MAJOR DEPRESSION AND ANTIOXIDANT CAPACITY

Abstract:

 Major depression is defined as a state of mind in which a person has feelings of great unhappiness and hopelessness and may be characterized by sadness, lethargy, thinking difficulty, an increase or decrease in appetite or an attempt to commit suicide. Due to depression, there is a disturbance in many functions of the body but mostly it could be the development of oxidative stress. Oxidative stress is the indication of imbalance between free radical productions, neutralization and leads to inflammation. Antidepressants used by patients usually result in damaging their liver enzymes. This research is based on the relation between the oxidative stress and depressed patients, where the results of catalase, CRP (C-reactive protein) and ALT (Alanine Aminotransferase) were significantly increased.

Keywords: Major depression– lethargy –Oxidative stress –Neutralization –Antidepressants –Inflammation

Introduction:

 Major depression is defined as a state of mind in which a person has feelings of great unhappiness and hopelessness. It is a physiological disorder described by changes in certain brain chemicals called neurotransmitters (Berk, M. 2011). The pathophysiology of depression is multifactorial and involves changes in brain monoaminergic transmission as well as increased oxidative stress. Oxidative stress has been defined as a loss of balance between reactive oxygen species production and antioxidant defenses (S., &Karlidag, R. 2009). Oxidative stress is one of the important mechanisms that cause the destruction of nerve cells by rapid lipid peroxidation of neuronal membrane lipids which are rich in highly polyunsaturated fatty acids (Oriani, G. 2012).

Catalase is one of the most efficient antioxidant enzymes for its capability to degrade hydrogen peroxide into water and oxygen. It prevents damage in the tissues done by accumulated peroxide (Karlidag, R. 2009). C-reactive protein (CRP) is a plasma protein that participates in the systematic response to inflammation and tissue damage. It is partly an innate immune response. Elevated CRP levels have been associated with depression.

Materials and Methods:

 

Study Design

The study included 60 fresh cases of major depressive disorder diagnosed as per the DSM IV, by the consultant psychiatrist. The control group of included age and sex matched 40 healthy control subjects taken from the general population (T. F. 2010). Patients were not using or were dependent on tobacco, alcohol or any other substance.

Specimen collection

The blood samples were collected from the cases and controls. Taking all aseptic precautions, about 5 ml of blood was drawn by venipuncture from peripheral vein, with a disposable syringe. The 5ml blood thus collected in clean dry glass tube was allowed to stand for 30 min at room temperature for the retraction of clot (Y. E.2014). This was then centrifuged at 3000 rpm for 10 min to separate the serum. The serum samples were stored at -800C in the refrigerator for analysis. Care was taken to avoid hemolysis of the sample.

Statistical Analysis

Statistical analysis was carried out by using Graph Pad Software. The results were expressed as Mean ± S.E.M.The two –tailed P values were used to calculate significance. (P< 0.05) was accepted as the significance level and the presence of statistical heterogeneity provided justification for a random effects approach to the meta-analysis. All analyses were conducted using STATA 11.0 (STATA Corp, College Station, TX).

Results and Discussion:

Major depression was most commonly measured using the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria (A., &Sezen, Y. 2010). A Cohen’s d effect size of 0.55 (95% confidence interval = 0.47–0.63) was found for the association between major depression and oxidative stress, indicating a roughly 0.55 of 1-standard-deviation increase in oxidative stress among individuals with depression compared with those without depression.

The studies varied widely in measures of both depression and of oxidative stress (Y. E.2014). Among the 23 studies, 7 different depression measures and 12 different oxidative stress markers were reported. Some of the oxidative stress measures analyzed exhibited stronger associations with depression than others (e.g., malondialdehyde and 8-oxo-2′-deoxyguanosine). The selection of study participants was dissimilar between the studies, with several performed in clinical populations and a few conducted using healthy volunteers from the community (Frey, B. N. 2012). A clinical population may have included patients with mild, moderate, or severe depression. This is important to consider when comparing results across these studies because the degree of depressive symptoms may impact the level of an oxidative stress or antioxidant status markers present in the body (Berk, M. 2011).

Conclusions:

Major Depression is a common physiological disorder involving an imbalance of brain chemicals called neurotransmitters. Major Depression and oxidative stress and antioxidant status across many different studies. Differences in measures of major depression and markers of oxidative stress and antioxidant status markers could account for the observed heterogeneity. These findings suggest that well-established associations between depression and poor health outcomes may be mediated by high oxidative stress.

By: Sonia Sharif

References:

Ø  Buyukhatipoglu, H., Kirhan, I., Dag, O. F., Turan, M. N., Vural, M., Taskin, A.,&Sezen, Y. (2010). Oxidative stress increased in healthcare workers working 24-hour on-call shifts. The American journal of the medical sciences, 340(6), 462-467.

Ø  Scapagnini, G., Davinelli, S., Drago, F., De Lorenzo, A., &Oriani, G. (2012). Antioxidants as antidepressants. CNS drugs, 26(6), 477-490.

Ø  Mohamadin, A. M., Habib, F. A., & Elahi, T. F. (2010). Serum paraoxonase 1 activity and oxidant/antioxidant status in Saudi women with polycystic ovary syndrome. Pathophysiology, 17(3), 189-196.

Ø  Maes, M., Galecki, P., Chang, Y. S., & Berk, M. (2011). A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro) degenerative processes in that illness. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 35(3), 676-692.

Ø  Maria Michel, T., Pulschen, D., &Thome, J. (2012). The role of oxidative stress in depressive disorders. Current pharmaceutical design, 18(36), 5890-5899.

Ø  Cumurcu, B. E., Ozyurt, H., Etikan, I., Demir, S., & Karlidag, R. (2009). Total antioxidant capacity and total oxidant status in patients with major depression: impact of antidepressant treatment. Psychiatry and clinical neurosciences, 63(5), 639-645.

Ø  Lee, G. J., Lee, S. K., Kim, J. M., Rhee, C. K., Lee, Y. K., Brainina, K. Z., & Kazakov, Y. E. (2014). Application feasibility of antioxidant activity evaluation using potentiometry in major depressive disorder. Electrochemistry, 82(4), 264-266.

Ø  Behr, G. A., Moreira, J. C., & Frey, B. N. (2012). Preclinical and clinical evidence of antioxidant effects of antidepressant agents: implications for the pathophysiology of major depressive disorder. Oxidative medicine and cellular longevity, 2012.