Journals / Journal of Mood Disorders / 2017 / Cilt: 7 - Sayı: 2

Paraoxonase (PON1) L55M and Q192R Polymorphisms in Major Depressive Disorder and Bipolar Disorder

Pages
86–92
Publication Date
2022-10-18
DOI
—
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

Polymorphisms wereanalyzed by using polymerase chain reaction.Results: There were no statistically significant differences between groups for the existence of PON1 genotypes.Additionally, there was no association between the PON1 genotypes and disease variables in both depressed and bipolarpatients.Conclusions: Evaluating the different stages of patients with mood disorders and examining the connection betweenPON1 polymorphisms and treatment outcomes will help us to clarify the relationship between PON1 and mood disorders.

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: Oxidative and nitrosative stress pathways, along with immune-inflammatory response, might play animportant role in the pathogenic mechanisms underlying major depressive disorder and bipolar disorder.
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Key Findings & Data:The aim of thepresent study is to investigate paraoxonase 1 polymorphisms and its correlations with disease parameters in patientswith major depressive disorder and bipolar disorder.Methods: PON1 L55M and Q192R single nucleotide polymorphisms were analyzed in a group consisted of 100 patientswith major depressive disorder, and 100 patients with bipolar disorder and 96 healthy controls.
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Conclusion & Impact:Polymorphisms wereanalyzed by using polymerase chain reaction.Results: There were no statistically significant differences between groups for the existence of PON1 genotypes.Additionally, there was no association between the PON1 genotypes and disease variables in both depressed and bipolarpatients.Conclusions: Evaluating the different stages of patients with mood disorders and examining the connection betweenPON1 polymorphisms and treatment outcomes will help us to clarify the relationship between PON1 and mood disorders.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Oxidative and nitrosative stress pathways, along with immune-inflammatory response, might play animportant role in the pathogenic mechanisms underlying major depressive disorder and bipolar disorder. The aim of thepresent study is to investigate paraoxonase 1 polymorphisms and its correlations with disease parameters in patientswith major depressive disorder and bipolar disorder.Methods: PON1 L55M and Q192R single nucleotide polymorphisms were analyzed in a group consisted of 100 patientswith major depressive disorder, and 100 patients with bipolar disorder and 96 healthy controls. Polymorphisms wereanalyzed by using polymerase chain reaction.Results: There were no statistically significant differences between groups for the existence of PON1 genotypes.Additionally, there was no association between the PON1 genotypes and disease variables in both depressed and bipolarpatients.Conclusions: Evaluating the different stages of patients with mood disorders and examining the connection betweenPON1 polymorphisms and treatment outcomes will help us to clarify the relationship between PON1 and mood disorders.

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Cite This Article

YİLDİZ, M., ERDOĞAN, S. T., BENLİ, I., CAM, F. C., ATES, O., DEMİR, O. (2022). Paraoxonase (PON1) L55M and Q192R Polymorphisms in Major Depressive Disorder and Bipolar Disorder. Journal of Mood Disorders, Cilt: 7 - Sayı: 2, 86–92. https://ajindex.com/articles/564531

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References (12)

  1. Siwek M, Sowa-Kucma M, Dudek D, Styczen K, Szewczyk B, Kotarska K, et al. Oxidative stress markers in affective disorders. Pharmacol Rep. 2013
  2. 65(6):1558-71. [CrossRef] 2. Moylan S, Berk M, Dean OM, Samuni Y, Williams LJ, O'Neil A, et al. Oxidative & nitrosative stress in depression: why so much stress? Neurosci Biobehav Rev. 2014
  3. [CrossRef] 3. Andreazza AC, Cassini C, Rosa AR, Leite MC, de Almeida LM, Nardin P, et al. Serum S100B and antioxidant enzymes in bipolar patients. J Psychiatr Res. 2007
  4. 41(6):5239. [CrossRef] 4. Machado-Vieira R, Dietrich MO, Leke R, Cereser VH, Zanatto V, Kapczinski F, et al. Decreased plasma brain derived neurotrophic factor levels in unmedicated bipolar patients during manic episode. Biol Psychiatry. 2007
  5. 61(2):1424. [CrossRef] 5. Berk M, Copolov DL, Dean O, Lu K, Jeavons S, Shapkaitz I, et al. Antioxidant treatment of the glutathione deficiency in bipolar disorder with N-acetylcysteine: a double-blind randomised placebo controlled trial. Bipolar Disord. 2007:9:89. 6. La Du BN, Aviram M, Billecke S, Navab M, Primo-Parmo S, Sorenson RC, et al. On the physiological role(s) of the paraoxonases. Chem Biol Interact. 1999
  6. [CrossRef] 7. Furlong CE, Suzuki SM, Stevens RC, Marsillach J, Richtera RJ, Jarvika GP, et al. Human PON1, a biomarker of risk of disease and exposure. Chem Biol Interact. 2010
  7. 187(1-3):35561. [CrossRef] 8. Primo-Parmo SL, Sorenson RC, Teiber J, La Du BN. The human serum paraoxonase/arylesterase gene (PON1) is one member of a multigene family. Genomics. 1996
  8. 33(3):498-507. [CrossRef] 9. Ezzaher A, Mouhamed DH, Mechri A, Neffati F, Rejeb J, Omezzine A, et al. Association between bipolar I disorder and the L55M and Q192R polymorphisms of the paraoxonase 1 (PON1) gene. J Affect Disord. 2012
  9. 139(1):127. [CrossRef] 10. Adkins S, Gan KN, Mody M, La Du BN. Molecular basis for the polymorphic forms of human serum paraoxonase/arylesterase: glutamine or arginine at position 191, for the respective A or B allozymes. Am J Hum Genet. 1993
  10. 52(3):598608. 11. Goswami B, Tayal D, Gupta N, Mallika V. Paraoxonase: a multifaceted biomolecule. Clin Chim Acta. 2009
  11. 410(1-2):112. [CrossRef] 12. Lawlor DA, Day IN, Gaunt TR, Hinks LJ, Timpson N, Ebrahim S, et al. The association of the paraoxonase (PON1) Q192R polymorphism with depression in older women: findings from the British Women's Heart and Health Study. J Epidemiol Community Health. 2007
  12. 61(1):857. [CrossRef] 13. Bortolasci CC, Vargas HO, Souza-Nogueira