No abstract

We investigated the effects of lamotrigine, aripiprazole and escitalopram administration and experimental depression on lipid peroxidation (LP) and antioxidant levels in cortex of the brain in rats. Forty male wistar rats were randomly divided into five groups. First group was used as control although second group was depression-induced group. Aripiprazole, lamotrigine and escitalopram per day were orally supplemented to chronic mild stress (CMS) depression-induced rats constituting the third, fourth and fifth groups for 28 days, respectively. Depression resulted in significant decrease in the glutathione peroxidase (GSH-Px) activity, reduced glutathione and vitamin C of cortex of the brain although their levels and beta-carotene concentrations were increased by the three drugs administrations to the animals of CMS induced depression group. The LP levels in the cortex of the brain and plasma of depression group were elevated although their levels were decreased by the administrations. The increases of antioxidant values in lamotrigine group were higher according to aripiprazole and escitalopram supplemented groups. Vitamin A level did not change in the five groups. In conclusion, the experimental depression is associated with elevated oxidative stress although treatment with lamotrigine has most protective effects on the oxidative stress within three medicines.

Diabetes mellitus (DM) is a frequently encountered metabolic disease with chronic features and involves numerous complications throughout its course, which causes severe restriction and disability in an individual's life. It has been reported that the incidence of depression is higher in diabetic patients and that diabetes is one of the risk factors in the development of depression. It has also been reported that co-morbid psychiatric disorders cause further deterioration in the quality of life in diabetic patients. The aim of this study was to investigate the effects of depression on the quality of life in type II DM patients. Sixty patients (30 females and 30 males) with current major depressive episode diagnosed according to DSM-IV criteria, and 48 type II DM patients (30 females and 18 males) without a major depressive episode (non-depressed group) were included in the study. All patients were evaluated with a semi-structured interview form to assess the clinical features of DM, Hamilton Rating Scale for Anxiety (HRSA), Hamilton Rating Scale for Depression (HRSD), and the Turkish version of The World Health Organization Quality of Life Assessment-Brief (WHOQOL-BREF). The HRSD and HRSA scores in the depressed group were 24.87+/-4.83 and 21.07+/-5.44, respectively, whereas those in the non-depressed group were 7.83+/-3.92 and 6.88+/-3.43, respectively. The physical health, psychological health, social relationship, environmental and social pressure domain, general health-related quality of life, overall quality of life, and WHOQOL-BREF total scores were found significantly lower in the depressed group than the non-depressed group. There were significant negative correlations between HRSD and HRSA scores and physical health, psychological health, social relationship, environmental and social pressure domain, general health-related quality of life, overall quality of life, and WHOQOL-BREF total scores. Furthermore, there were significant negative correlations between the HbA1c level and physical health, social relationship, environmental domain, social pressure domain, general health-related quality of life, overall quality of life, and WHOQOL-BREF total scores. However, there was a significant positive correlation between the level of education and physical health, psychological health, social relationship, environmental social pressure domain, overall quality of life, and WHOQOL-BREF total scores. There were significant negative correlations between social relationship domain score, and age and duration of illness. Our study demonstrates that the presence of depression in type II DM further deteriorates the quality of life of the patients. Since treating depression would have a beneficial effect on the quality of life, clinicians should carefully assess for depression associated with type II DM.

Venlafaxine is an approved antidepressant that is an inhibitor of both serotonin and norepinephrine transporters. Medical treatment with oral venlafaxine can be beneficial to depression due to reducing free radical production in the brain and medulla of depression-induced rats because oxidative stress may a play role in some depression. We investigated the effect of venlafaxine administration and experimental depression on lipid peroxidation and antioxidant levels in cortex brain, medulla and erythrocytes of rats. Thirty male wistar rats were used and were randomly divided into three groups. Venlafaxine (20 mg/kg) was orally supplemented to depression-induced rats constituting the first group for four week. Second group was depression-induced group although third group was used as control. Depressions in the first and second groups were induced on day zero of the study by chronic mild stress. Brain, medulla and erythrocytes samples were taken from all animals on day 28. Depression resulted in significant decrease in the glutathione peroxidase (GSH-Px) activity and vitamin C concentrations of cortex brain, glutathione (GSH) value of medulla although their levels were increased by venlafaxine administration to the animals of depression group. The lipid peroxidation levels in the three tissues and nitric oxide value in cortex brain elevated although their levels were decreased by venlafaxine administration. There were no significant changes in cortex brain vitamin A, erythrocytes vitamin C, GSH-Px and GSH, medulla vitamin A, GSH and GSH-Px values. In conclusion, cortex brain within the three tissues was most affected by oxidative stress although there was the beneficial effect of venlafaxine in the brain of depression-induced rats on investigated antioxidant defenses in the rat model. The treatment of depression by venlafaxine may also play a role in preventing oxidative stress.

It is well known that oxidative stress damages biomolecules such as DNA and lipids. No study is available on the morphine-induced oxidative damage and fatty acids changes in brain and spinal tissues. The aim of this work was to determine the effects of morphine on the concentrations and compositions of fatty acid in spinal cord segments and brain tissues in rabbits as well as lipid peroxidation (LP) and glutathione (GSH) levels in cortex brain. Twelve New Zealand albino rabbits were used and they were randomly assigned to two groups of 6 rabbits each. First group used as control although morphine administrated to rats in second group. Cortex brain and (cervical, thoracic, lumbar) samples were taken. The fatty acids between n:18.0 and 21.0 were present in spinal cord sections and n:10 fatty acids in control animals were present in the brain tissues. Compared to n:20.0-24.0 fatty acids in spinal cord sections and 8.0 fatty acids in the brain tissues of drug administered animals. The concentration and composition of the fatty acid methyl esters in spinal cord and brain tissues was decreased by morphine treatments. LP levels in the cortex brain were increased although GSH levels were decreased by the morphine administration. In conclusion, unsaturated fatty acids contents in brain and spinal cord sections and GSH were reduced by administrating spinal morphine although oxidative stress as LP increased. The inhibition oxidative damage may be a useful strategy for the development of a new protection for morphine administration as well as opiate abuse.