Peroksydacja lipidów i aktywność cynkowo-miedziowej dysmutazy ponadtlenkowej u osób leczonych fluoksetyną z powodu pierwszego epizodu depresji             615-624
Psychiatr Pol 2007;41(5):615-624
In recent years researchers have made a lot of studies to determine the molecular and neurochemical mechanisms which are the basis of depressive disorders. Apoptosis is a cause of the limbic system neuronal cells defect in patients suffering from depression. The antioxidant system is the best known molecular mechanism which protects the cells from apoptosis. This system exists inside and outside of the cells compartments. There is much evidence that antioxidant enzymes keep neuronal cells safe from apoptosis, which is a result of oxidative stress. It also limits the premature ageing of cells. Aim. We tried to give an answer to three questions. I. Is the activity of cooper-zinc superoxide dismutase (CuZnSOD) and lipid peroxydation level (TBARS) different in patients and the healthy control group? 2. Does the activity of CuZnSOD change due to fluoxetine treatment? 3. What is the difference of TBARS concentration in platelets isolated from patients before and after treatment? Method. The study comprised of 32 patients diagnosed with depression. The activity of CuZnSOD in platelets was measured by Misra and Fridovich's method. The thrombocyte concentration of TBARS was measured by Placer and coop. method. Results and conclusions. 1. The activity of CuZnSOD in platelets of depressive patients is lower than in the healthy control group, but the differences are not significant. 2. The activity of CuZnSOD rises after fluoxetine treatment. 3. The concentration of TBARS is higher in patients than in the healthy control group. 4. The intensity of lipid peroxydation is statistically lower after fluoxetine treatment.
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