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Biomarkers used to assess radio- and chemotherapy-induced lymphocyte genome instability in a case of cerebral infarction during relapse of a testicular seminoma

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Gamulin M., Pastuhović A., Šantek F., Grgić M., Kopjar N.
Biomonitoring
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2014
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vol. 1
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issue 1
EN
We report a case of a testicular seminoma patient with relapse who was irradiated after acute cerebral infarction induced by cisplatin-based chemotherapy. Lymphocytic genome instability was studied using an alkaline comet assay, analysis of structural chromosome aberrations, and cytokinesis-block micronucleus assay in blood samples collected before and after PET CT scanning that preceded radiotherapy, as well as before the administration of the first and after the administration of the last fraction of 3D conformal radiation. A challengetest with hydrogen peroxide (H2O2) was performed on isolated peripheral blood lymphocytes in order to establish to what extent earlier therapies had modified the response of the patient’s DNA to external stimuli with a genotoxic chemical. Levels of primary DNA damage in lymphocytes increased after diagnostic exposure, lowered prior to administration of a conformal 3D radiotherapy, and were the highest at the end of radiotherapy. Ex vivo exposure to H2O2 caused additional lymphocyte DNA damage, which gradually increased 15 and 30 minutes after treatment. Diagnostic and therapeutic exposure to radiation caused measurable cytogenetic damage that was subjected to extensive repair. All of the obtained results point to increased genomic instability in the patient which should be taken into account in his future medical surveillance.
2
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Changes in phosphorylation of histone H2A.X and p53 in response of peripheral blood lymphocytes to gamma irradiation

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Vilasová Z., Řezáčová M., Vávrová J., Tichý A., Vokurková D., Zoelzer F., Řeháková Z., Osterreicher J., Lukášová E.
Acta Biochimica Polonica
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2008
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vol. 55
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issue 2
381-390
EN
The main aim of this study was to compare the reaction of quiescent and proliferating, i.e. phytohemagglutinin (PHA)-stimulated, human peripheral blood mononuclear cells (PBMCs) to γ-radiation, and analyse changes of proteins related to repair of DNA damage and apoptosis, such as γH2A.X, p53, p53 phosphorylation at serines-15 and -392, and p21 and their dose dependence. Freshly isolated PBMCs in peripheral blood are predominantly quiescent, in G0 phase, and with very low amounts of proteins p53 and p21. Using confocal microscopy we detected dose dependent (0.5-5 Gy) induction of foci containing γH2A.X (1 h after γ-ray exposure), which are formed around radiation-induced double strand breaks of DNA. Apoptosis was detected from 24 h after irradiation by the dose of 4 Gy onwards by Annexin V binding and lamin B cleavage. Seventy two hours after irradiation 70% of CD3+ lymphocytes were A+. Neither increase in p53 nor its phosphorylation on serine-392 after irradiation was detected in these cells. However, massive increase in p21 (cyclin-dependent kinase inhibitor 1A) was detected after irradiation, which can be responsible for late occurrence of apoptosis in these quiescent cells. PHA-stimulation itself (72 h) caused an increase in early apoptosis (A+PI-) in comparison to non-stimulated PBMCs (38% A+ resp. 13.4%). After PHA-stimulation also the amount of γH2A.X, p53, and p21 increased, but no phosphorylation of p53 on serine-392 or -15 was detected. Reaction to γ-radiation was different in PHA-stimulated lymphocytes: the p53 pathway was activated and p53 was phosphorylated on serines-15 and -392 4 h after irradiation by the dose of 4 Gy. Phosphorylation of p53 at serine-15 increased in a dose-dependent manner in the studied dose range 0.2-7.5 Gy. Also the amount of p21 increased after irradiation. Seventy two hours after irradiation of PHA-stimulated CD3+ T lymphocytes by the dose of 4 Gy 65% of cells were A+.
3
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Helicobacter pylori increases expression of proapoptotic markers Fas and FasL on CD4 lymphocytes in children

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Kotłowska-Kmieć A., Bąkowska A., Szarszewski A., Kamińska B., Łuczak G., Radys W., Landowski P., Brodzicki J., Korzon M., Liberek A.
Acta Biochimica Polonica
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2009
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vol. 56
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issue 3
433-438
EN
The pathomechanism of Helicobacter pylori action upon gastric mucosa and its role in the pathogenesis of gastritis have not been fully elucidated. The aim of this study was to evaluate the most prevalent lymphocyte subpopulations of the gastric mucosa in gastritis in children, as well as to evaluate the expression of Fas and Fas ligand receptors (FasL), periapoptotic markers of gastric mucosa lymphocytes before and after H. pylori eradication. Forty nine patients aged 6 to 17 years, investigated due to chronic abdominal pain, were studied. The obtained tissue samples were analysed by immunohistochemistry. Different lymphocyte subsets were quantified on the basis of surface antigen expression (CD3, CD4, CD8, CD20), secreted cytokines (IL-4, IL-6, IFNγ) and Fas and FasL proteins in the gastric mucosa. B and T helper lymphocytes were found to play a major role in the inflammatory infiltration in the gastric mucosa in children during H. pylori infection. Their expression was found to decrease after eradication. The enhanced expression of Fas receptor on lymphocytes before treatment and a decrease of this expression after eradication of H. pylori were shown. It was demonstrated that there is a correlation between CD4 and Fas receptor expression that may induce apoptosis of the helper lymphocytes in infected children.
4
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Role of T-lymphocytes in Radiation-Impaired Wound Healing

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Schäffer M., Stülten C., Viebahn R.
Polish Journal of Surgery
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2007
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vol. 79
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issue 4
312-318
EN
Radiation impairs healing, although the underlying mechanisms are not clearly defined. T-lymphocytes have been shown to be critical for wound healing. We hypothesized that radiation-impaired healing may affect different subtypes of T cells.The aim of the study. We studied the effect of local electron irradiation on standard parameters of dermal wound healing in rats and correlated the outcome of healing with the expression of different lymphocyte subtypes in the wound.Material and methods. Groups of 10 rats were irradiated using single dose 12 or 24 Gray electron radiation at the dorsal skin. Control rats were sham-irradiated. On day 5, a skin incision in the irradiated area was performed and polyvinyl alcohol sponges were inserted subcutaneously. Rats were sacrificed 10 days later to determine the wound breaking strength and reparative collagen deposition. Blood lymphocytes were analyzed by FACS. Immunohistochemistry was performed on wound sections.Results. Irradiation significantly reduced wound collagen deposition and wound breaking strength (p <0.05), leading to a 78% reduction in collagen deposition and 47% reduction in breaking strength in 24 Gy animals. Blood lymphocytes were not affected by electron-irradiation, suggesting that the wound was not affected by radiation-induced systemic effects. Impaired healing was reflected, however, in increased expression of wound CD8 cells and decreased expression of CD25 (IL-2 receptor) (p <0.01). No effect was seen on wound CD4 cells. In addition, the ratio of CD4/CD8 was significantly decreased (p <0.05).Conclusions. Radiation-impaired healing is reflected in impaired expression of wound lymphocyte subtypes. Altered lymphocyte subtypes may affect the outcome of healing in irradiated wounds.
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