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Effect of Increased Urea Levels on Mouse Preimplantation Embryos Developed in Vivo and in Vitro


High plasma urea nitrogen concentration has been proposed as an important factor contributing to the decline in reproductive parameters of domestic animals. The aim of this study was to evaluate the effect of urea on the development of preimplantation embryos in a mouse model. During in vivo tests, acute renal failure (ARF) accompanied by hyper-uraemia was induced by intramuscular administration of glycerol (50%) into hind limbs of fertilised dams. During in vitro tests, embryos collected from healthy dams were cultured in a medium with the addition of various concentrations of urea from the 4-cell stage to the blastocyst stage. Stereomicroscopic evaluation and fluorescence staining of embryos obtained from dams with ARF showed that high blood urea is connected with an increase in the number blastocysts containing at least one apoptotic cell and in the incidences of dead cells per blastocyst, but it did not affect their ability to reach the blastocyst stage. In vitro tests showed that culture of embryos with urea at concentration of 10 mM negatively affected the quality of obtained blastocysts. Blastocysts showed significantly lower numbers of cells and increased incidence of dead cells. An increase in apoptosis incidence was observed even in blastocysts obtained from cultures with 5 mM urea. Urea at concentrations 50 mM and higher negatively affected the ability of embryos to reach the blastocyst stage and the highest used concentrations (from 500 mM) caused overall developmental arrest of embryos at the 4- or 5- cell stage. These results show that elevated levels of urea may cause changes in the microenvironment of developing preimplantation embryos, which can negatively affect their quality. Embryo growth remains un-affected up to very high concentrations of urea.

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Analysis of Sister Chromatid Exchanges and Proliferation of Human Peripheral Blood Lymphocytes Exposed to Epoxiconazole

epoxiconazole in bovine peripheral lymphocytes in vitro . Chemosphere , 193, 82—88. 12. Taxvig, C., Hass, U., Axelstad, M., Dalgaard, M., Boberg, J., Andeasen, H. L., et al., 2007: Endocrine-disrupting activities in vivo of the fungicides tebuconazole and epoxiconazole. Toxicol. Sci. Off. J. Soc. Toxicol. , 100, 464—473. 13. Terzoudi, G. I., Malik, S. I., Pantelias, G. E., Margaritis, K., Manola, K., Makropoulos, W., 2003: A new cytogenetic approach for the evaluation of mutagenic potential of chemicals that induce cell cycle arrest in the G 2 phase

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Adriamycin activity's durational governance of different cell death types and zonality in rat liver acinus. Immunohistochemical studies

., Halicka H.D., Li C.J., Bhalla K., Bronde E.V., Blagosklonny M.V.: Pharmacological induction of HSp 70 protects apoptosis-prone cells from doxorubicin: comparison with caspase-inhibitor and cycle-arrest-mediated cytoprotection. Cell Death Differ Abstr 2006, 13, 1434-1441. 4. Faubel S., Ljubanovic D., Reznikow L., Somerset H., Dinarello C.A.: Caspase-1-deficient mice are protected against cisplatin- induced apoptosis and acute tubular necrosis. Kidney Int 2004, 66, 2202-2213. 5. Gumucio J.J., Miller D.L.: Functional implications of liver

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A Histopathological Study of Ischemic and Compressive Paraplegia in Dogs

References 1. Acher, C., Wynn, M., 2012: Paraplegia after thoracoabdominal aortic surgery: not just assisted circulation, hypothermic arrest, clamp and sew, or TEVAR. Ann. Cardiothorac. Surg., 1, 365-372. 2. Adams, F., 1849: The Genuine Works of Hippocrates. Translated from Greek. Section II. Hippocratic Treatises. S. 24-132. London, Sydenham Society. 3. Ahuja, C. S., Fehlings, M., 2016: Concise review: Bridging the gap: Novel neuroregenerative and neuroprotective strategies in spinal cord injury. Stem Cell

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Identification of Human Hepatocyte Proliferation Related Gene C2orf69

(temsirolimus) induces antiproliferative effects through inhibition of mTOR in Bel-7402 liver cancer cells. Cancer Cell Int 2013; 13(1):30. 11. Choi HJ, Fukui M, Zhu BT. Role of cyclin B1/Cdc2 upregulation in the development of mitotic prometaphase arrest in human breast cancer cells treated with nocodazole. PLoS One 2011; 6(8):e24312. 12. Motokura T, Bloom T, Kim HG, Jüppner H, Ruderman JV, Kronenberg HM, et al. A novel cyclin encoded by a bcl1-linked candidate oncogene. Nature 1991; 350(6318):512-515. 13. Thompson MD, Monga SP

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Biomarkers of injury to neural tissue in veterinary medicine

W.J., Das C., Hsu S.T., Jackson S.E.: The effect of Parkinson's-disease-associated mutations on the deubiquitinating enzyme UCH-L1. J Mol Biol 2011, 407, 261–272. 4. Arnaoutakis G.J., George T.J., Wang K.K., Wilson M.A., Allen J.G., Robinson C.W., Haggerty K.A., Weiss E.S., Blue M.E., Talbot C.C., Jr., Troncoso J.C., Johnston M.V., Baumgartner W.A.: Serum levels of neuron-specific ubiquitin carboxyl-terminal esterase-L1 predict brain injury in a canine model of hypothermic circulatory arrest. J Thorac Cardioc Sur 2011, 142, 902–910. 5. Babcock L

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Acquisition and Expansion of Adult Rat Bone Marrow Multipotent Mesenchymal Stromal Cells

elicited by cardiac arrest in a dog brain. Folia Veterinaria , 50, 73—75. 10. Kim, B. G., Hwang, D. H., Lee, S. I., Kim, E. J., Kim, S. N., 2007: Stem cell-based cell therapy for spinal cord injury. Cell Transplant. , 16, 355—364. 11. Maženský, D., Flešárová, S., 2016: Importance of the arterial blood supply to the rabbit and guinea pig spinal cord in experimental ischemia. In Schaller, B. (Ed.): Ischemic Stroke — Updates . Tech., Croatia, 59—86. 12. Michalczyk, K., Ziman, M., 2005: Nestin structure and predicted function in cellular

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Influence of post-mortem muscle glycogen content on the quality of beef during aging

–266. 4. Díaz M.T., Vieira C., Pérez C., Lauzurica S., González de Chávarri E., Sánchez M., De la Fuente J.: Effect of lairage time (0 h, 3 h, 6 h or 12 h) on glycogen content and meat quality parameters in suckling lambs. Meat Sci 2014, 96, 653–660. 5. England E.M., Matarneh S.K., Oliver E.M., Apaoblaza A., Scheffler T.L., Gerrard D.E.: Excess glycogen does not resolve high ultimate pH of oxidative muscle. Meat Sci 2015, 114, 95–102. 6. England E.M., Matarneh S.K., Scheffler T.L., Wachet C., Gerrard D.E.: pH inactivation of phosphofructokinase arrests

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Cytotoxicity of iron (III), molybdenum (III), and their mixtures in BALB/3T3 and HepG2 cells

-Khedhairy A.A., Pant A.B.: Molybdenum nanoparticles-induced cytotoxicity, oxidative stress, G2/M arrest, and DNA damage in mouse skin fibroblast cells (L929), Colloids and Surfaces B: Biointerfaces 2014, 125, 73–81. 19. Tallkvist J., Oskarsson A.: Chapter 47, Molybdenum, In: Handbook on the Toxicology of Metals, edited by Nordberg G.F., Fowler B.A., Elsevier, 2015, pp. 1077–1089. 20. Terpiłowska S., Siwicki A.K.: Interactions between chromium (III) and iron (III), molybdenum (III) or nickel (II): cytotoxicity, genotoxicity, and mutagenicity studies

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Radix Glehniae extract inhibits migration and invasion of lung cancer cells

”, “softening hardness and loosing knot”, and so on. Some low-toxic and nontoxic Chinese herbs have played a role in tumor treatment [ 4 ]. Radix Glehniae is a commonly used nontoxic herb with the functions of “Yang yin qing fei”, promoting the secretion of saliva or body fluid, and “expelling phlegm and arresting cough”. It is useful for treating lung diseases and has been widely used in prescriptions against lung cancer [ 5 ]. Here, for the first time, we investigated the effect of Radix Glehniae on the migration and invasion abilities of lung cancer cells, as well as

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