Ukr.Biochem.J. 2017; Volume 89, Issue 5, Sep-Oct, pp. 84-95

doi: https://doi.org/10.15407/ubj89.05.084

Thiamine diphosphate synthesis and redox state indicator in rat brain during of B(1) hypovitaminosis

Yu. M. Parkhomenko, A. S. Pavlova, O. A. Mejenskaya,
S. P. Stepanenko, L. I. Chekhivska

Palladin Istitute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
e-mail: yupark@biochem.kiev.ua

The main aim of this study was to reveal the relationship between thiamine metabolism and the redox balance of cellular metabolism in chronic alimentary thiamine deficiency. On the experimental model of chronic alimentary thiamine deficiency (hypovitaminosis) the dynamics of changes in the indicators of thiamine diphosphate (ThDP) synthesis and the redox state in rat brain tissue were studied. In the whole brain homogenate of the rat, the levels of ThDP and thiamine pyrophosphokinase (TPK) activity as well as the levels of free SH-groups and reactive oxygen species (ROS) were measured. The results obtained showed, even with a very limited intake of thiamine into the body (model of alimentary hypovitaminosis), there was no increase in the level of ROS (one of the signs of oxidative stress) in the brain tissue, while the level of free SH-groups significantly decreased. Under these conditions, the content of the coenzyme form of thiamine, ThDP, in brain tissue changes insignificantly, which suggests that there are non-coenzymatic mechanisms of vitamin B1 involvement in maintaining cellular redox homeostasis. The analysis of changes in the ThDP content and the TPK activity in the cerebral cortex, cerebellum and hippocampus of the rats’ brain in the dynamics of  hypovitaminosis  development and TPK immunoreactivity at the end of the experiment  showed that the ThDP synthesis in cells of various brain regions under the indicated conditions does not depend  on the redox  state, but is regulated by the level of ThDP.

Keywords: , , , , , ,


References:

  1. Butterworth RF, Kril JJ, Harper CG. Thiamine-dependent enzyme changes in the brains of alcoholics: relationship to the Wernicke-Korsakoff syndrome. Alcohol Clin Exp Res. 1993 Oct;17(5):1084-8. PubMed, CrossRef
  2. Lu’o’ng Kv, Nguyen LT. Role of thiamine in Alzheimer’s disease. Am J Alzheimers Dis Other Demen. 2011 Dec;26(8):588-98. PubMed, CrossRef
  3. Lu’o’ng Kv, Nguyên LT. Thiamine and Parkinson’s disease. J Neurol Sci. 2012 May 15;316(1-2):1-8. PubMed, CrossRef
  4. Liu D, Ke Z, Luo J. Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy. Mol Neurobiol. 2017 Sep;54(7):5440-5448. PubMed, PubMedCentral, CrossRef
  5. Parkhomenko YuM, Pavlova AS, Mezhenskaya OA. Mechanisms responsible for the high sensitivity of neural cells to vitamin B1 deficiency. Neurophysiol. 2016; 48(6): 429-448.  CrossRef
  6. Jhala SS, Hazell AS. Modeling neurodegenerative disease pathophysiology in thiamine deficiency: consequences of impaired oxidative metabolism. Neurochem Int. 2011 Feb;58(3):248-60.  PubMed, CrossRef
  7. Gaüzère BA, Aubry P. The disease called “Barbiers” in the 19th century. Med Sante Trop. 2014 Jul-Sep;24(3):241-6. PubMed
  8. Prinzo ZW. Thiamine deficiency. World Health Organization, 1999. 52  p.
  9. Tumanov VN, Trebukhina RV. Interstitial thiamine redistribution during the development of vitamin B1 deficiency in mice. Vopr Pitan. 1987 Nov-Dec;(6):49-52. (In Russian). PubMed
  10. Parkhomenko YM, Kudryavtsev PA, Pylypchuk SY, Chekhivska LI, Stepanenko SP, Sergiichuk AA, Bunik VI. Chronic alcoholism in rats induces a compensatory response, preserving brain thiamine diphosphate, but the brain 2-oxo acid dehydrogenases are inactivated despite unchanged coenzyme levels. J Neurochem. 2011 Jun;117(6):1055-65. PubMed, CrossRef
  11. Oktyabrsky ON, Smirnova GV. Redox regulation of cellular functions. Biochemistry (Mosc). 2007 Feb;72(2):132-45. PubMed, CrossRef
  12. Kulinsky VI, Kolesnichenko LS. The biological role of glutathione.  Usp Sovrem Biol. 1990; 110(1):20-23.
  13. Robaczewska J, Kedziora-Kornatowska K, Kozakiewicz M, Zary-Sikorska E, Pawluk H, Pawliszak W, Kedziora J. Role of glutathione metabolism and glutathione-related antioxidant defense systems in hypertension. J Physiol Pharmacol. 2016 Jun;67(3):331-7. PubMed
  14. Bai P, Bennion M, Gubler CJ. Biochemical factors involved in the anorexia of thiamin deficiency in rats. J Nutr. 1971 Jun;101(6):731-7. PubMed
  15. Pavlova AS, Stepanenko SP, Chehovskaya LI, Tihomirov AA, Parkhomenko YuM. Dependence of vitamin B1 metabolism and the state of astroglia in the rat brain on the supply with this vitamin. Neurophysiology. 2016;48(5):336–345.  CrossRef
  16. Zapadnyuk IP, Zapadnyuk VI, Zakhariya EA. Laboratory animals. Breeding, content, use in the experiment, K: Vishcha shk., 1983. 383 p. (in Russian).
  17. Ostrovsky YuM. Experimental vitaminology. M: Science and technology, 1979. 551 p. (in Russian).
  18. Laemmli UK. Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature. 1970 Aug 15;227(5259):680-5. PubMed, CrossRef
  19. Zhang X, Cao J, Jiang L, Zhong L. Suppressive effects of hydroxytyrosol on oxidative stress and nuclear Factor-kappaB activation in THP-1 cells. Biol Pharm Bull. 2009 Apr;32(4):578-82. PubMed, CrossRef
  20. Severin SYe, Solovieva GA. Practical work on biochemistry. Moscow: MSU, 1989. 509 p. (in Russian).
  21. Gibson GE, Zhang H. Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration. Neurochem Int. 2002 May;40(6):493-504. PubMed, CrossRef
  22. Rindi G, Comincioli V, Reggiani C, Patrini C. Nervous tissue thiamine metabolism in vivo. II. Thiamine and its phosphoesters dynamics in different brain regions and sciatic nerve of the rat. Brain Res. 1984 Feb 20;293(2):329-42. PubMed, CrossRef
  23. Ferreira-Vieira TH, de Freitas-Silva DM, Ribeiro AF, Pereira SR, Ribeiro ÂM. Perinatal thiamine restriction affects central GABA and glutamate concentrations and motor behavior of adult rat offspring. Neurosci Lett. 2016 Mar 23;617:182-7.  PubMed, CrossRef
  24. Vetreno RP, Hall JM, Savage LM. Alcohol-related amnesia and dementia: animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment. Neurobiol Learn Mem. 2011 Nov;96(4):596-608. PubMed, PubMedCentral, CrossRef
  25. Parkhomenko YuM, Stepuro II, Donchenko GV, Stepuro VI. Oxidized derivatives of thiamine: formation, properties, biological role. Ukr Biokhim Zhurn. 2012 Nov-Dec;84(6):5-24. (In Russian). PubMed
  26. Agrawal A, Rathor R, Suryakumar G. Oxidative protein modification alters proteostasis under acute hypobaric hypoxia in skeletal muscles: a comprehensive in vivo study. Cell Stress Chaperones. 2017 May;22(3):429-443. PubMed, PubMedCentral, CrossRef
  27. Korolainen MA, Goldsteins G, Nyman TA, Alafuzoff I, Koistinaho J, Pirttilä T. Oxidative modification of proteins in the frontal cortex of Alzheimer’s disease brain. Neurobiol Aging. 2006 Jan;27(1):42-53. PubMed, CrossRef.
  28. Vignisse J, Sambon M, Gorlova A, Pavlov D, Caron N, Malgrange B, Shevtsova E, Svistunov A, Anthony DC, Markova N, Bazhenova N, Coumans B, Lakaye B, Wins P, Strekalova T, Bettendorff L. Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels. Mol Cell Neurosci. 2017 Jul;82:126-136.  PubMed, CrossRef

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