Homocysteine and Asymmetric Dimethylarginine (ADMA) in Neurological Diseases
DOI:
https://doi.org/10.24297/jac.v6i2.6584Keywords:
Biothiols, dimethylarginine, pathogenesis, therapy effectsAbstract
Homocysteine (Hcy) is formed from methionine (Met) and is distributed in two metabolic pathways: in the process of remethylation to Met and in the process of transsulfuration to cysteine. Hyperhomocysteinemia (HHcy) is a risk factor for cardiovascular and neurological diseases such as: Alzheimer’s and Parkinson’s diseases, multiple sclerosis, and stroke. Increased Hcy level may lead to endothelial dysfunction due to impaired bioavailability of endothelium-derived nitric oxide (NO). The molecular mechanism decreasing the levels of NO in HHcy conditions is incompletely understood, but it seems that asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, may be a key factor. ADMA is formed from L-arginine by enzymes in the family of protein N-methyltransferases (PRMT) and may undergo hydrolysis to L-citrulline and dimethylamine with the participation of dimethylaminohydrolase (DDAH). In pathological conditions such as neurodegenerative diseases, Hcy may lead to increased ADMA concentrations by inhibiting the activity of DDAH. Several drugs, such L-dopa, antiepileptic drugs, and lipid-lowering drugs, may interfere with the metabolic pathways of thiols, leading to an alteration of plasma Hcy and ADMA levels. It seems that administration of L-arginine, in conjunction with B vitamins, to patients with HHcy may be a new method in the treatment of neurodegenerative diseases.
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References
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[18] Boysen, G., Brander, T., Christensen, H., Gideon, R. and Truelsen, T. 2003. Homocysteine and risk of recurrent stroke. Stroke 34 (May 2003), 1258-1261.
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[23] Fuso, A., Seminara, L., Cavallaro, R.A., D'Anselmi, F. and Scarpa, S. 2005. S-adenosylmethionine/homocysteine cycle alterations modify DNA methylation status with consequent deregulation of PS1 and BACE and beta-amyloid production. Mol. Cell Neurosci. 28 (Jan. 2005), 195-204.
[24] Borowczyk, K., Tisonczyk, J. and Jakubowski, H. 2012. Metabolism and neurotoxicity of homocysteine thiolactone in mice: protective role of bleomycin hydrolase. Amino Acids 43 (Sep. 2012), 1339-1348.
[25] Boger, R.H., Bode-Boger, S.M., Sydow, K., Heistad, D.D. and Lentz, S.R. 2000. Plasma concentration of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, is elevated in monkeys with hyperhomocyst(e)inemia or hypercholesterolemia. Arterioscler. Thromb. Vasc. Biol. 20 ( 2000), 1557-1564.
[26] Smith, M.A., Vasák, M., Knipp, M., Castellani, R.J. and Perry, G. 1998. Dimethylargininase, a nitric oxide regulatory protein, in Alzheimer disease. Free Radic. Biol. Med. 25 (Nov. 1998), 898-902.
[27] Selley, M.L. 2003. Increased concentration of homocysteine and asymmetric dimethylarginine and decreased concentrations of nitric oxide in the plasma of patients with Alzheimer’s disease. Neurobiol. Aging 24 (Nov. 2003), 903-907.
[28] de la Torre, J.C. 2002. Alzheimer disease as a vascular disorder: nosological evidence. Stroke 33 (Apr. 2002), 1152-1162.
[29] Chen, M., Jiang, P., Lu, J., Xiang, Z.H. and Jiao, B.H. 2010. The correlation of asymmetrical dimethylarginine level and oxidative stress to the onset of Alzheimer's disease. Yao Xue Xue Bao 45 (Aug. 2010), 1001-1005.
[30] Gorell, J.M., Johnson, C.C. and Rybicki, B.A. 1994. Parkinson’s disease and its comorbid disorders: an analysis of Michigan mortality data, 1970 to 1990. Neurology 44 (Oct. 1994), 1865-1868.
[31] Muller, T. 2008. Role of homocysteine in the treatment of Parkinson’s disease. Expert. Rev. Neurother. 8 ( 2008), 957-967.
[32] Duan, W., Ladenheim, B., Cutler, R.G., Kruman, I.I., Cadet, J.L. and Mattson, M.P. 2002. Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson’s disease. J. Neurochem. 80 (Jan. 2002), 101-110.
[33] Padovan-Neto, F.E., Echeverry, M.B., Tumas, V. and Del-Bel, E.A. 2009. Nitric oxide synthase inhibition attenuates L-DOPA-induced dyskinesias in a rodent model of Parkinson’s disease. Neuroscience 159 (Mar. 2009), 927-935.
[34] Qureshi, G.A., Baig, S., Bednar, I., Södersten, P., Forsberg, G. and Siden, A. 1995. Increased cerebrospinal fluid concentration of nitrite in Parkinson’s disease. Neuroreport 6 (Aug. 1995), 1642-1644.
[35] Turski, L. and Turski, W.A. 1993. Towards an understanding of the role of glutamate in neurodegenerative disorders: energy metabolism and neuropathology. Experimentia 49 (Dec. 1993), 1064-1072.
[36] Teunissen, C.E., Killestein, J., Kragt, J.J., Polman, C.H., Dijkstra, C.D. and Blom, H.J. 2008. Serum homocysteine levels in relation to clinical progression in multiple sclerosis. J. Neurol. Neurosurg. Psychiatry 79 (Dec. 2008), 1349-1353.
[37] Hyka, N., Dayer, J.M., Modoux, C., Kohno, T., Edwards, C.K. 3rd, Roux-Lombard, P. and Burger, D. 2001. Apolipoprotein A-I inhibits the production of interleukin-1beta and tumor necrosis factor-alpha by blocking contact-mediated activation of monocytes by T lymphocytes. Blood 97 (Apr. 2001), 2381-2389.
[38] Hoffmann, S., Tittgemeyer, M. and von Cramon, D.Y. 2007. Cognitive impairment in multiple sclerosis. Curr. Opin. Neurol. 20 (Jun. 2007), 275-280.
[39] Rio, J., Montalban, J., Tintore, M., Codina, A. and Malinow, M.R. 1994. Serum homocysteine levels in multiple sclerosis. Arch. Neurol. 51 (Dec. 1994), 1181.
[40] Sydow, K., Schwedhelm, E., Arakawa, N., Bode-Böger, S.M., Tsikas, D., Hornig, B., Frölich, J.C. and Böger, R.H. 2003. ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins. Cardiovasc. Res. 57 (Jan. 2003), 244-252.
[41] Oz, O., Gokcil, Z., Bek, S., Cakir, E. and OdabaÅŸi, Z. 2009. Is asymmetric dimethylarginine responsible for the vascular events in patients under antiepileptic drug treatment? Epilepsy Res. 87 (Nov. 2009), 54-58.
[42] Sniezawska, A., Dorszewska, J., Rozycka, A., Przedpelska-Ober, E., Lianeri, M., Jagodziński, P.P. and Kozubski, W. 2011. MTHFR, MTR, and MTHFD1 gene polymorphisms compared to homocysteine and asymmetric dimethylarginine concentrations and their metabolites in epileptic patients treated with antiepileptic drugs. Seizure 20 (Sep. 2011), 533-540.[43] Bochynska, A., Lipczynska-Lojkowska, W., Gugala-Iwaniuk, M., Lechowicz, W., Restel, M., Graban, A., Lipska, B. and Gryglewicz, D. 2012. The effect of vitamin B supplementation on homocysteine metabolizm and clinical state of patients with chronic epilepsy treated with carbamazepine and valproic acid. Seizure 21 (May 2011), 276-281.
[44] Jonasson, T.F., Hedner, T., Hultberg, B. and Ohlin, H. 2003. Hyperhomocysteinaemia is not associated with increased levels of asymmetric dimethylarginine in patients with ischaemic heart disease. Eur. J. Clin. Invest. 33 (Jul. 2003), 543-549.
[45] Wanby, P., Brattstrom, L., Brudin, L., Hultberg, B. and Teerlink, T. 2003. Asymmetric dimethylarginine and total homocysteine in plasma after oral methionine loading. Scand. J. Clin. Lab. Invest. 63, 347-353.
[46] Mattson, M.P. 2008. Glutamate and neurotrophic factors in neuronal plasticity and disease. Ann. NY Acad. Sci. 1144 (Nov. 2008), 97-112.
[47] Dayal, S. and Lentz, S.R. 2005. ADMA and hyperhomocysteinemia. Vasc. Med. 10 ( 2005), Suppl 1, 27-33.
[48] Maas, R. 2005. Pharmacotherapies and their influence on asymmetric dimethylarginine (ADMA). Vasc. Med. 10, 49-57.
[49] Dorszewska, J., Winczewska-Wiktor, A., Sniezawska, A., Kaczmarek, I. and Steinborn, B. 2009. Homocysteine and asymmetric dimethylarginine (ADMA) in epilepsy. Prz. Lek. 66, 448-452 (in polish
[2] Mamatha, S.N., Nagaraja, D., Philip, M. and Christopher, R. 2011. Asymmetric dimethylarginine as a risk marker for early-onset ischemic stroke in Indian population. Clin. Chim. Acta 412 (Jan. 2011), 139-142.
[3] Rueda-Clausen, C.F., Córdoba-Porras, A., Bedoya, G., Silva, F.A., Zarruk, J.G., López-Jaramillo, P. and Villa, L.A. 2012. Increased plasma levels of total homocysteine but not asymmetric dimethylarginine in Hispanic subjects with ischemic stroke FREC-VI sub-study. Eur. J. Neurol. 19 (Mar. 2012), 417-425.
[4] Selley, M.L. 2004. Homocysteine increases the production of asymmetric dimethylarginine in cultured neurons. J. Neurosci. Res. 77 (Jul. 2004), 90-93.
[5] Arlt, S., Schulze, F., Eichenlaub, M., Maas, R., Lehmbeck, J.T., Schwedhelm, E., Jahn, H. and Böger, R.H. 2008. Asymmetrical dimethylarginine is increased in plasma and decreased in cerebrospinal fluid of patients with Alzheimer's disease. Dement. Geriatr. Cogn. Disord. 26, 58-64.
[6] Dorszewska, J., Florczak, J., Jaroszewska-Kolecka, J. and Kozubski W. 2008. Homocysteine and asymmetric dimethylarginine (ADMA) in the plasma of patients with Alzheimer's disease. Folia Neuropathol. 46, 296-297.
[7] Dorszewska, J. and Kozubski, W. 2011. Oxidative DNA damage and the level of biothiols, and L-dopa therapy in Parkinson’s disease. In: Qayyum Rana, A. (Ed.) Etiology and Pathophysiology of Parkinson's Disease, InTech, pp. 349-372.
[8] Rawal, N., Lee, Y.J., Whitaker, J.N., Park JO, Paik, W.K. and Kim, S. 1995. Urinary secretion of NG-dimethylarginines in multiple sclerosis patients: preliminary observations. J. Neurol. Sci. 129 (Apr. 1995), 186-191.
[9] Masuda, H. and Azuma, H. 2002. Biological and pathophysiological roles of endogenous methylarginines as inhibitors of nitric oxide synthase. Nihon Yakurigaku Zasshi 119, 29-35.
[10] Triantafyllou, N., Evangelopoulos, M.E., Kimiskidis, V.K., Kararizou, E., Boufidou, F., Fountoulakis, K.N., Siamouli, M., Nikolaou, C., Sfagos, C., Vlaikidis, N. and Vassilopoulos, D. 2008. Increased plasma homocysteine levels in patients with multiple sclerosis and depression. Ann. Gen. Psychiatry 7 (Sep. 2008), 17.
[11] Siniscalchi, A., Mancuso, F., Gallelli, L., Ferreri Ibbadu, G., Biagio Mercuri, N. and De Sarro, G. 2005. Increase in plasma homocysteine levels induced by drug treatments in neurologic patients. Pharmacol. Res. 52 (Nov. 2005), 367-375.
[12] McCarty, M.F. 2004. Vascular endothelium is the organ chiefly responsible for the catabolism of plasma asymmetric dimethylarginine-an explanation for the elevation of plasma ADMA in disorders characterized by endothelial dysfunction. Med. Hypotheses 63 ( 2004), 699-708.
[13] Lu, T.M., Ding, Y.A., Leu, H.B., Yin, W.H., Sheu, W.H. and Chu, K.M. 2004. Effect of rosuvastatin on plasma levels of asymmetric dimethylarginine in patients with hypercholesterolemia. Am. J. Cardiol. 94 (Jul. 2004), 157-161.
[14] Oguz, A. and Uzunlulu, M. 2008. Short term fluvastatin treatment lowers serum asymmetric dimethylarginine levels in patients with metabolic syndrome. Int. Heart J. 49 (May 2008), 303-311.
[15] Rho, J., Choi, S., Seong, Y.R., 2001. Prmt5, which forms distinct homo-oligomers, is a member of the protein-arginine methyltransferase family. J. Biol. Chem. 276 (Apr. 2001), 11393-11401.
[16] Leiper, J.M., Santa Maria, J., Chubb, A., MacAllister, R.J., Charles, I.G., Whitley, G.S. and Vallance, P. 1999. Identification of two human dimethylarginine dimethylaminohydrolases with distinct tissue distributions and homology with microbial arginine deiminases. Biochem. J. 343 (Oct. 1999), 209-214.
[17] Ueda, S., Kato, S., Matsuoka, H., Kimoto, M., Okuda, S., Morimatsu, M. and Imaizumi, T. 2003. Regulation of cytokine-induced nitric oxide synthesis by asymmetric dimethylarginine: role of dimethylarginine dimethylaminohydrolase. Circ. Res. 92 (Feb. 2003), 226-33.
[18] Boysen, G., Brander, T., Christensen, H., Gideon, R. and Truelsen, T. 2003. Homocysteine and risk of recurrent stroke. Stroke 34 (May 2003), 1258-1261.
[19] van Guldener, C., Nanayakkara, P.W. and Stehouwer, C.D. 2007. Homocysteine and asymmetric dimethylarginine (ADMA): biochemically linked but differently related to vascular disease in chronic kidney disease. Clin. Chem. Lab. Med. 45, 1683-1687.
[20] Nanayakkara, P.W., Kiefte-de Jong, J.C., ter Wee, P.M., Stehouwer, C.D., van Ittersum, F.J., Olthof, M.R., Teerlink, T., Twisk, J.W., van Guldener, C. and Smulders, Y.M. 2009. Randomized placebo-controlled trial assessing a treatment strategy consisting of pravastatin, vitamin E, and homocysteine lowering on plasma asymmetric dimethylarginine concentration in mild to moderate CKD. Am. J. Kidney Dis. 53 (Jan. 2009), 41-50.[21] Seshadri, S., Beiser, A., Selhub, J., Jacques, P.F., Rosenberg, I.H., D'Agostino, R.B., Wilson, P.W. and Wolf, P.A. 2002. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. N. Engl. J. Med. 346 (Feb. 2002), 476-483.
[22] Dorszewska, J., Florczak-Wyspianska, J., Oczkowska, A., Dezor, M., Prendecki M. and Kozubski W. 2013. Homocysteine and asymmetric dimethylarginine concentrations in the plasma of Alzheimer's disease patients with varying degrees of dementia. Adv. Alzheimers Dis. 1, 1-6.
[23] Fuso, A., Seminara, L., Cavallaro, R.A., D'Anselmi, F. and Scarpa, S. 2005. S-adenosylmethionine/homocysteine cycle alterations modify DNA methylation status with consequent deregulation of PS1 and BACE and beta-amyloid production. Mol. Cell Neurosci. 28 (Jan. 2005), 195-204.
[24] Borowczyk, K., Tisonczyk, J. and Jakubowski, H. 2012. Metabolism and neurotoxicity of homocysteine thiolactone in mice: protective role of bleomycin hydrolase. Amino Acids 43 (Sep. 2012), 1339-1348.
[25] Boger, R.H., Bode-Boger, S.M., Sydow, K., Heistad, D.D. and Lentz, S.R. 2000. Plasma concentration of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, is elevated in monkeys with hyperhomocyst(e)inemia or hypercholesterolemia. Arterioscler. Thromb. Vasc. Biol. 20 ( 2000), 1557-1564.
[26] Smith, M.A., Vasák, M., Knipp, M., Castellani, R.J. and Perry, G. 1998. Dimethylargininase, a nitric oxide regulatory protein, in Alzheimer disease. Free Radic. Biol. Med. 25 (Nov. 1998), 898-902.
[27] Selley, M.L. 2003. Increased concentration of homocysteine and asymmetric dimethylarginine and decreased concentrations of nitric oxide in the plasma of patients with Alzheimer’s disease. Neurobiol. Aging 24 (Nov. 2003), 903-907.
[28] de la Torre, J.C. 2002. Alzheimer disease as a vascular disorder: nosological evidence. Stroke 33 (Apr. 2002), 1152-1162.
[29] Chen, M., Jiang, P., Lu, J., Xiang, Z.H. and Jiao, B.H. 2010. The correlation of asymmetrical dimethylarginine level and oxidative stress to the onset of Alzheimer's disease. Yao Xue Xue Bao 45 (Aug. 2010), 1001-1005.
[30] Gorell, J.M., Johnson, C.C. and Rybicki, B.A. 1994. Parkinson’s disease and its comorbid disorders: an analysis of Michigan mortality data, 1970 to 1990. Neurology 44 (Oct. 1994), 1865-1868.
[31] Muller, T. 2008. Role of homocysteine in the treatment of Parkinson’s disease. Expert. Rev. Neurother. 8 ( 2008), 957-967.
[32] Duan, W., Ladenheim, B., Cutler, R.G., Kruman, I.I., Cadet, J.L. and Mattson, M.P. 2002. Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson’s disease. J. Neurochem. 80 (Jan. 2002), 101-110.
[33] Padovan-Neto, F.E., Echeverry, M.B., Tumas, V. and Del-Bel, E.A. 2009. Nitric oxide synthase inhibition attenuates L-DOPA-induced dyskinesias in a rodent model of Parkinson’s disease. Neuroscience 159 (Mar. 2009), 927-935.
[34] Qureshi, G.A., Baig, S., Bednar, I., Södersten, P., Forsberg, G. and Siden, A. 1995. Increased cerebrospinal fluid concentration of nitrite in Parkinson’s disease. Neuroreport 6 (Aug. 1995), 1642-1644.
[35] Turski, L. and Turski, W.A. 1993. Towards an understanding of the role of glutamate in neurodegenerative disorders: energy metabolism and neuropathology. Experimentia 49 (Dec. 1993), 1064-1072.
[36] Teunissen, C.E., Killestein, J., Kragt, J.J., Polman, C.H., Dijkstra, C.D. and Blom, H.J. 2008. Serum homocysteine levels in relation to clinical progression in multiple sclerosis. J. Neurol. Neurosurg. Psychiatry 79 (Dec. 2008), 1349-1353.
[37] Hyka, N., Dayer, J.M., Modoux, C., Kohno, T., Edwards, C.K. 3rd, Roux-Lombard, P. and Burger, D. 2001. Apolipoprotein A-I inhibits the production of interleukin-1beta and tumor necrosis factor-alpha by blocking contact-mediated activation of monocytes by T lymphocytes. Blood 97 (Apr. 2001), 2381-2389.
[38] Hoffmann, S., Tittgemeyer, M. and von Cramon, D.Y. 2007. Cognitive impairment in multiple sclerosis. Curr. Opin. Neurol. 20 (Jun. 2007), 275-280.
[39] Rio, J., Montalban, J., Tintore, M., Codina, A. and Malinow, M.R. 1994. Serum homocysteine levels in multiple sclerosis. Arch. Neurol. 51 (Dec. 1994), 1181.
[40] Sydow, K., Schwedhelm, E., Arakawa, N., Bode-Böger, S.M., Tsikas, D., Hornig, B., Frölich, J.C. and Böger, R.H. 2003. ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins. Cardiovasc. Res. 57 (Jan. 2003), 244-252.
[41] Oz, O., Gokcil, Z., Bek, S., Cakir, E. and OdabaÅŸi, Z. 2009. Is asymmetric dimethylarginine responsible for the vascular events in patients under antiepileptic drug treatment? Epilepsy Res. 87 (Nov. 2009), 54-58.
[42] Sniezawska, A., Dorszewska, J., Rozycka, A., Przedpelska-Ober, E., Lianeri, M., Jagodziński, P.P. and Kozubski, W. 2011. MTHFR, MTR, and MTHFD1 gene polymorphisms compared to homocysteine and asymmetric dimethylarginine concentrations and their metabolites in epileptic patients treated with antiepileptic drugs. Seizure 20 (Sep. 2011), 533-540.[43] Bochynska, A., Lipczynska-Lojkowska, W., Gugala-Iwaniuk, M., Lechowicz, W., Restel, M., Graban, A., Lipska, B. and Gryglewicz, D. 2012. The effect of vitamin B supplementation on homocysteine metabolizm and clinical state of patients with chronic epilepsy treated with carbamazepine and valproic acid. Seizure 21 (May 2011), 276-281.
[44] Jonasson, T.F., Hedner, T., Hultberg, B. and Ohlin, H. 2003. Hyperhomocysteinaemia is not associated with increased levels of asymmetric dimethylarginine in patients with ischaemic heart disease. Eur. J. Clin. Invest. 33 (Jul. 2003), 543-549.
[45] Wanby, P., Brattstrom, L., Brudin, L., Hultberg, B. and Teerlink, T. 2003. Asymmetric dimethylarginine and total homocysteine in plasma after oral methionine loading. Scand. J. Clin. Lab. Invest. 63, 347-353.
[46] Mattson, M.P. 2008. Glutamate and neurotrophic factors in neuronal plasticity and disease. Ann. NY Acad. Sci. 1144 (Nov. 2008), 97-112.
[47] Dayal, S. and Lentz, S.R. 2005. ADMA and hyperhomocysteinemia. Vasc. Med. 10 ( 2005), Suppl 1, 27-33.
[48] Maas, R. 2005. Pharmacotherapies and their influence on asymmetric dimethylarginine (ADMA). Vasc. Med. 10, 49-57.
[49] Dorszewska, J., Winczewska-Wiktor, A., Sniezawska, A., Kaczmarek, I. and Steinborn, B. 2009. Homocysteine and asymmetric dimethylarginine (ADMA) in epilepsy. Prz. Lek. 66, 448-452 (in polish
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2017-04-24
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Dorszewska, J. (2017). Homocysteine and Asymmetric Dimethylarginine (ADMA) in Neurological Diseases. JOURNAL OF ADVANCES IN CHEMISTRY, 6(2), 930–939. https://doi.org/10.24297/jac.v6i2.6584
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