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      Examination of the effect of ovarian radiation injury induced by hysterosalpingography on ovarian proliferating cell nuclear antigen and the radioprotective effect of amifostine: an experimental study

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          The aim of this study was to examine the effect of amifostine on cellular injury in the ovarian tissue induced by hysterosalpingography (HSG).


          In total, forty 4-month old female Wistar Albino rats were assigned into 8 groups. Each group contained 5 rats. Group 1 (G1): rats were decapitated without any procedure. Group 2 (G2): rats were decapitated after 3 hours of total body irradiation. Group 3 (G3): rats were decapitated 3 hours after HSG procedure. Group 4 (G4): rats were decapitated 3 hours after HSG procedure performed 30 min after receiving amifostine 200 mg/kg intraperitoneally. Group 5 (G5): rats were decapitated after 1 month without any procedure. Group 6 (G6): rats were decapitated after 1 month of total body irradiation. Group 7 (G7): rats were decapitated 1 month after HSG procedure. Group 8 (G8): rats were decapitated 1 month after HSG procedure performed 30 min after receiving amifostine 200 mg/kg intraperitoneally. After rats were decapitated under general anesthesia in all groups, blood samples were obtained and bilateral ovaries were removed. One of the ovaries was placed in 10% formaldehyde solution for histological germinal epithelial degeneration, apoptosis and proliferating cell nuclear antigen scoring. The other ovary and blood sera were stored at −80°C. TNF-α, total antioxidant status, total oxidant status, and malondialdehyde levels were studied in tissue samples and anti-mullerian hormone levels in blood samples.


          At the end of the first month, there was significant ovarian germinal epithelium degeneration. Proliferating cell nuclear antigen immunoreactivity was significantly reduced in all other groups when compared with G1 and G5.


          In conclusion, amifostine could significantly reduce the ovarian cellular injury induced by HSG.

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          Most cited references 40

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          p63 protects the female germ line during meiotic arrest.

          Meiosis in the female germ line of mammals is distinguished by a prolonged arrest in prophase of meiosis I between homologous chromosome recombination and ovulation. How DNA damage is detected in these arrested oocytes is poorly understood, but it is variably thought to involve p53, a central tumour suppressor in mammals. While the function of p53 in monitoring the genome of somatic cells is clear, a consensus for the importance of p53 for germ line integrity has yet to emerge. Here we show that the p53 homologue p63 (refs 5, 6), and specifically the TAp63 isoform, is constitutively expressed in female germ cells during meiotic arrest and is essential in a process of DNA damage-induced oocyte death not involving p53. We also show that DNA damage induces both the phosphorylation of p63 and its binding to p53 cognate DNA sites and that these events are linked to oocyte death. Our data support a model whereby p63 is the primordial member of the p53 family and acts in a conserved process of monitoring the integrity of the female germ line, whereas the functions of p53 are restricted to vertebrate somatic cells for tumour suppression. These findings have implications for understanding female germ line fidelity, the regulation of fertility and the evolution of tumour suppressor mechanisms.
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            A perpetual cascade of cytokines postirradiation leads to pulmonary fibrosis.

            Radiation-induced pulmonary reactions have classically been viewed as distinct phases--acute pneumonitis and, later, fibrosis--occurring at different times after irradiation and attributed to different target cell populations. We prefer to view these events as a continuum, with no clear distinction between the temporal sequence of the different pulmonary reactions; the progression is the result of an early activation of an inflammatory reaction, leading to the expression and maintenance of a cytokine cascade. In the current study, we have examined the temporal and spatial expression of cytokine and extracellular matrix messenger ribonucleic acid (mRNA) abundance in fibrosis-sensitive mice after thoracic irradiation. Radiation fibrosis-prone (C57BL/6) mice received thoracic irradiation of 5 and 12.5 Gy. At Day 1, and 1, 2, 8, 16, and 24 weeks after treatment, animals were killed and lung tissue processed for light microscopy and isolation of RNA. Expression of cytokine and extracellular matrix mRNA abundance was evaluated by slot-blot analysis and cellular localization by in situ hybridization and immunochemistry. One of the cytokines responsible for the inflammatory phase (IL-1 alpha) is elevated at 2 weeks, returns to normal baseline values, then increases at 8 weeks, remaining elevated until 26 weeks when lung fibrosis appears. Transforming growth factor-beta (TGF beta), a proliferative cytokine, is elevated at 2 weeks, persists until 8 weeks, and then returns to baseline values. In parallel with the cytokine cascade, the fibrogenic markers for CI/CIII/IV (collagen genes) correlate by showing a similar early and then later elevation of activity. For instance, the collagen gene expression of CI/CIII is a biphasic response with an initial increase at 1-2 weeks that remits at 8 weeks, remains inactive from 8 to 16 weeks, and then becomes elevated at 6 months when collagen deposition is recognized histopathologically. These studies clearly demonstrate the early and persistent elevation of cytokine production following pulmonary irradiation. The temporal relationship between the elevation of specific cytokines and the histological and biochemical evidence of fibrosis serves to illustrate the continuum of response, which, we believe, underlies pulmonary radiation reactions and supports the concept of a perpetual cascade of cytokines produced immediately after irradiation, prompting collagen genes to turn on, and persisting until the expression of late effects becomes apparent pathologically and clinically.
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              The pathology of ionizing radiation as defined by morphologic patterns.

              This article presents a brief description of the effects of ionizing radiation in human tissues, as seen by the Pathologist. The lesions that occur in multiple organ/tissues will be discussed, dividing them into those that affect (a) the parenchyma or epithelia, (b) the stromal elements, and (c) the blood vessels. Since not all lesions fit into these patterns, the exceptions will be described as characteristic organ lesions. Unless specified otherwise the alterations presented are those that result from electromagnetic radiation (x-rays and gamma rays) as used for clinical radiation therapy. Most of the material presented will be delayed injury (i.e. months-to-years after exposure). The epithelial/parenchymal lesions include atrophy, necrosis, metaplasia, cellular atypia, dysplasia, and neoplasia. The common stromal lesions--the best recognized by pathologists--include fibrosis, fibrinous exudates, necrosis (with a paucity of cellular inflammatory exudates), and atypical fibroblasts. The vascular lesions are quite consistent: most often they affect the microvessels (capillaries, sinusoids) producing lethal and sublethal damage to the endothelial cells, with capillary rupture or thrombosis. Medium-size vessels show neointimal proliferation, fibrinoid necrosis, thrombosis, or acute arteritis. Damage in large vessels is less common; it occurs more in arteries than in veins and includes neointimal proliferation, atheromatosis, thrombosis and rupture (a dramatic complication). Some of the characteristic organ lesions are veno-occlusive liver disease, acute radiation pneumonitis, permanent bone marrow hypoplasia or aplasia, and colitis cystica profunda. Neoplasms are a well-recognized delayed complication of radiation and will not be described in detail. It is important to remember that there are no pathognomonic features of injuries produced by ionizing radiation. Nonetheless, although not specific individually, the combined features are characteristic enough to be recognized.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Drug Design, Development and Therapy
                Dove Medical Press
                25 May 2018
                : 12
                : 1491-1500
                [1 ]Department of Obstetrics and Gynecology, Firat University School of Medicine, Elazig, Turkey
                [2 ]Department of Histology and Embryology, Firat University School of Medicine, Elazig, Turkey
                [3 ]Department of Obstetrics and Gynecology, Maltepe University School of Medicine, Istanbul, Turkey
                [4 ]Department of Biochemistry, Firat University School of Medicine, Elazig, Turkey
                Author notes
                Correspondence: Remzi Atilgan, Department of Obstetrics and Gynecology, School of Medicine, Firat University, Firat Medical Center, 23119 Elazig, Turkey, Tel +90 42 4233 3555 ext 2118, Fax +90 42 4237 9138, Email remzi_atilgan@ 123456hotmail.com
                © 2018 Can et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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