Aim: The purpose of the present study was to investigate whether total antioxidant capacity (TAC) and total oxidant status (TOS) are associated with major depressive disorder (MDD) and to evaluate the impact of antidepressant treatment on TAC and TOS in MDD.
Methods: Fifty‐seven MDD patients and 40 healthy controls participated in the study. Serum TAC and TOS were measured both in patients and controls using Erel's methods. Patients were treated with antidepressant drugs for 12 weeks. The treatment course was evaluated using the Montgomery–Asberg Depression Rating Scale (MADRS) in all patients.
Results: TOS and oxidative stress index (OSI) were higher (P = 0.0001 for both) and TAC was lower (P = 0.0001) in the MDD group compared with those of the controls. After 3 months of antidepressant treatment, TOS and OSI were decreased and TAC was increased compared with the pretreatment values (P = 0.0001, for all). Furthermore, there were significant positive correlations between the severity of the disease and serum TOS and OSI (r = 0.584, P = 0.0001; r = 0.636, P = 0.0001, respectively). A negative correlation was found between the severity of the disease and serum TAC (r = −0.553, P = 0.0001) at the pre‐treatment stage.
Conclusion: Treatment administered for 3 months to MDD patients increases TAC while decreasing TOS and OSI.
Cisplatin-induced nephrotoxicity is associated with an increase in lipid peroxidation and oxygen free radicals in rat kidneys. In this study, the effects of desferrioxamine were compared to vitamin C and E on cisplatin-induced lipid peroxidation and antioxidant enzyme activities in rat kidneys. Rats were divided into five groups, with 15 Wistar rats in each group. In the control group, rats received 1 mL/100 g isotonic saline solution intraperitoneally (i.p.). In Group II, 10 mg/kg cisplatin i.p. was injected to rats. Thirty minutes before the same dosage of cisplatin administration, 100 mg/kg i.p. vitamin C or E was given to rats in groups III and IV, respectively. Rats in Group V received 250 mg/kg desferrioxamine i.p., before the same dose of cisplatin administration. All rats were killed by cervical dislocation after 72 hours. The kidneys were immediately removed and washed in cold saline. Spectrophotometric method was used for all analyses. While catalase, glutathione reductase (GR), and super oxide dismutase (SOD) levels were found to be significantly decreased (P B < 0.001), malondialdehyde (MDA) (P < 0.05) and hydrogen peroxide (H2O2) (P < 0.001) levels were significantly increased in the cisplatin group when compared to the controls. MDA levels were decreased by desferrioxamine (P < 0.005) as well as vitamin C and E (P < 0.05 and P < 0.001, respectively). These three compounds induced a significant increase in SOD levels (P B < 0.05), but only in the vitamin C group, were SOD levels not significantly different than the levels of the controls (P > 0.05). In the desferrioxamine (P < 0.05), vitamin C and E groups (P < 0.001 for both), the cisplatin elevated H2O2 levels were decreased. None of these drugs had any effect on GR and catalase levels (P > 0.05). Desferrioxamine is useful to prevent cisplatin-induced lipid peroxidation, however, vitamin C and E are more effective on antioxidant enzymes than desferrioxamine.
Studies attempting to clarify the relationship between major depressive disorder (MDD) and the immune system have been increasing in recent years. It was reported that increased production of the main proinflammatory cytokines, such as interleukin-1, interleukin-6, and tumor necrosis factor-alpha, and that of acute phase reactants may play a role in the etiopathogenesis of depression. Stress and depression were reported to increase leukocyte and neutrophil counts and to decrease lymphocyte count. Biological determinants affecting the diagnosis, therapy, and prognosis of depression are quite limited. Therefore, new etiological models are needed to explain the pathophysiology of depression. In recent years, neutrophil–lymphocyte ratio (NLR) was determined to be a good indicator of inflammatory status. There is no study in the literature investigating NLR in MDD. This study aims to examine the role of inflammation in the etiology of depression based on the NLR in MDD patients who are undergoing no pharmacological therapy. A total of 41 patients diagnosed with MDD, who received no antidepressant therapy within the past 1 month, were included in the study, which took place between January and March 2015. The control group consisted of 47 healthy subjects with no psychiatric disorders. A sociodemographic information form and a Beck Depression Scale were administered, and the blood was taken for biochemical analysis. Significant differences were identified in the NLR, neutrophil count, lymphocyte percentage, and leukocyte values of the patient group when compared with the control group (P<0.05). Our study is the first in which NLR was investigated in MDD. The findings of the study reveal that NLR tends to be higher in patients with MDD, and a high NLR value supports the view that inflammation is a critical factor in the etiology of MDD.
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