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Lead stimulates the glutathione system in selective regions of rat brain.
Folia Neuropathol. 2002: 40 (4) s.203-209, il., bibliogr. 44 poz.
Hasła klasyfikacyjne GBL:
Lead (Pb) is a highly neurotoxic agent that causes functional and structural abnormalities in the brain. Glutathione (GSH) is a main molecule involved in the protection mechanisms against Pb itself and against reactive oxygen species generated by the metal. This study was carried out to investigate the effect of Pb on the glutathione system in several regions of adult rat brain. In the model of Pb toxicity, adult Wistar rats were exposed to 25 mg of lead acetate/kg b.w. for 3 days. Glutathione and the related enzymes i.e. ç-glutamylcysteine synthetase (ç-GCS), glutathione reductase (GR) and glutathione S-transferases (GSTs) were examined in the hippocampus, cerebellum and forebrain. In the cystolic fraction the concentration of total GSH and the activity of GR increased only in the cerebellum of Pb-exposed rats. Higher increases of both parameters were observed in mitochondrial fraction obtained from the cerebellum and hippocampus. The activity of cystolic enzyme - ç-GCS was enhanced only in the forebrain. Regarding cytosolic GSTs, changes in the activity together with enhanced relative density of enzyme protein were found in the cerebellum and hippocampus. Generally, activation of the glutathione system observed shortly after Pb treatment suggests the protective response of the brain in toxic insult. Regional differences in the pattern of these changes may coincide with different susceptibility to Pb. Present results suggest also that mitochondrial mechanisms might account for lead toxicity.
Experimental and human ischaemia: is the penumbra present in human ischaemic stroke?
Folia Neuropathol. 2002: 40 (4) s.211-217, il., bibliogr. 60 poz.
Hasła klasyfikacyjne GBL:
Experimental occlusion of the middle cerebral artery and reduction of cerebral blood flow (CBF) below 15 ml/100 gm/per minute cause failure of the somatosensory evoked response and lethargy of cortical neurones. Increase of CBF to normal value normalises the bioelectrical activity within the "penumbra"- the zone surrounding the necrotic area. In this "risk zone" neurones can survive only a few hours. So the penumbra is a "therapeutic window" in which therapy can save some neurones from death. However, if decrease of CBF is continued, numerous cells within the penumbra gradually die. The phenomenon of the penumbra, based on experiments, was applied to human ischaemic stroke; however great differences between experimental and human brain ischaemia do exist. The human course of disease and the size of necrotic lesions depend on numerous additional factors. The three very important critical values of CBF which decrease in human brain ischaemia are difficult to examine. New imaging methods play a great diagnostic role in searching for the penumbra, but their diagnostic possibilities and results are limited. In the short-time duration of the therapeutic window both CT and MRI often do not indicate ischaemic lesion. So, it is known whether the penumbra is present or not. Conclusive estimation of MRI diffusion-weighted imaging and perfusion-imaging and of their coefficient is impossible to obtain in the timee exceeding the "therapeutic window". Numerous additional various diseases and compensatory vascular mechanisms influence the necrotic zone in human focal ischaemia...
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