-ß (TGF-ß) affect differentiation, pro­liferation and carcinogenesis of epithelial cells. The effect of both compounds on the proliferation of cells of the hormone sensitive human breast cancer cell line (ER+) MCF-7 was assessed in the presence of estradiol and tamoxifen. The assay was based on [ 3H] thymidine incorporation and the proliferative activity of PCNA- and Ki 67-positive cells. The apoptotic index and expression of the Bcl-2 and p53 antigens in MCF-7 cells were also determined. Exogenous TGF-ß1 added to the cell culture showed antiproliferative activity within the concentration range of 0.003-30 ng/ml. Irrespective of TGF-ß 1 concentrations, a marked reduction in the stimulatory action of estradiol (10-9 and 10-8 M) was observed whereas in combination with tamoxifen (10 -7 and 10 -6 M) only 30 ng/ml TGF-ß 1 caused a statistically significant reduction to aproximately 30% of the proliferative cells. In further experiments we examined the effect of exposure of breast cancer cells to retinoids in combination with TGF-ß 1. The incorporation of [3H]thymidine into MCF-7 cells was inhibited to 52 ± 19% (con­trol = 100%) by 3 ng/ml TGF-ß1, and this dose was used throughout. It was found that addition of TGF-ß1 and isotretinoin to the culture did not decrease proliferation, while TGF-ß1 and tretinoin at low concentrations (3 x 10 -8 and 3 x 10-7 M) reduced the percentage of proliferating cells by aproximately 30% (67±8% and 67±5%, P < 0.05 compared to values in the tretinoin group). Both retinoids also led to a sta­tistically significant decrease in the stimulatory effect of 10-9 M estradiol, attenu­ated by TGF-ß1. In addition, the retinoids in combination with TGF-ß1 and tamoxifen (10–6 M) caused a further reduction in the percentage of proliferating cells. Immunocytochemical analysis showed that all the examined compounds gave a statistically significant reduction in the percentage of cells with a positive reaction to PCNA and Ki 67 antigen. TGF-ß1, isotretinoin and tretinoin added to the culture resulted in the lowest percentage of PCNA positive cells. However, the lowest fraction of Ki 67 positive cells was observed after addition of isotretinoin. The obtained results also confirm the fact that the well-known regulatory proteins Bcl-2 and p53 play an important role in the regulation of apoptosis in the MCF-7 cell line, with lowered Bcl-2 expression accompanying easier apoptotic induction. The majority of the examined compounds act via the p53 pathway although some bypass this important proapoptotic factor.
Objectives: Molecular mechanism of carcinogenesis associated with high risk (HR) type HPV is related to the activity of virus oncoproteins E5, E6 and E7. Their task is to bring the cells to a state enabling synthesis of viral DNA, copying viral particles and promotion of uncontrolled cell growth. Proliferative factors of a feminine genital tract epithelium are also sex hormones — estradiol and progesterone. Steroids influence the transcription of genes involved in cell cycle, acting through specific nuclear receptors (ER and PR). The aim of this study was evaluation of the effect of selected concentrations of 17ß-estradiol and progesterone on survival and proliferation of HeLa line cells. Material and methods: The study was done on a transformed HeLa cell line containing integrated genome HPV of type 18. The lines were incubated in the presence of 17ß-estradiol at the concentrations of lx10-4M, lx10-5M, lx10-7M, lx10-8M. Cell survival was determined with the use of 0.5% of water solution of toluidine blue and the cell proliferation rate were evaluated with the use of BrdU Labelling and Detection Kit and the method ELISA (Roche). Results: The obtained results point to 10% toxic influence on HeLa line cells of 17ß-estradiol at high concentrations after 72 h of incubation. The influence of the hormone on proliferation rate was diversified depending on the hormone concentration and time.
The aims of the study were to compare the in vitro effects of daidzein or 17ß-estradiol (E2) on: 1) progesterone (P4) secretion by luteinized granulosa cells harvested from large porcine follicles, as well as 2) estrogen receptor and ß (ER and ERß) mRNA and protein expression in the cells. In addition, the effect of daidzein on E2 secretion and viability of the granulosa cells was examined. We found that basal and gonadotropin-stimulated P4 secretion were inhibited in granulosa cells cultured in the presence of daidzein either for 24 or 48 hours. In contrast to daidzein, E2 reduced P4 secretion only during 24-hour cell cultures increasing it during longer cultures. Daidzein did not affect E2 secretion by granulosa cells. The expression of ER and ERß mRNA, as well as ERß protein, was up-regulated by daidzein but unaffected by E2. To conclude, the soy estrogen daidzein acts directly on the porcine ovary to decrease progesterone production and to increase expression of ERß mRNA and protein. Daidzein actions in porcine luteinized granulosa cells differ from those of estradiol and it may suggest disadvantageous effects of the phytoestrogen on reproductive processes in females.
The relationship between HPV (Human Papillomavirus) and cervical carcinoma is very strong, causal, constant, specific and universal. HPV infection precedes the occurrence of preinvasive carcinoma and the evidence for biological probability of such relationship does not leave any doubt. Out of high-risk HPV types, the most often occurring in cervical infections types 16 and 18 were placed in the first group of human carcinogens. However, HPV infection is not the only factor of malignant neoplasm development. Neuroplastic transformation of cervical epithelium requires the presence of cofactors. In recent years, higher role is ascribed to the influences of steroid hormones, including estradiol and progesterone. In normal and neoplastic cells of uterine cervix, the occurrence of receptors for steroid hormones was described. In the regulatory region of oncogenic HPV hormone response elements were found. Receptors combined with steroid hormones functioning as transcription factors may influence the expression of viral oncogens E6 and E7 through stimulation of proliferation and transformation. The aim of this study was to analyse the influence of 17ß-estradiol on the amount of proteins E6 and E7 HPV 18 and to evaluate the transcript E6/E7 after incubation of HeLa line cells with 17ß-estradiol. The results revealed stimulating influence of the hormone on the expression of proteins and mRNA at concentrations of lx10-7M. At high concentrations of 1x10- 4M, estradiol was inhibiting transcription and expression of oncoproteins.
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