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Etiopathogenesis of schizophrenia development is unknown yet in 1% of human population. There is damaged metabolism of biological membranes, abused production of free radicals and altered activity of antioxidant enzymes in patients with schizophrenia. Recently, a study showed that many of the genes and proteins whose expression is modified in the schizophrenic brain are related to glutathione and oxidative stress pathways. According to the researchers changes in permeability of biological membranes in brain could involve the pathophisiology of all--subtypes of schizophrenia as a result of oxidative stress. Brain is particularly sensitive to oxidative damage. There is a lot of phospholipids and polyunsaturated fatty acids in brain tissue under physiological conditions. The changes in polyunsaturated fatty acids metabolism, increased lipid peroxidation and the presence of oxidative stress are found in schizophrenia. They can course to appear instabilities of neuron membranes or even cell death owing to oxidative stress. Mainly to getting to know the molecular disease mechanism is associated with a disorder of the brain. The results suggest that at least some of the schizophrenia disease process can be traced in peripheral tissue like plasma, blood cells or liver. In various types of schizophrenia antipsychotic treatment affects oxidative state of erythrocyte membranes in a different way. Research into changes of antioxidant enzymes level during the treatment of typical and atypical neuroleptic drugs could contribute to widening the knowledge on the reasons of undesirable effects during pharmacotherapy with typical neuroleptic drugs.

This article presents the latest study results on lead (Pb2+) neurotoxicity, in order to draw attention of the Polish public to the issue and initiate a nation-wide programme eliminating lead contamination effects, especially in children. We discuss the after-effect of exposure to lead in concentrations lower than presently accepted as 'safe'. The pathway of lead transport to the brain, and the effects of lead accumulation in neurons, oligodendroglia and astroglia, are examined. We also present the impairing influence of lead on the cognitive brain functions and learning abilities as a result of affecting three main neurotransmission systems: dopaminergic, cholinergic and glutaminergic. The present knowledge on the influence of lead on receptors, neutransmitter release and synaptic proteins.

Clinical and experimental studies indicate that stress and depression are associated with the up-regulation of the immune system, including increased production of pro-inflammatory cytokines. When administered to patients or laboratory animals, some of these cytokines induce typical symptoms of depression. It is known that cytokines modulate brain neurotransmission and the activity of the hypothalamic-pituitary-adrenal axis, both of which are disturbed in depression. This review summarizes in vivo, ex vivo and in vitro clinical and experimental studies of the effect of antidepressants on cytokine production. In vitro culture and animal studies in particular suggest that antidepressants of several classes decrease the production of pro-inflammatory cytokines and shift the pro/anti-inflammatory cytokine balance towards the latter. Some studies suggest that immunological disturbances, including changes in cytokine levels, are not shared by all depressive patients, which means that only in certain groups of patients may the immunomodulatory action of antidepressants play a significant role in producing the therapeutic effect.

The aim of this research was to define the influence of long-term ethanol intoxication on the changes in end products of lipid peroxidation, reacting with thiobarbituric acid (TBA-reactive products) and free SH-groups concentrations in rat brains. The experiment was conducted on male Lewis rats. The experimental groups received a 1-molar ethanol solution and the control group received tap water. The animals were killed after 4, 8 and 12 weeks of intoxication and their brains were collected for further examination, encompassing measurement of the concentration of TBA-reactive products and free SH-groups. A statistically significant increase in the concentration of TBA-reactive products in 4th week of intoxication and decrease in the concentration of free SH-groups in 8th and 12th week of intoxication--compared to the control group--was noticed.

The experiment was carried out on male guinea pigs exposed to NO2 at a constant concentration of 0.1 ppm 24 h daily for 1, 2.5 and 6 months, or NO2 concentration was increased to 0.5 ppm twice daily, between 7:00 and 8:00 AM and 4:00 and 5:00 PM. After the exposure to NO2 was over the animals were killed by decapitation. The cranium was opened and the brain removed, and afterwards at 0 degrees C the left hemisphere was dissected into discrete areas which were then frozen on dry ice and weighed. The tissues were kept for 2-3 days at -20 degrees C, and afterwards the content of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindole-acetic acid was estimated spectrofluorometrically in examined parts of the brain (thalamus--hypothalamus pons + medulla oblongata hippocampus, cortex frontalis). It was shown that the applied NO2 concentrations brought about slight and nonspecific alterations in the content of the investigated amines in guinea pigs' brain.