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Abstract

Objective: Prolidase enzyme, which exists in plasma, brain and various organs, is a cytosolic exopeptidase, that divisor the imidodipeptides with carboxyl terminal position of proline and hydroxyproline. The aim of the present study was to investigate serum prolidase activity level in major depressive disorder (MDD).Methods: This study included 22 patients with MDD as the study group, and 26 healthy subjects without any psychiatric disorders as the control group. Each patient underwent a detailed diagnostic evaluation by experienced psychiatrists. The sociodemographic information form given to both patients and the control subjects, while Hamilton Depression Scale Scoring (HDS), Hamilton Anxiety Scale Scoring (HAS), Clinical Global Impression Scoring (CGI) applied to patients. Blood samples were obtained for biochemical analyses.Results: The mean age of the patient group was 31.3±10.1 years old, whereas the mean age of the control group was 32.3±8.8 years old. The mean duration of the education for the patient group was 8.1±6.2 years, whereas for the control group was 10.2±3.8 years. There was no significant differences in terms of the mean age of participants and the mean duration of the education between two groups (p>0.05). The level of prolidase activity of patient group was 510.3±480.8 U/L, whereas the level of prolidase activity of control group was 457.8±386.0 U/L. No significant difference was observed in serum prolidase activity between patient and the control groups (p>0.05). Conclusion: In our study similar level of prolidase activity was found in MDD and healthy subjects. We suggest that this finding may be an evidence indicating that MDD and bipolar depression may be different clinical entities. J Clin Exp Invest 2015; 6 (3): 296-300

Keywords

• Major depressive disorder, prolidase activity, etiology

Major depresif bozuklukta prolidaz aktivitesi

Öz

Amaç: Prolidaz enzimi dipeptitlerin karboksil terminal pozisyondaki prolin veya hidroksiprolini ayıran plazma, beyin ve çeşitli organlarda bulunan bir egzopeptidazdır. Biz bu çalışmada major depresif bozukluk (MDB)’da prolidaz aktivitesini araştırmayı amaçladık. Yöntemler: Çalışmamızda hasta grubu major depresif bozukluk 22 kişiden oluşurken kontrol grubu ise herhangi bir psikiyatrik rahatsızlığı olmayan sağlıklı 26 kişiden oluşmaktaydı. Her hasta deneyimli psikiyatristler tarafından ayrıntılı tanısal değerlendirmeye alındı. Hasta ve kontrol grubuna sosyodemografik bilgi formu verilirken, hasta grubuna Hamilton Depresyon Derecelendirme Ölçeği (HDDÖ), Hamilton Anksiyete Derecelendirme Ölçeği (HADÖ), Klinik Global İzlem Ölçeği (KGİ) uygulandı. Biyokimyasal analizler için kan alındı. Bulgular: Hasta grubunun yaş ortalaması 31,3±10,1 yıl, kontrol grubunun yaş ortalaması ise 32,3±8,8 yıl idi. Eğitim süresi hasta grubunun 8,1±6,2 yıl, kontrol grubunda 10,2±3,8 yıl idi. Gruplar arasında yaş ve eğitim süresi açısından istatistiksel olarak anlamlı farklılık belirlenmedi (p > 0,05). Prolidaz aktivitesinin hasta grubunda 510.3±480.8 U/L iken kontrol grubunda 457,8±386,0 U/L olduğu görüldü. Prolidaz aktivitesi bakımında hasta ve kontrol grubu arasında anlamlı farklılık gözlenmedi (p > 0,05). Sonuç: Çalışmamızda prolidaz aktivitesi MDB’ta sağlıklı kişilerle benzer bulunmuştur. Bu verinin MDB ve bipolar depresyonun farklı klinik antiteler olduğunu biyokimyasal düzeyde gösteren bir bulgu olabileceğini önermekteyiz

Anahtar Kelimeler

• Major depresif bozukluk, prolidaz aktivitesi, etyoloji

References

1. Zanaboni G, Dyne KM, Rossi A, et al. Prolidase deficiency: biochemical study of erythrocyte and skin fibroblast prolidase activity in Italian patients. Haematologica 1994;79:13-18.
2. Palka JA, Phang JM. Prolidase activity in fibroblasts is regulated by interaction of extracellular matrix with cell surface integrin receptors. J Cell Biochem 1997;67:166-175.
3. McRae PA, Porter BE. The perineuronal net component of the extracellular matrix in plasticity and epilepsy. Neurochem Int 2012;61:963-972.
4. Hauptmann M, Wilson DF, Erecinska M. High affinity proline uptake in rat brain synaptosomes. FEBS Lett 1983;161:301-305.
5. Crump FT, Fremeau RT, Craig AM. Localization of the brain-specific high-affinity I-proline transporter in cultured hippocampal neurons:molecular heterogeneity of synaptic terminals. Mol Cell Neurosci 1999;13:25-39.
6. Selek S, Altindag A, Saracoglu G, et al. Prolidase activity and its diagnostic performance in bipolar disorder. J Affect Disord 2011;129:84-86.
7. Mandel H, Abeling N, Gutman A, et al. Prolidase deficiency among an Israeli population: prenatal diagnosis in a genetic disorder with uncertain prognosis. Prenatal Diagnosis 2000;20:927-929.
8. Aslan M, Nazligul Y, Horoz M, et al. Serum prolidase activity and oxidative status in Helicobacter pylori infection. Clin Biochem 2007;40:37-40.

9. Cakmak A, Zeyrek D, Atas A, et al. Serum prolidase activity and oxidative status in patients with bronchial asthma. J Clin Lab Anal 2009;23:132-138.
10. Cakmak A, Soker M, Koc A, Aksoy N. Prolidase activity and oxidative status in patients with thalassemia major. J Clin Lab Anal 2010;24:6-11.
11. Bahceci B, Bagcioglu E, Kokacya MH, et al. Prolidase activity and oxidative stress in patients with schizophrenia: A preliminary study. J Pak Med Assoc 2015;65:131-135.
12. Gibbon AS, Brooks L, Scarr E, Dean B. AMPA receptor expression is increased post-mortem samples of the anterior cingulated from subjects with major depressive disorder. J Affect Disord 2012;136:1232-1237.
13. Cohen S, Nadler J. Proline-induced potentiation of glutamate
14. transmission. Brain Research 1997;761:271-282.
15. Guy W. ECDEU Assessment Manual for Psychopharmacology. Revised US Dept Health, Education and Welfare publication (ADM), Rockville, Md; National Institude of Mental Health, 1976;76-338.
16. Akdemir A, Örsel SD, Dağ İ, et al. Hamilton depresyon derecelendirme ölçeğinin geçerlililği-güvenirliliği ve klinikte kullanımı. Psikiyatri Psikoloji ve Psikofarmakoloji Dergisi 1996;4:251-259.
17. Yazıcı MK, Demir B, Tanrıverdi N, et al. Hamilton Anksiyete
18. Değerlendirme Ölçeği, değerlendiriciler arası güvenirlik ve geçerlik çalışması. Türk Psikiyatri Dergisi 1998;9:114-117.
19. Cumurcu BE, Ozyurt H, Etikan I, et al. Total antioxidant capacity and total oxidant status in patients with major depression: impact of antidepressant treatment. Psychiatry Clin Neurosci 2009;63:639-645.
20. Galecki P, Szemraj J, Bienkiewicz M, et al. Oxidatif stress parameters after combined fluoxetine and acetylsalisilic acid therapy in depressive patients. Hum Psychopharmacol 2009;24:277-286.
21. American Psychiatric Association. Diagnostic and statistical
22. manual of mental disorders (5th ed.). Washington, DC: 2013.
23. Sayar K. İki uçlu bozukluk 1 ve iki uçlu bozukluk 2 depresyon edavisi arasindaki farklar. Journal of Mood Disorders 2013;3:37-38.
24. Aydemir Ö. Major depresif bozuklukta tedavi hedefleri ve tedavinin izlenmesi. Klinik Psikofarmakoloji Bülteni 2011;21:1-9.
25. Murray RK, Mayes PA, Granner DK, Rodwell VW. Hayper’s Biochemistry Appleton &Lange 22. International press (çev ed: Menteş, G., & Biltan, E.) İstanbul, Barış Kitapevi 1990:336-338.
26. Delwing D, Bavaresco CS, Wannmacher CM, et al. Proline induces oxidative stress in cerebral cortex of rats. International Journal of Developmental Neuroscience 2003;21:105-110.
27. Arikanoglu A, Akil E, Varol S, et al. Relationship of cognitive performance with prolidase and oxidative stress in Alzheimer disease. Neurol Sci 2013;34:2117-2121.
28. Serafini G, Gonda X, Rihmer Z, et al. NMDA receptor antagonists for depression: Critical considerations. Ann Clin Psychiatry 2015;27:213-220.
29. Levine J, Panchalingam K, Rapoport A, et al. Increased cerebrospinal fluid glutamine in depressed patients. Biol Psychiatry 2000;47:586-593.
30. Altamura C, Maes M, Dai J, Meltzer HY. Plasma concentrations
31. of excitatory amino acids, serine, glycine, taurine and histidine in major depression. Eur Neuropsychopharmacol 1995;5:71-75.
32. Maes M, Verkerk R, Vandoolaeghe E, et al. Serum levels of excitatory amino acids, serine, glycine, histidine, threonine, taurine, alanine and arginine in treatmentresistant depression: Modulation by treatment with antidepressants and prediction of clinical responsivity. Acta Psychiatr Scand 1998;97:302-308.
33. Francis PT, Poynton A, Lowe SL, et al. Brain amino acid concentrations and Ca++ dependent release in intractable depression assessed antemortem. Brain Res 1989;494:315-324.
34. Holemans S, De Paermentier F, Horton RW, et al. NMDA glutamatergic receptors, labeled with [3H]MK- 801, in brain samples from drug-free depressed suicides. Brain Res 1993;616:138-143.
35. Auer DP, Pütz B, Kraft E, et al. Reduced glutamate in the anterior cingulated cortex in depression: an in vivo proton magnetic resonance spectroscopy study. Biol Psychiatry 2000;47:305-313.
36. Sanacora G. Evidence for GABAergic and glutamatergic involvement in the pathophysiology and treatment of depressive disorders. Biological Psychiatry HAH D’haenen. JA denBoer, P Willner (Ed), West Sussex, John Wiley & Sons, 2002;739-749.
37. Kokacya MH, Bahceci B, Bahceci I, et al. Prolidase activity and oxidative stress in patients with major depressive disorder. Psychiatr Danub 2014;26:314-318.