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Yaşlanma sürecinde melatoninin rolü

The role of melatonın durıng agıng

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Abstract (2. Language): 
Pineal is a gland that has different functions on various organisms and is under photoneuroendocrine control. The gland produces a hormone called melatonin (N-acetyl 5-methoxitryptamine), which is secreted especially in darkness. Melatonin is a potent free radical scavenger that protects tissues from oxidant damage. Aging in human and animals decreases the production of melatonin by pineal gland obviously. According to an accepted theory about aging, the anatomical and functional degeneration formed in organs while aging is bound to the damage caused by free radicals. In elderly, the free radical attack on neurons or neural tissue is important since aging facilitates the neurodegenerative situations. The excitatory amino acid neurotransmitters, especially, are much more harmful on neurons because they cause the formation of free radicals. por that reason, the brain areas having neuron endings are more likely to be damaged than the other areas of brain are, since they secrete excitatory amino acids. Defense mechanisms to stresses and toxic agents exposure mediated free radicals generations are become insufficient with aging like decreased melatonin production in pineal gland. Pineal gland and melatonin are thought, for years, to be related to aging. Many theories about melatonin and aging have been suggested. The decrease of melatonin levels related to age and this situation, to increase the degeneration in organism is one of the sources of all these theories. In conclusion, melatonin is suggested to play a preservative role in preventing the neurodegenerative disorders becomes in elderly.
Abstract (Original Language): 
Pineal be z çeşitli canlılarda farklı fonksiyonlara sahip bir bez olup fotonöroendokrin kontrol altındadır. Bez özellikle karanlıkta sentezlenen melatonin (N-Asetil-5-Metoksitriptamin) adı verilen bir hormon üretir. Melatonin güçlü bir oksijen radikal toplayıcısıdır ve bu yüzden dokuların hasara uğramasının gecikmesine destek olabilmektedir. Pineal bezden melatonin üretimi insan ve hayvanlarda yaşlanmayla birlikte belirgin olarak azalmaktadır. Yaşlanmayla ilgili kabul gören bir teoriye göre, yaşlanma esnasında organlarda oluşan anatomik ve fonksiyonel dejenerasyon, serbest radikallerin oluşturduğu hasara bağlanmaktadır. Yaşlılıkta nöronlar veya nöral doku üzerine serbest radikal saldırısı birçok nörodejeneratif durumların oluşumunu kolaylaştırması bakımından önemlidir. Eksitatör aminoasit nörotransmiterler, serbest radikal oluşumuna neden olduğundan dolayı nöronlar üzerine özellikle daha tahripkardır. Bundan dolayı, sinir sonlanmaları ihtiva eden beyin alanları eksitatör aminoasitleri salgıladığından, bu alanlar beynin diğer alanlarına nazaran daha çabuk tahrip olurlar. Yaşlanmayla birlikte, stres veya toksik ajanlara maruz kalma sonucu serbest radikal oluşumunu engelleyen süreçler de tıpkı melatonin seviyelerinde olduğu gibi azalmaktadır. Pineal bez ve melatoninin yıllardır yaşlanmayla ilgili olduğu düşünülmüştür. Melatonin ve yaşlanmayla ilgili birçok teori öne sürülmüştür. Yaşla ilişkili olarak melatonin seviyesinin azalması ve bu durumun organizmadaki dejenerasyonu ilerletmesi, bütün bu teorilerin dayanak noktalarından birisidir. Bu bilgiler ışığında melatoninin yaşlılarda ortaya çıkan nörodejeneratif hastalıkların önlenmesinde koruyucu bir rol oynayabileceği düşünülmektedir.
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REFERENCES

References: 

1. Reiter RJ, Tan D, Sainz RM, Mayo JC, Silvia LB. Melatonin: reducing the toxicity and increasing the efficacy ofdrugs. J Pharmacy and Pharmacology 2002; 54:1299-1321
2. Brzezinski A. Melatonin in humans. The New England JournalofMedicine 1997; 336:186-195
3. Axelrod J. The pineal gland: A neurochemical transducer. Science 1974; 184:1341-1348
4. Waldhauser F, Dietzel M. Daily and annual rhythms in human melatonin secretion: role in puberty control. AnnNYAcadSci 1985;453:205-214
5. Iguchi H, Kato KI, Ibayashi Y. Melatonin serum levels and metabolic clearance rate in patients with liver cirrhosis. J Clin Endocrinol Metab 1982; 54:1025¬1027
6.
Üstünda
ğ B, Canatan H. Melatonin: Güçlü bir antioksidan ve serbest radikal giderici!.. Fırat Tıp Dergisi 1999; 1(7):502-512
7. Harman D. Free radical theory ofaging. Mutat Res 1992; 275:257-266
8. Reiter RJ. Pineal function during aging; attenuation of the melatonin rhythm and its neurobiological consequences. ActaNeurobiol Exp. 1994; 54
(Suppl):31-39
9. Iguchi H, Kato K, Ibayashi H. Age dependent reduction in serum melatonin concentration in healthy human subjects. J Clin Endoerinol Metab 1982; 52:27-29.
10. Poeggeler B, Reiter RJ, Tan DX, Chen LD, Manchester LC. Melatonin, hydroxyl radical mediated oxidative damageandaging. JPinealRes. 1993; 14:151-168
11. Halliwel B, Aruoma 0.1. DNA damage by oxygen
derived species. FEBS Lett 1991; 281:9-19
12. Tan DX, Poeggeler B, Reiter RJ, Chen LD, Chen S, Manchester LC, Barlow-Walden LR. The pineal hormone melatonin inhibits DNA-adduct formation induced by the chemical carcinogen safrole in vivo. CancerLett 1993; 70:65-71
13. Hardeland R, Reiter RJ, Poeggeler B, Tan DX. The significance ofthe metabolism ofthe neurohormone melatonin: Antioxidative protection and phonation of bioactive substances. Neuroscience and Biobehavioral Reviews. 1993; 17:347-357
14. Acuna-Castroviejo D, Reiter RJ, Menendez-Pelaez A, Pablos MI, Burgos A. Characterization ofhigh-affinity melatonin binding sites in purified cell nuclei ofrat liver. J Pineal Res 1994; 16(2):100-112
15. Reiter RJ. The aging pineal gland and its physiological consequences. Bio Essays 1992; 14:169-175
16. Nair NPV, Hariharasubramanian N, Pilapil C, Isaac I, Thavundayil JX. Plasma melatonin An Index ofBrain Aging in Humans. Biol Psychiatry 1986; 21:141-150
17. Okatani Y, Wakatsuki A, Reiter RJ, Miyahara Y. Melatonin reduces oxidative damage of neural lipids and proteins in senescence-accelerated mouse. Neurobiology Agini 2002; 23:639-644
18. Sandyk R. Possible role ofpineal melatonin in the mechanism ofaging. Intern J Neuroscience 1990;
52:85-92
19. Srinivasan V. Melatonin oxidative stress and neurodegenerative diseases. Indian J Exp Biol 2002;
40(6):668-679
20. Jenner P. Oxidative Stress in Parkinson's Disease. Ann Neurol 2003; 53(suppl 3):26-38
21. Maurizi CP. Alzheimer's disease: roles for mitochondrial damage, the hydroxyl radical and cerebrospinal fluid deficiency ofmelatonin. Med Hypotheses 2001; 57(2):156-160
22.
Özgüne
r F, Özcankaya R, Delibaş N, Koyu A, Çalışkan S. Melatonin ve klinik önemi. SDÜ Tıp Fakültesi Dergisi 1995;2(4):1-6
23. Miguez JM, Recio J, Sanchez-Barcelo E, Aldegunde M. Changes with age in daytime and nighttime contents ofmelatonin, indoleamines, and catecholamines in the pineal gland: a comparative study in rat and Syrian hamster. J Pineal Res 1998; 25(2):106-115
24. Maestroni G, Conti A, Pierpaoli W. Pineal melatonin, its fundamental immunoregulatory role in aging and cancer. Annals NY Acad Sciences 1988;521:140-148
25. Weiss B, Greenberg LH, Cantor E. Denervation supersensitivity and beta-adrenergic receptors as a function ofage. Adv Biochem Psychopharmacol 1980; 21:461-472
26. Schmid HA. Decreased melatonin biosynthesis, calcium flux, pineal gland calcification and aging: a hypothetical framework. Gerontology 1993; 39(4):189-199
27. Anisimov VN, Khavinson VKh, Morozov VG. Twenty years ofstudy on effects ofpineal peptide preparation: epithalamin in experimental gerontology and oncology. AnnNYAcadSci 1994; 31;719:483-493

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