Dergiler / International Journal of Secondary Metabolite / 2026 / Volume: 5 Issue: 3

Effect of Pre-/ Postnatal Hypoxia on Pyruvate Kinase in Rat Brain

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Yayın Tarihi
2018-09-15
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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

An explanation of the obtained results suggested can be considered as an evidence of the realization of the biological effect of hypoxia through the oxidative mechanism.

📌 3 Maddede Bu Makale

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Amaç & Hipotez:The effect of hypoxic hypoxia on the pyruvate kinase (PK) activity in the brain structures of white rats during ontogenesis in a comparative aspect has been studied.
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Temel Bulgular & Veri:A clear dependence could be established in the increase of PK activity from an oxygen deficient state, the age of animals, the studied structure of the brain and the prolonged effect of hypoxia.
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Sonuç & Katkı:An explanation of the obtained results suggested can be considered as an evidence of the realization of the biological effect of hypoxia through the oxidative mechanism.
🔬Tür:Research Article
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Albino rats · Age · Hypoxia

Özet

The effect of hypoxic hypoxia on the pyruvate kinase (PK) activity in the brain structures of white rats during ontogenesis in a comparative aspect has been studied. A clear dependence could be established in the increase of PK activity from an oxygen deficient state, the age of animals, the studied structure of the brain and the prolonged effect of hypoxia. Prenatal exposure to hypoxia has shown that the PK activity is not restored to the control value level in postnatal development. After postnatal exposure to hypoxia with increasing age in animals, the PK activity gets more resistant to the effect of stress-factors. The data analysis indicates that the increasing exhaustion of energy resources necessary for normal cell functioning makes an important contribution to the development of hypoxic state and the insufficiency of mitochondrial oxidative phosphorylation, the main energy forming system which underlies these disturbances. Energy-shortage, in its turn causes a variety of secondary negative metabolic alterations and gives rise to free radical oxidation in the cells. An explanation of the obtained results suggested can be considered as an evidence of the realization of the biological effect of hypoxia through the oxidative mechanism.

Abstract

The effect of hypoxic hypoxia on the pyruvate kinase (PK) activity in the brain structures of white rats during ontogenesis in a comparative aspect has been studied. A clear dependence could be established in the increase of PK activity from an oxygen deficient state, the age of animals, the studied structure of the brain and the prolonged effect of hypoxia. Prenatal exposure to hypoxia has shown that the PK activity is not restored to the control value level in postnatal development. After postnatal exposure to hypoxia with increasing age in animals, the PK activity gets more resistant to the effect of stress-factors. The data analysis indicates that the increasing exhaustion of energy resources necessary for normal cell functioning makes an important contribution to the development of hypoxic state and the insufficiency of mitochondrial oxidative phosphorylation, the main energy forming system which underlies these disturbances. Energy-shortage, in its turn causes a variety of secondary negative metabolic alterations and gives rise to free radical oxidation in the cells. An explanation of the obtained results suggested can be considered as an evidence of the realization of the biological effect of hypoxia through the oxidative mechanism.

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Bu Makaleye Atıf Yap

Rashidova, A. M. (2018). Effect of Pre-/ Postnatal Hypoxia on Pyruvate Kinase in Rat Brain. International Journal of Secondary Metabolite, Volume: 5 Issue: 3. https://doi.org/10.21448/ijsm.450963

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Kaynakça (30)

  1. Shvyreva, E., Graf, A., Maslova, M., Maklakova, A., Sokolova, N. (2017). Acute hypoxic stress in the critical periods of embryogenesis: the influence on the offspring developmentin the early postnatal period. European Neuropsycho pharmacology, ed. Elsevier BV (Netherlands), 27(9), 105. https://istina.msu.ru/publications/article/74505542/
  2. Menshchikova, E.B., Lankin, V.Z., Zenkov, N.K. (2006). In: Oxidative stress. Proxidants and antioxidants. M.: “Slovo”, 556 p. https://www.twirpx.com/file/908751/
  3. Anisimov, V.N. (2008). Molecular and Physiological Mechanisms of Aging., v1, 481 p., St. Petersburg. http://www.gerontology.ru/PDF_library/Book-Anisimov_t-1-2008.pdf
  4. Zhuravin, I.A., Tumanova, N.L., Ozirskaya, E.V., Vasiliev, D.S., Dubrovskaya, N.M. (2007). Formation of structural and ultrastructural organization of striatum in postnatal ontogenesis of rats with changing conditions of their embryonic development. J.Evol. Biochim. Fiziol., 43(2), 229-239. DOI 10.1134/50022093007020123
  5. Mishra, O.P., Delivoria-Papadopoulos, M. (1999). Cellular mechanisms of hypoxic injury in the developing brain. Brain Res Bull., 48(3), 233-238. PMID 10229330; https://www.ncbi.nlm.nih.gov/pubmed/10229330
  6. Pellerin, L., Magistretti, P.J. (2003). How to balance the brain energy budget while spending glucose differently. J. Physiology, 546(2), 325. DOI: 10.1113/jphysiol.2002.035105. PMCID: PMC2342533. PMID: 12527720.
  7. Semenza, G.L. (2012). Hypoxia-inducible factors in physiology and medicine. Cell. Feb 3; 148(3), 399-408. DOI: 10.1016/j.cell.2012.01.021.
  8. Рашидова, А.М., Гашимова, У.Ф. (2017). Зависимость активности ферментов ЛДГ и ПК в тканях структур головного мозга белых крыс от уровня гипоксии, перенесенной на стадии органогенеза ж.Известия НАНА, 72(1), 121-125. http://www.jbio.az/uploads/journal/e70929ecd0b2172f1485c15aaed81c57.pdf
  9. Belova, N.G., Zhelev, V.A., Agarkova, L.A., Kolesnikova I.A., Gabitova N.A. (2008). Features of energy metabolism of cells in the mother-fetus-newborn system in pregnancy complicated by gestosis. Сибирский медицинский журнал, 4-1(23), 7-10.
  10. Лукьянова, Л. Д. (2001). Митохондриальные дисфункции при гипоксии -типовой патологический процесс.//Митохондрии в патологии. Материалы всероссийского рабочего совещания.-Пущино, 2001.-С. 66-67; https://readera.ru/metabolicheskaja-moduljacija-protivoopuholevogo-jeffekta-citostatikov-v-14045499
  11. Prabhakar, N.R. (2013). Sensing hypoxia: physiology, genetics and epigenetics. J. Physiol., 591(9), 2245-2257. DOI: 10.1113/jphysiol.2012.247759
  12. Zamenina, E.V., Panteleeva, N.I., Roshchevskaya, I.M. (2017). The heart electric field of man during ventricularrepolarization under hypoxic influence. Russian J. of Physiology,103(11). 1330-1339. https://elibrary.ru/item.asp?id=30511338
  13. Chinopoulos, C., Zhang, S.F., Thomas, B., Ten, V., Starkov, A.A. (2011). Isolation and functional assessment of mitochondria from small amounts of mouse brain tissues. Methods Mol. Biol., 793, 311-324. DOI: 10.1007/978-1-61779-328-8_20
  14. Bergmeyer, H.U. (1975). Biochemica information. In: Methods of Enzymatic Analysis, II. 82-83. https://books.google.az/books?id=jgIlBQAAQBAJ&pg=PA157&dq=Bergmeyer+H.U.+(1975).+Biochemica+information.&hl=ru&sa=X&ved=0ahUKEwiNnt3b06PcAhUDlSwKHWbJDQgQ6AEILDAB#v=onepage&q=Bergmeyer%20H.U.%20(1975).%20Biochemica%20information.&f=false
  15. Kruger, N.J. (2009). The Bradford method for protein quantitation. The protein Protocols Handbook, 3-rd ed. Ed. by J.M.Walker, Humana press Inc., Totowa N.J.,: 17-24. https://www.springer.com/gb/book/9781588298805
  16. Fatemi, A., Wilson, M.A., Johnston, M.V. (2009). Hypoxic Ischemic Encephalopathy in the Term Infant. Clin Perinatol., 36(4), 835. DOI: 10.1016/j.clp.2009.07.011
  17. Граф, А.В., Гончаренко, Е.Н., Соколова, Н.А., Ашмарин, И.П. (2008). Антенатальная гипоксия: участие в развитии патологий ЦНС в онтогенезе. Нейрохимия, 25(1-2), 11-16. http://naukarus.com/antenatalnaya-gipoksiya-uchastie-v-razvitii-patologiy-tsns-v-ontogeneze
  18. Zhuravin, I.A., Tumanova, N.L., Vasilyev, D.S. (2009). Change in adaptive mechanisms of the brain in the ontogenesis of rats underwent prenatal hypoxia. Reports of the Academy of Sciences, 425(1), 123-125. http://naukarus.com/izmenenie-adaptivnyh-mehanizmov-mozga-v-ontogeneze-krys-perenesshih-prenatalnuyu-gipoksiyu
  19. Stroyev, S.A., Tyulkova, E.I., Vataeva, L.A., Samoilov, M.O., Pelto-Huikko, M.T. (2011). Effect of prenatal hypoxia on the expression of thioredoxin-1 in the rat hippocampus at different times. Нейрохимия, 28(3), 226-231. https://elibrary.ru/item.asp?id=16655351
  20. Speakman, J. R., Selman, C. (2011). The free-radical damage theory: Accumulating evidence against a simple link of oxidative stress to ageing and lifespan. BioEssays: news and reviews in molecular, cellular and developmental biology, 33(4), 255-259. DOI:10.1002/bies.201000132.
  21. Harman, D. (2006). Free Radical Theory of Aging: An Update Increasing the Functional Life Span. Annals of the NY Academy of Sciences, 10 May: 10-21. DOI:10.1196/annals.1354.003
  22. Huseynov, A. H. (2017) Mechanism of impaсt of hypoxia on general activity of brain cortex. Russian Journal of Physiology, 103(11), 1209-1224. https://elibrary.ru/item.asp?id=30511329
  23. Ballanyi, K.J. (2004). Protective role of neuronal KATP channels in brain hypoxia. J. Exp. Biol., 207, 3201-3212. DOI: 10.1242/jeb.01106
  24. Nieber, K. (1999). Hypoxia and neuronal function under in vitro conditions. Pharmacol. Ther., 82(1), 71-86. PMID: 10341358; https://www.ncbi.nlm.nih.gov/pubmed/10341358
  25. van Os, S., Ruitenbeek, W., Hopman, J., van de Bor, M. (2006). Excitatory amino acid release and electrocortical brain activity after hypoxemia in near–term lambs. Brain Dev., 28, 380-388. DOI: 10.1016/j.braindev.2005.12.002
  26. Luhmann, H.J., Kral, T., Heinemann, U. (1993). Influence of hypoxia on excitation and GABA–ergic inhibition in mature and developing rat neocortex. Exp. Brain Res., 97, 209-224. https://link.springer.com/article/10.1007/BF00228690
  27. Nolan P.C., Waldrop T.G.(1996). In vitro responses of VLM neurons to hypoxia after 320 normobaric hypoxic acclimatization. Respiration Physiology, 105(1-2), 23-33; DOI.ORG/10.1016/0034-5687(96)00033-3; https://www.sciencedirect.com/science/article/pii/0034568796000333
  28. Hanse E., Taira T., Lauri S., Groc L. (2009). Glutamate synapse in developing brain an integrative perspective beyond the silent state. Trends Neurоsci., 32(10), 532-537. DOI: 10.1016/j.tins.2009.07.003. Epub 2009 Sep 4.
  29. ГоранчукВ.В., СаповаН.И., ИвановА.О. (2003). Гипокситерапия. Изд-во ЭЛБИ-СПб.; 536 с. https://www.mmbook.ru/catalog/raznoe/101625-detail
  30. Лукьянова, Л.Д., Ушаков, И.Б. (2004). Проблемы гипоксии: молекулярные, физиологические и медицинские аспекты. М., Истоки., 584 с., https://elibrary.ru/item.asp?id=19523467