A DEFICIÊNCIA DE TIAMINA PODE AJUDAR NA COMPREENSÃO DOS MECANISMOS NEURODEGENERATIVOS?
Palabras clave:
Tiamina, Deficiência de Tiamina, Álcool, NeurodegeneraçãoResumen
A deficiência de tiamina é utilizada por pesquisadores para estudar condições neurodegenerativas. Por isso, conhecer o papel dessa vitamina no metabolismo e os efeitos que sua deficiência pode causar é tão importante. O objetivo desse ensaio é revisar o que se sabe sobre a atuação da vitamina B1 no metabolismo e os efeitos neuroquímicos e comportamentais que sua deficiência, associada ou não ao consumo de álcool, pode provocar. Essa revisão mostra que a tiamina parece ter mais papéis do que exclusivamente a de coenzima do metabolismo energético, participando também de processos neurais. Mostra ainda que são vários os efeitos neuroquímicos e comportamentais decorrentes da deficiência de tiamina associada ou não ao consumo de álcool. Concluímos que a tiamina parece ser um alvo importante de investigação para o entendimento das condições neurodegenerativas.
Citas
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[18] LIU, D.; KE, Z.; LUO, J. Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy. Molecular Neurobiology, v. 54, n. 7, p. 5440–5448, 2017.
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[20] KE, Z.J.; GIBSON, G.E. Selective response of various brain cell types during neurodegeneration induced by mild impairment of oxidative metabolism. Neurochemistry International, v. 45, n. 2–3, p. 361–369, 2004.
[21] ANDERSEN, B.B. Reduction of Purkinje cell volume in cerebellum of alcoholics. v. i, p. 10–18, 2004.
[22] BONTHIUS, D.J. et al. NeuroToxicology The protective effect of neuronal nitric oxide synthase ( nNOS ) against alcohol toxicity depends upon the NO-cGMP-PKG pathway and NF- k B. v. 29, p. 1080–1091, 2008.
[23] OSIEZAGHA, K. et al. Thiamine deficiency and delirium. Innovations in Clinical Neuroscience, v. 10, n. 4, p. 26–32, 2013.
[24] GANGOLF, M. et al. Thiamine triphosphate synthesis in rat brain occurs in mitochondria and is coupled to the respiratory chain. Journal of Biological Chemistry, v. 285, n. 1, p. 583–594, 2010.
[25] SINGLETON, C. K.; MARTIN, P.R. Molecular Mechanisms of Thiamine Utilization. Current Molecular Medicine, v. 1, n. 2, p. 197–207, 2001.
[26] NAVARRO, D. et al. Brain Lactate Synthesis in Thiamine Deficiency : A Re-evaluation Using 1 H- 13 C Nuclear Magnetic Resonance Spectroscopy. Journal of Neuroscience Research, v. 41, p. 33–41, 2005.
[27] TORVIK, A. Topographic distribution and severity of brain lesions in Wernicke's encephalopathy. Clinical Neuropathology, 6(1):25-29, 1986.
[28] SAVAGE, L.M.; HALL, J.M.; RESENDE, L.S. Translational Rodent Models of Korsakoff Syndrome Reveal the Critical Neuroanatomical Substrates of Memory Dysfunction and Recovery. v. 22, n. 2, p. 195–209, 2012.
[29] FREITAS-SILVA, D.M.; RESENDE, L.S.; PEREIRA, S.R.C.; FRANCO, G.C.; RIBEIRO, A.M. Behavioural Brain Research, 211(1):33-40. 2010.
[30] SCHOUSBOE et al. Energy Substrates to Support Glutamatergic and GABAergic Synaptic Function: Role of Glycogen, Glucose and Lactate. Neurotoxicity Research, 12(4):263-268. 2007.
[2] THOMSON, A. D.; BAKER, H.; LEEVY, C. M. Patterns of 35S-thiamine hydrochloride absorption in the malnourished alcoholic patient. J Lab Clin Med, 76(1):34-45, 1970.
[3] SECHI, G.; SERRA, A. Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management. The Lancet Neurology, 6(5):442-455, 2007.
[4] BUTTERWORTH R. F. Maternal thiamine deficiency. A factor in intrauterine growth retardation. Annals of the New York Academy of Sciences, 678, 325–329, 1993.
[5] BAKER, H.; HOCKSTEIN, S.; DEANGELIS, B. & HOLLAND, B. K. Thiamin status of gravidas treated for gestational diabetes mellitus compared to their neonates at parturition. International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition, 70(6), 317–320, 2000.
[6] ALCAIDE, M. L.; JAYAWEERA, D.; ESPINOZA, L. & KOLBER, M. Wernicke's encephalopathy in AIDS: a preventable cause of fatal neurological deficit. International journal of STD & AIDS, 14(10), 712–713, 2003.
[7] BUTTERWORTH, R.F. Thiamine deficiency-related brain dysfunction in chronic liver failure. Metab Brain Dis, 24(1):189-96, 2009.
[8] HOYUMPA A. M., Jr. Mechanisms of thiamin deficiency in chronic alcoholism. The American journal of clinical nutrition, 33(12), 2750–2761, 1980.
[9] TALLAKSEN, C. M.; BØHMER, T.; & BELL, H. Blood and serum thiamin and thiamin phosphate esters concentrations in patients with alcohol dependence syndrome before and after thiamin treatment. Alcoholism, clinical and experimental research, 16(2), 320–325, 1992.
[10] ZHAO, R. & GOLDMAN, I.D. Folate and Thiamine Transporters mediated by Facilitative Carriers (SLC19A1-3 and SLC46A1) and Folate Receptors. Mol Aspects Med, 34, 2013.
[11] HAAS, R.H. Thiamin and the brain. Ann Ver Nutr, 8: 483-515,1988.
[12] YAMASHIRO, T.; YASUJIMA, T.; SAID, H. M. & YUASA, H. pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates. The Journal of biological chemistry, 295(50), 16998–17008, 2020
[13] MAYR, J.A. et al. Thiamine pyrophosphokinase deficiency in encephalopathic children with defects in the pyruvate oxidation pathway. Am J Hum Genet, 89(6):806-12, 2011.
[14] Aleshin, V.A.; Mkrtchyan, G.V.; Bunik, V.I. Mechanisms of Non-coenzyme Action of Thiamine: Protein Targets and Medical Significance. Biochemistry (Mosc), 84(8):829-850, 2019.
[15] Bunik, V.I.; Aleshin, V.A.; Zhou, X.; Krishnan, S.; Karlsson, A. Regulation of Thiamine (Vitamin B1)-Dependent Metabolism in Mammals by p53. Biochemistry (Mosc), 85(7):801-807, 2020.
[16] BETTENDORFF, L.; WINS, P. Thiamin diphosphate in biological chemistry: New aspects of thiamin metabolism, especially triphosphate derivatives acting other than as cofactors. FEBS Journal, v. 276, n. 11, p. 2917–2925, 2009.
[17] GIGLIOBIANCO, T. et al. An alternative role of F o F 1 -ATP synthase in Escherichia coli : synthesis of thiamine triphosphate. Scientific Reports, v. 1, 2013.
[18] LIU, D.; KE, Z.; LUO, J. Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy. Molecular Neurobiology, v. 54, n. 7, p. 5440–5448, 2017.
[19] BUENO, K.O. et al. Spatial cognitive deficits in an animal model of Wernicke–Korsakoff syndrome are related to changes in thalamic VDAC protein concentrations. Neuroscience, v. 294, p. 29–37, 2015.
[20] KE, Z.J.; GIBSON, G.E. Selective response of various brain cell types during neurodegeneration induced by mild impairment of oxidative metabolism. Neurochemistry International, v. 45, n. 2–3, p. 361–369, 2004.
[21] ANDERSEN, B.B. Reduction of Purkinje cell volume in cerebellum of alcoholics. v. i, p. 10–18, 2004.
[22] BONTHIUS, D.J. et al. NeuroToxicology The protective effect of neuronal nitric oxide synthase ( nNOS ) against alcohol toxicity depends upon the NO-cGMP-PKG pathway and NF- k B. v. 29, p. 1080–1091, 2008.
[23] OSIEZAGHA, K. et al. Thiamine deficiency and delirium. Innovations in Clinical Neuroscience, v. 10, n. 4, p. 26–32, 2013.
[24] GANGOLF, M. et al. Thiamine triphosphate synthesis in rat brain occurs in mitochondria and is coupled to the respiratory chain. Journal of Biological Chemistry, v. 285, n. 1, p. 583–594, 2010.
[25] SINGLETON, C. K.; MARTIN, P.R. Molecular Mechanisms of Thiamine Utilization. Current Molecular Medicine, v. 1, n. 2, p. 197–207, 2001.
[26] NAVARRO, D. et al. Brain Lactate Synthesis in Thiamine Deficiency : A Re-evaluation Using 1 H- 13 C Nuclear Magnetic Resonance Spectroscopy. Journal of Neuroscience Research, v. 41, p. 33–41, 2005.
[27] TORVIK, A. Topographic distribution and severity of brain lesions in Wernicke's encephalopathy. Clinical Neuropathology, 6(1):25-29, 1986.
[28] SAVAGE, L.M.; HALL, J.M.; RESENDE, L.S. Translational Rodent Models of Korsakoff Syndrome Reveal the Critical Neuroanatomical Substrates of Memory Dysfunction and Recovery. v. 22, n. 2, p. 195–209, 2012.
[29] FREITAS-SILVA, D.M.; RESENDE, L.S.; PEREIRA, S.R.C.; FRANCO, G.C.; RIBEIRO, A.M. Behavioural Brain Research, 211(1):33-40. 2010.
[30] SCHOUSBOE et al. Energy Substrates to Support Glutamatergic and GABAergic Synaptic Function: Role of Glycogen, Glucose and Lactate. Neurotoxicity Research, 12(4):263-268. 2007.
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Publicado
2021-09-04
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de Freitas Lacerda, R. ., & Sena Romano, I. C. (2021). A DEFICIÊNCIA DE TIAMINA PODE AJUDAR NA COMPREENSÃO DOS MECANISMOS NEURODEGENERATIVOS?. South American Journal of Basic Education, Technical and Technological, 8(2), 932–939. Recuperado a partir de https://periodicos.ufac.br/index.php/SAJEBTT/article/view/4577
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