Wpływ kwasu α-liponowego, monofosforanu urydyny i witamin z grupy B na funkcję ośrodkowego i obwodowego układu nerwowego Artykuł przeglądowy
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Opublikowane:
wrz 30, 2019
Słowa kluczowe:
α-lipoic acid, uridine, vitamin B, vitamin E, selenium, diabetic neuropathy, Wernicke-Korsakov syndrome, pelagra, Alzheimer disease
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Abstrakt
Celem pracy jest aktualizacja wiedzy klinicznej dotyczącej leczenia chorób neurologicznych związanych z niedoborem kluczowych składników odżywczych: witamin z grupy B, kwasu α-liponowego, monofosforanu urydyny, witaminy E oraz selenu. Optymalne funkcjonowanie ośrodkowego oraz obwodowego układu nerwowego zależy od stałej podaży owych składników. W artykule omówiono objawy neurologiczne najczęstszych chorób niedoborowych.
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Jak cytować
Widera, M., & Berkowicz , T. (2019). Wpływ kwasu α-liponowego, monofosforanu urydyny i witamin z grupy B na funkcję ośrodkowego i obwodowego układu nerwowego. Medycyna Faktów , 12(3(44), 282-289. https://doi.org/10.24292/01.MF.0319.17
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Artykuły
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Bibliografia
1. Smith A.R., Shenvi S.V., Widlansky M. et al.: Lipoic acid as a potential therapy for chronic diseases associated with oxidative stress. Curr. Med. Chem. 2004; 11: 1135-1146.
2. Scott B.C., Aruoma O.I., Evans P.J. et al.: Lipoic and dihydrolipoic acids as antioxidants. A critical evaluation. Free Radic. Res. 1994; 20: 119-133.
3. Devasagayam T.P., Subramanian M., Pradhan D.S., Sies H.: Prevention of singlet oxygen-induced DNA damage by lipoate. Chem. Biol. Interact. 1993; 86: 79-92.
4. Cenini G., Lloret A., Cascella R.: Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View. Oxidative Medicine and Cellular Longevity 2019.
5. Singh A., Kukreti R., Saso L., Kukreti S.. Oxidative Stress: A Key Modulator in Neurodegenerative Diseases. Molecules 2019; 24(8). pii: E1583. doi: 10.3390/molecules24081583.
6. Liu J., Head E., Gharib A.M. et al.: Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha – lipoic acid. Proc. Natl. Acad. Sci. U S A 2002; 99: 2356-2361.
7. Suh J.H., Shenvi S.V., Dixon B.M. et al.: Decline in transcriptional activity of Nrf2 causes age-related loss of glutathione synthesis, which is reversible with lipoic acid. Proc. Natl. Acad. Sci. U S A 2004; 101: 3381-3386.
8. Lodge J.K., Traber M.G., Packer L.: Thiol chelation of Cu2+ by dihydrolipoic acid prevents human low density lipoprotein peroxidation. Free Radic Biol. Med. 1998; 25: 287-297.
9. Anuradha B., Varalakshmi P.: Protective role of DL-alpha-lipoic acid against mercury-induced neural lipid peroxidation. Pharmacol. Res. 1999; 39: 67-80.
10. Han D., Sen C.K., Roy S. et al.: Protection against glutamate-induced cytotoxicity in C6 glial cells by thiol antioxidants. Am. J. Physiol. 1997; 273: R1771-1778.
11. Streeper R.S., Henriksen E.J., Jacob S. et al.: Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am. J. Physiol. 1997; 273: E185-191.
12. Hughes V.A., Fiatarone M.A., Fielding R.A. et al.: Exercise increases muscle GLUT-4 levels and insulin action in subjects with impaired glucose tolerance. Am. J. Physiol. 1993; 264: E855-E862.
13. Jacob S., Streeper R.S., Fogt D.L. et al.: The antioxidant alpha-lipoic acid enhances insulin-stimulated glucose metabolism in insulin-resistant rat skeletal muscle. Diabetes 1996; 45: 1024-1029.
14. Jacob S., Henriksen E.J., Schiemann A.L. et al.: Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung 1995; 45: 872-874.
15. Konrad T., Vicini P., Kusterer K. et al.: alpha-lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes. Diabetes Care 1999; 22: 280-287.
16. Marracci G.H., Marquardt W.E., Strehlow A. et al.: Lipoic acid downmodulates CD4 from human T lymphocytes by dissociation of p56(Lck). Biochem. Biophys. Res. Commun. 2006; 344: 963-971.
17. Schillace R.V., Pisenti N., Pattamanuch N. et al.: Lipoic acid stimulates cAMP production in T lymphocytes and NK cells. Biochem. Biophys. Res. Commun. 2007; 354: 259-264.
18. Larghero P., Vene R., Minghelli S. et al.: Biological assays and genomic analysis reveal lipoic acid modulation of endothelial cell behavior and gene expression. Carcinogenesis 2007; 28: 1008-1020.
19. He Y., Sanderson I.R., Walker W.A.: Uptake, transport and metabolism of exogenous nucleo-sides in intestinal epithelial cell cultures. J. Nutr. 1994; 124: 1942-1949.
20. Ikeda U., Ito T., Shimada K.: Interleukin-6 and acute coronary syndrome. Clin. Cardiol. 2001; 24: 701-704.
21. Battisti E., Albanese A., Guerra L.: Alpha lipoic acid and superoxide dismutase in the treatment of chronic low back pain. Eur. J. Phys. Rehabil. Med. 2013; 49: 1-6.
22. Monroy Guízar E.A., García Benavides L., Ambriz Plascencia A.R. et al.: Effect of Alpha-Lipoic Acid on Clinical and Neurophysiologic Recovery of Carpal Tunnel Syndrome: A Double-Blind, Randomized Clinical Trial. J. Med. Food Vol. 2018; 21(5).
23. Connolly G.P., Duley J.A.: Uridine and its nucleotides: biological actions, therapeutic potentials. Trends Pharmacol. Sci. 1999; 20: 218-225.
24. Kondo D.G., Sung Y.H., Hellem T.L. et al.: Open-Label Uridine for Treatment of Depressed Adolescents with Bipolar Disorder. J. Child Adolesc. Psychopharmacol. 2011; 21(2): 171-175.
25. Carlezon W.A., Mague S.D., Parow A.M. et al.: Antidepressant-like effects of uridine and omega-3 fatty acids are potentiated by combined treatment in rats. Biol. Psychiatry 2005; 57(4): 343-350.
26. Grimble G.K.: Dietary nucleotides and gut mucosal defence. Gut 1994; 35: S46-51.
27. He Y., Sanderson I. R., Walker W.A.: Uptake, transport and metabolism of exogenous nucleo-sides in intestinal epithelial cell cultures. J. Nutr. 1994; 124: 1942-1949.
28. Cansev M.: Uridine and cytidine in the brain: Their transport and utilization. Brain Res. Rev. 2006; 52: 389-339.
29. Cornford E.M., Oldendorf W.H.: Independent blood-brain barrier transport systems for nucleic acid precursors. Biochim. Biophys. Acta 1975; 394: 211-219.
30. van Groeningen C.J., Peters G.J., Pinedo H.M.: Reversal of 5-fluorouracil-induced toxicity by oral administration of uridine. Ann. Oncol. 1993; 4: 317-320.
31. Page T., Yu A., Fontanesi J., Nyhan W.L.: Developmental disorder associated with increased cellular nucleotidase activity. Proc. Natl. Acad. Sci. U S A. 1997; 94(21): 11601-1106.
32. van der Beek E.M., Kamphuis P.: The potential role of nutritional components in the management of Alzheimer’s Disease. Eur. J. Pharmacol. 2008; 585: 197-207.
33. Cansev M., Ulus I.H., Wang L. et al.: Restorative effects of uridine plus docosahexaenoic acid in a rat model of Parkinson’s disease. Neurosci. Res. 2008; 62: 206-209.
34. Wurtman R.J., Cansev M., Ulus I.H.: Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phosphatides. J. Nutr. Health Aging 2009; 13: 189-197.
35. Kamphuis P.J., Wurtman R.J.: Nutrition and Alzheimer’s disease: pre-clinical concepts. Eur. J. Neurol. 2009; 16: 12-18.
36. Myers C.S., Fisher H., Wagner G.C.: Uridine potentiates haloperidol’s disruption of conditioned avoidance responding. Brain Res. 1994; 651: 194-198.
37. Agnati L.F., Fuxe K., Ruggeri M.: Effects of chronic treatment with uridine on striatal dopamine release and dopamine related behaviours in the absence or the presence of chronic treatment with haloperidol. Neurochem. Int. 1989; 15: 107-113.
38. Moszczyński P., Pyć R.: Biochemia witamin. Część I. Witaminy grupy B i koenzymy. PWN, Warszawa–Łódź 1998; 11-201.
39. Ziemlański Ś., Bułhak-Jachymczyk B., Niedźwiecka-Kącik D. et al.: Normy żywienia człowieka. Fizjologiczne podstawy. PZWL, Warszawa 2001: 211-280.
40. Gubler C.J.L: Thiamine. W: Handbook of vitamins (ed. Machlin L.J.). New York 1984.
41. Murray R.K., Granner D.K., Mayes P.A. et al.: Biochemia Harpera. PZWL, Warszawa 1994: 693-708.
42. Depeint F., Bruce W.R., Shangari N. et al.: Mitochondrial function and toxicity: Role of the B vitamin family on mitochondrial energy metabolism. Chem. Biol. Interact. 2006; 163: 94-112.
43. Coimbra C.G., Junquiera V.B.C.: Hight doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parcinsons disease patients. Braz. J. Med. Biol. Res. 2003; 36: 1409-1417.
44. Atamna H.: Heme iron and the mitochondrial decay of ageing. Ageing Res. Rev. 2003; 3: 303-313.
45. Stepuro A.I., Piletskaya T.P., Stepuro I.I. et al.: Thiamin oxidative transformation catalyzed by copper ions and ascorbic acid. Biochem. Russia 1997; 62: 1409-1414.
46. Chawla J., Kvarnberg D.: Hydrosoluble vitamins. Handb. Clin. Neurol. 2014; 120: 891Y914. DOI: 10.1016/B978-0-7020-4087-0.00059-0.
47. Bourgeois C., Cervantes-Laurean D., Moss J.: Niacin. W: Shils M.E., Shike M., Ross A.C. et al. (eds): Modern nutrition in health and disease. 10th ed. Baltimore, MD: Lippincott Williams & Wilkins 2006: 442-451.
48. Sung S., Yao Y., Uryu K. et al.: Early vitamin E supplementation in young but not aged mice reduces Abeta levels and amyloid deposition in a transgenic model of Alzheimer’s disease. FASEB J. 2004; 18(2): 323-325.
49. Mangialasche F., Solomon A., Kåreholt I. et al.: Serum levels of vitamin E forms and risk of cognitive impairment in a Finnish cohort of older adults. Exp. Gerontol. 2013; 48(12): 1428-1435.
50. Dominiak A., Wilkaniec A., Wroczyński P., Adamczyk A.: Selenium in the Therapy of Neurological Diseases. Where is it Going? Curr. Neuropharmacol. 2016; 14(3): 282-229.
2. Scott B.C., Aruoma O.I., Evans P.J. et al.: Lipoic and dihydrolipoic acids as antioxidants. A critical evaluation. Free Radic. Res. 1994; 20: 119-133.
3. Devasagayam T.P., Subramanian M., Pradhan D.S., Sies H.: Prevention of singlet oxygen-induced DNA damage by lipoate. Chem. Biol. Interact. 1993; 86: 79-92.
4. Cenini G., Lloret A., Cascella R.: Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View. Oxidative Medicine and Cellular Longevity 2019.
5. Singh A., Kukreti R., Saso L., Kukreti S.. Oxidative Stress: A Key Modulator in Neurodegenerative Diseases. Molecules 2019; 24(8). pii: E1583. doi: 10.3390/molecules24081583.
6. Liu J., Head E., Gharib A.M. et al.: Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha – lipoic acid. Proc. Natl. Acad. Sci. U S A 2002; 99: 2356-2361.
7. Suh J.H., Shenvi S.V., Dixon B.M. et al.: Decline in transcriptional activity of Nrf2 causes age-related loss of glutathione synthesis, which is reversible with lipoic acid. Proc. Natl. Acad. Sci. U S A 2004; 101: 3381-3386.
8. Lodge J.K., Traber M.G., Packer L.: Thiol chelation of Cu2+ by dihydrolipoic acid prevents human low density lipoprotein peroxidation. Free Radic Biol. Med. 1998; 25: 287-297.
9. Anuradha B., Varalakshmi P.: Protective role of DL-alpha-lipoic acid against mercury-induced neural lipid peroxidation. Pharmacol. Res. 1999; 39: 67-80.
10. Han D., Sen C.K., Roy S. et al.: Protection against glutamate-induced cytotoxicity in C6 glial cells by thiol antioxidants. Am. J. Physiol. 1997; 273: R1771-1778.
11. Streeper R.S., Henriksen E.J., Jacob S. et al.: Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am. J. Physiol. 1997; 273: E185-191.
12. Hughes V.A., Fiatarone M.A., Fielding R.A. et al.: Exercise increases muscle GLUT-4 levels and insulin action in subjects with impaired glucose tolerance. Am. J. Physiol. 1993; 264: E855-E862.
13. Jacob S., Streeper R.S., Fogt D.L. et al.: The antioxidant alpha-lipoic acid enhances insulin-stimulated glucose metabolism in insulin-resistant rat skeletal muscle. Diabetes 1996; 45: 1024-1029.
14. Jacob S., Henriksen E.J., Schiemann A.L. et al.: Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung 1995; 45: 872-874.
15. Konrad T., Vicini P., Kusterer K. et al.: alpha-lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes. Diabetes Care 1999; 22: 280-287.
16. Marracci G.H., Marquardt W.E., Strehlow A. et al.: Lipoic acid downmodulates CD4 from human T lymphocytes by dissociation of p56(Lck). Biochem. Biophys. Res. Commun. 2006; 344: 963-971.
17. Schillace R.V., Pisenti N., Pattamanuch N. et al.: Lipoic acid stimulates cAMP production in T lymphocytes and NK cells. Biochem. Biophys. Res. Commun. 2007; 354: 259-264.
18. Larghero P., Vene R., Minghelli S. et al.: Biological assays and genomic analysis reveal lipoic acid modulation of endothelial cell behavior and gene expression. Carcinogenesis 2007; 28: 1008-1020.
19. He Y., Sanderson I.R., Walker W.A.: Uptake, transport and metabolism of exogenous nucleo-sides in intestinal epithelial cell cultures. J. Nutr. 1994; 124: 1942-1949.
20. Ikeda U., Ito T., Shimada K.: Interleukin-6 and acute coronary syndrome. Clin. Cardiol. 2001; 24: 701-704.
21. Battisti E., Albanese A., Guerra L.: Alpha lipoic acid and superoxide dismutase in the treatment of chronic low back pain. Eur. J. Phys. Rehabil. Med. 2013; 49: 1-6.
22. Monroy Guízar E.A., García Benavides L., Ambriz Plascencia A.R. et al.: Effect of Alpha-Lipoic Acid on Clinical and Neurophysiologic Recovery of Carpal Tunnel Syndrome: A Double-Blind, Randomized Clinical Trial. J. Med. Food Vol. 2018; 21(5).
23. Connolly G.P., Duley J.A.: Uridine and its nucleotides: biological actions, therapeutic potentials. Trends Pharmacol. Sci. 1999; 20: 218-225.
24. Kondo D.G., Sung Y.H., Hellem T.L. et al.: Open-Label Uridine for Treatment of Depressed Adolescents with Bipolar Disorder. J. Child Adolesc. Psychopharmacol. 2011; 21(2): 171-175.
25. Carlezon W.A., Mague S.D., Parow A.M. et al.: Antidepressant-like effects of uridine and omega-3 fatty acids are potentiated by combined treatment in rats. Biol. Psychiatry 2005; 57(4): 343-350.
26. Grimble G.K.: Dietary nucleotides and gut mucosal defence. Gut 1994; 35: S46-51.
27. He Y., Sanderson I. R., Walker W.A.: Uptake, transport and metabolism of exogenous nucleo-sides in intestinal epithelial cell cultures. J. Nutr. 1994; 124: 1942-1949.
28. Cansev M.: Uridine and cytidine in the brain: Their transport and utilization. Brain Res. Rev. 2006; 52: 389-339.
29. Cornford E.M., Oldendorf W.H.: Independent blood-brain barrier transport systems for nucleic acid precursors. Biochim. Biophys. Acta 1975; 394: 211-219.
30. van Groeningen C.J., Peters G.J., Pinedo H.M.: Reversal of 5-fluorouracil-induced toxicity by oral administration of uridine. Ann. Oncol. 1993; 4: 317-320.
31. Page T., Yu A., Fontanesi J., Nyhan W.L.: Developmental disorder associated with increased cellular nucleotidase activity. Proc. Natl. Acad. Sci. U S A. 1997; 94(21): 11601-1106.
32. van der Beek E.M., Kamphuis P.: The potential role of nutritional components in the management of Alzheimer’s Disease. Eur. J. Pharmacol. 2008; 585: 197-207.
33. Cansev M., Ulus I.H., Wang L. et al.: Restorative effects of uridine plus docosahexaenoic acid in a rat model of Parkinson’s disease. Neurosci. Res. 2008; 62: 206-209.
34. Wurtman R.J., Cansev M., Ulus I.H.: Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phosphatides. J. Nutr. Health Aging 2009; 13: 189-197.
35. Kamphuis P.J., Wurtman R.J.: Nutrition and Alzheimer’s disease: pre-clinical concepts. Eur. J. Neurol. 2009; 16: 12-18.
36. Myers C.S., Fisher H., Wagner G.C.: Uridine potentiates haloperidol’s disruption of conditioned avoidance responding. Brain Res. 1994; 651: 194-198.
37. Agnati L.F., Fuxe K., Ruggeri M.: Effects of chronic treatment with uridine on striatal dopamine release and dopamine related behaviours in the absence or the presence of chronic treatment with haloperidol. Neurochem. Int. 1989; 15: 107-113.
38. Moszczyński P., Pyć R.: Biochemia witamin. Część I. Witaminy grupy B i koenzymy. PWN, Warszawa–Łódź 1998; 11-201.
39. Ziemlański Ś., Bułhak-Jachymczyk B., Niedźwiecka-Kącik D. et al.: Normy żywienia człowieka. Fizjologiczne podstawy. PZWL, Warszawa 2001: 211-280.
40. Gubler C.J.L: Thiamine. W: Handbook of vitamins (ed. Machlin L.J.). New York 1984.
41. Murray R.K., Granner D.K., Mayes P.A. et al.: Biochemia Harpera. PZWL, Warszawa 1994: 693-708.
42. Depeint F., Bruce W.R., Shangari N. et al.: Mitochondrial function and toxicity: Role of the B vitamin family on mitochondrial energy metabolism. Chem. Biol. Interact. 2006; 163: 94-112.
43. Coimbra C.G., Junquiera V.B.C.: Hight doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parcinsons disease patients. Braz. J. Med. Biol. Res. 2003; 36: 1409-1417.
44. Atamna H.: Heme iron and the mitochondrial decay of ageing. Ageing Res. Rev. 2003; 3: 303-313.
45. Stepuro A.I., Piletskaya T.P., Stepuro I.I. et al.: Thiamin oxidative transformation catalyzed by copper ions and ascorbic acid. Biochem. Russia 1997; 62: 1409-1414.
46. Chawla J., Kvarnberg D.: Hydrosoluble vitamins. Handb. Clin. Neurol. 2014; 120: 891Y914. DOI: 10.1016/B978-0-7020-4087-0.00059-0.
47. Bourgeois C., Cervantes-Laurean D., Moss J.: Niacin. W: Shils M.E., Shike M., Ross A.C. et al. (eds): Modern nutrition in health and disease. 10th ed. Baltimore, MD: Lippincott Williams & Wilkins 2006: 442-451.
48. Sung S., Yao Y., Uryu K. et al.: Early vitamin E supplementation in young but not aged mice reduces Abeta levels and amyloid deposition in a transgenic model of Alzheimer’s disease. FASEB J. 2004; 18(2): 323-325.
49. Mangialasche F., Solomon A., Kåreholt I. et al.: Serum levels of vitamin E forms and risk of cognitive impairment in a Finnish cohort of older adults. Exp. Gerontol. 2013; 48(12): 1428-1435.
50. Dominiak A., Wilkaniec A., Wroczyński P., Adamczyk A.: Selenium in the Therapy of Neurological Diseases. Where is it Going? Curr. Neuropharmacol. 2016; 14(3): 282-229.