OKSİDATİF STRES VE PARKİNSON HASTALIĞI

Yıl 2019, Cilt: 43 Sayı: 1, 94 - 116, 31.01.2019

Selma Nergis Aslan , Bensu Karahalil

Öz

            Amaç: Parkinson Hastalığı (PH) beyinde dopaminerjik
nöronların kaybıyla ilişkili kronik ve progresif nörodejeneratif bir
hastalıktır. Yaşlılık tüm nörodejeneratif hastalıklarda olduğu gibi PH’nın
oluşumunda da kanıtlanmış tek faktördür. Yaşlılıkta daha fazla tetiklenen
oksidatif stresin dopaminerjik nörotoksisite oluşumunda önemli bir rol oynadığı
düşünülmektedir. Bu derlemede oksidatif stres ve PH arasındaki ilişki
irdelenecektir.

        Gereç ve Yöntem: PH ile
oksidatif stres arasındaki ilişkinin tespiti için yapılmış çalışmaların
kapsamlı olarak derlenebilmesi için sağlık bilimleri alanındaki veri tabanları
kullanılmıştır. Web of Science gibi temel atıf indekslerinde daha önce
yayımlanmış makalelerden yararlanılmıştır.

        Sonuç ve Tartışma: Parkinson
çok sayıda temel hücresel süreci etkileyen genetik ve çevresel faktörlerin
kompleks etkileşiminden kaynaklanan nörodejeneratif bir hastalıktır. Oksidatif
stres genetik bütünlüğü tehdit eder ve PH’nın gelişimine katkı sağlar.
Oksidatif strese bağlı olarak meydana gelen hasar ürünlerinden kaçınmak ve bu
çizgide koruyucu tedavi protokolü çizmek sağlıklı beyin fonksiyonlarının devamı
ve organizmayı Parkinson gibi nörodejeneratif hastalıklardan korumak adına önemli
bir strateji olabilir.

Anahtar Kelimeler

Parkinson hastalığı (PH), oksidatif stres, reaktif oksijen türler (ROT), yaşlanma, nörodejeneratif hastalık

OXIDATIVE STRESS AND PARKINSON DISEASE

Öz

         Objective: Parkinson's
Disease (PD) is a chronic and progressive neurodegenerative disease in the
brain associated with the loss of dopaminergic neurons. Old age is the only
proven factor in the development of PD. It is thought that oxidative stress
which is more triggered in old age plays a vital role in the formation of
dopaminergic neurotoxicity. In this review, the relationship between oxidative
stress and PD will be examined.

        Material and Method: The databases in the health sciences field were
used to compile the studies conducted to determine the relationship between PH
and oxidative stress. Previously published articles such as Web of Science have
been used.

        Result and Discussion: Parkinson's is a neurodegenerative disease
resulting from the complex interaction of genetic and environmental factors that
affect on many basic cellular process. Oxidative stress threatens genetic
integrity and contributes to the development of PH. Avoiding
damage products due to oxidative stress and drawing a protective treatment
protocol may be a crucial strategy for maintaining healthy brain function and
protecting the organism from neurodegenerative diseases such as Parkinson's
disease.

Anahtar Kelimeler

Parkinson's disease (PD), oxidative stress, reactive oxygen species (ROS), aging, neurodegenerative disease

Kaynakça

• Hipkiss, A.R. (2007). Biological aspects of ageing. El Sevier Psychiatry, 6(12), 476-79, https://doi.org/10.1016/j.mppsy.2007.09.003.
• Skinner, J.S. (2005). Exercise testing and exercise prescription for special cases: theoretical basis and clinical application, (Ed.), Lippincott Williams & Wilkins, Baltimore.
• Amor, S., Peferoen, L.A., Vogel, D.Y., Breur, M., van der Valk, P., Baker, D., van Noort J.M. (2013). Inflammation in neurodegenerative diseases – an update. Immunology,142,151-166
• Radak, Z., Zhao, Z., Goto, S., Koltai, E. (2011). Age-associated neurodegeneration and oxidative damage to lipids, proteins and DNA. Molecular Aspect of Medicine, 32, 305-315
• Aydın, A. (2015) Oksidanlar&Antioksidanlar. Yeditepe Üniversitesi Sağlık Bilimleri Enstitüsü, Turkheltox Toksikoloji Kongresi; 2015 Ekim 21-24; İzmir.
• Dorsey, E.R., Constantinescu, R., Thompson J.P., Biglan, K.M., Holloway R.G., Kieburtz K., Marshall, F.J., Ravina, B.M., Schifitto, G., Siderowf, A., Tanner, C.M. (2007) Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030. Neurology, 68 (5), 384-6
• Willis, A., Evanoff, B.A., Lian, M., Criswell, S.R., Racetta, B.A. (2010). Geographic and Ethnic Variation in Parkinson Disease: A Population-Based Study of US Medicare Beneficiaries. Neuroepide, 4 (3), 143-51
• Olanow, C.W., Brundin, P. (2013). Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion-Like Disorder? Movement Disorders, 28(1), 31-4. Retrieved February 6,2013 from https://doi.org/10.1002/mds.25373.
• Olanow, C.W., Kordower, J.H., Lang, A.E., Obeso, J.A. (2009). Dopaminergic transplantation for Parkinson’s disease: Current status and future prospects. Annals of Neurology, 66 (5), 591-6
• Kalia, L.V., Lang, A.E. (2015). Parkinson’s Disease. Lancet, 386 (9996), 896-912
• Gazewood, J.D., Richard, D.R.,Clebak, K. (2013). Parkinson Disease: an update. Am.Fam.Physician, 87 (4), 267-273
• Hou, Y., Zhang, J., Chen, B., Wu, T. (2015). Local brain activity in different motor subtypes of Parkinson's disease with fMRI, Europe PMC, 95 (7), 483-8
• Connoly, B.S., Lang, A.E. (2014). Pharmacological treatment of Parkinson disease: a review. JAMA, 311 (16), 1670-83.
• Lev, N., Melamed, E. (2001). Heredity in Parkinson's Disease: New Findings. IMAJ, 3, 435-438
• Langston, J.W., Ballard, P., Tetrud, J.W., Irwin, I. (1983). Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. Science, 219 (4587), 979-80.
• Richards, R. I, Robertson, S. A, O'Keefe, L. V, Fornarino D, Scott A, Lardelli M, & Baune B.T. (2016). The Enemy Within: Innate Surveillance-mediated Cell Death, the common mechanism of neurodegenerative disease. Frontiers in Neuroscience, 10, 193. Retrieved May 10, 2016 from https://doi.org/10.3389/fnins.2016.00193.
• Uttara, B.,Singh, A.V., Zamboni, P., Mahajan, R.T. (2009). Bentham Science Publishers Ltd. Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options. Current Neuropharmacology,7, 65-74
• Bolisetty, S., Jaimes, E.A. (2013). Mitochondria and reactive oxygen species: physiology and pathophysiology. International Journal of Molecular Science, 14 (3), 6306-44.
• Ding, Y., Chen, J., Okon, I.S., Zou, M.H., Song, P. (2016). Absence of AMPKα2 accelerates cellular senescence via p16 induction in mouse embryonic fibroblasts. The International Journal of Biochemistry & Cell Biology, 71, 72-80.
• Kim, G., Kim, J.E., Rhie, S., Yoon, S. (2015). The Role of Oxidative Stress in Neurodegenerative Diseases. Experimental Neurology, 24 (4), 325-340
• Hybertson, B., Gao, B., Bose, S. (2011). Oxydative Stress in Health and Disease. Molecular Aspect of Medicine, 32, 234-246
• Babusikova, E., Evinova, A., Hatok, J., Dobrota, D., Jurecekova, J. (2012). Oxidative Changes and Possible Effects of Polymorphism of Antioxidant Enzymes in Neurodegenerative Disease. Kishore, U(Ed). Neurodegenerative Diseases, DOI: 10.5772/54619. Retrieved May 15, 2016 from https://www.intechopen.com.
• Dizdaroglu, M., Jaruga, P., Birincioglu, M., Rodriguez, H. (2002). Free radical-induced damage to DNA: mechanisms and measurement. Free Radical Biology and Medicine, 32 (11), 1102-15.
• Boiteux, S., Gellon, L., Guibourt, N. Repair of 8-oxoguanine in Saccharomyces cerevisiae: interplay of DNA repair and replication mechanisms. Free Radical Biology of Medicine, 32 (12), 1244-53.
• Hirano, T., Tamae, K. (2012). Differentiation of Embryonic Stem Cells and Oxidative DNA Damage / DNA Repair Systems. Stem Cell Research and Therapy,10:1-5
• De Martinis, B. S., Bianchi, M.D.L.P. (2002). Methodology for urinary 8-hydroxy-2′-deoxyguanosine analysis by HPLC with electrochemical detection. Pharmacolological Research, 46 (2), 129-131.
• Sheng, Z., Oka, S., Tsuchimoto, D.,Abolhassani, N.,Nomaru, H.,Sakumi, K., Yamada, H., Nakabeppu, Y. (2012). 8-Oxoguanine causes neurodegeneration during MUTYH-mediated DNA base excision repair. The Journal of Clinical Investigation, 122, 4344-4361.
• Luo, Y., Hoffer, A., Hoffer, B. (2015). Mitochondria: A Therapeutic Target for Parkinson’s Disease? International Journal of Molecular Sciences, 16, 20704-20730.
• Calabrese, V., Lodi, R., Tonon, C. (2005). Oxidative stress, mitochondrial dysfunction and cellular stress response in Friedreich’s ataxia. International Journal of Molecular Sciences, 233, 145-162.
• Büeler, H. (2009). Impaired Mitokondrial Dynamics and Function in the Pathogenesis of Parkinson Disease. Experimental Neurology, 218, 235-246.
• Stockum, S., Nardin, A., Schrepfer, E. (2016). Mitochondrial dynamics and mitophagy in Parkinson's disease: A fly point of view. Neurological Disease, 90, 58-67.
• Reed, T. (2011). Lipid peroxidation and neurodegenerative disease. Free Radical Biology of Medicine, 51, 1302-1319
• Azevedo, F.A., Carvalho, L.R., Grinberg, L.T., Farfel, J.M., Ferretti, R.E, Leite, R.E., Jacob, Filho W. (2009). Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain, The Journal of Comparative Neurology, 513 (5), 532-41.
• Amor, S., Puentes, F., Baker, D., van der Valk, P. (2010). Inflammation in Neurodegenerative Diseases. Immunology, 129 (2), 154-69.
• Fischer, R., Maier, O. (2015). Interrelation of oxidative stress and inflammation in neurodegenerative disease: role of TNF. Oxidative Medicine and Cellular Longevity, 610813.
• Dias, V., Junn, E., Mouradian, M.M. (2013). The role of oxidative stress in Parkinson's disease. Journal of Parkinson’sDisease, (4), 461-91. Retrieved2013from https://content.iospress.com/articles/journal-of-parkinsons-disease/jpd130230.
• Gao, H.M., Zhang, F., Zhou, H., Kam, W., Wilson, B., Hong, J.S. (2011). Neuroinflammation and α-synuclein dysfunction potentiate each other, driving chronic progression of neurodegeneration in a mouse model of Parkinson's disease. Environmental Health Perspective,119 (6), 807-14.
• Hofman, F.M., Hinton, D.R., Johnson, K., Merrill, J.E. (1989). Tumor necrosis factor identified in multiple sclerosis brain. Journal of Experimental Medicine,170 (2), 607-12.
• McCoy, M.K., Tansey, M.G. (2008). TNF signaling inhibition in the CNS: implications for normal brain function and neurodegenerative disease. Journal of Neuroinflammation,5, 45.
• Segura-Aguilar, J., Paris, I., Munoz, P., Ferrari, E., Zecca, L., Zucca, F.A. (2014). Protective and toxic roles of dopamine in Parkinson's disease. J Neurochem, 129 (6), 898-915.
• Zucca, F.A., Basso, E., Cupaioli, F.A., Ferrari, E., Sulzer, D., Casella, L., Zecca, L.(2014). Neuromelanin of the human substantia nigra: an update. Neurotoxicity Research, 25 (1), 13-23.
• Caudle, W.M., Richardson, J.R., Wang, M.Z., Taylor, T.N., Guillot, T.S., McCormack, A.L., Colebrooke, R.E., Di Monte, D.A., Emson. P.C. (2007). Reduced vesicular storage of dopamine causes progressive nigrostriatal neurodegeneration. The Journal of Neuroscience, 27 (30), 8138-48.
• Van Laar, V.S., Berman, S.B. (2013). The interplay of neuronal mitochondrial dynamics and bioenergetics: implications for Parkinson's disease. Neurobiology of Disease, 51, 43-55.
• Sulzer, D., Zecca, L. (2000). Intraneuronal dopamine-quinone synthesis: a review. Neurotoxicity Research, (3), 181-95.
• Belluzzi, E., Bisaglia, M., Lazzarini, E., Tabares, L.C., Beltramini, M., Bubacco, L. (2012). Human SOD2 modification by dopamine quinones affects enzymatic activity by promoting its aggregation: possible implications for Parkinson's disease. PLoS One, 7 (6), e38026.
• Kuhn, D.M., Arthur, R.E., Thomas, D.M., Elferink, L.A. (1999). Tyrosine hydroxylase is inactivated by catechol-quinones and converted to a redox-cycling quinoprotein: possible relevance to Parkinson's disease. Journal of Neurochemistry, 73 (3), 1309-17.
• Sulzer, D., Bogulavsky, J., Larsen, K.E., Behr, G., Karatekin, E., Kleinman, M.H, Turro, N., Krantz, D., Edwards, R.H, Greene, L.A, Zecca, L. (2000). Neuromelanin biosynthesis is driven by excess cytosolic catecholamines not accumulated by synaptic vesicles. PNAS, 97 (22), 11869-74.
• Ohtsuka, C., Sasaki, M., Konno, K., Koide, M., Kato, K., Takahashi, J., Takahashi, S., Kudo, K., Yamashita, F. (2013). Changes in substantia nigra and locus coeruleus in patients with early-stage Parkinson's disease using neuromelanin-sensitive MR imaging. Neuroscience Letters, 541, 93-8.