Exposure of school children to polycyclic aromatic hydrocarbons, heavy metals and radionuclides in the urban soil of Kragujevac city, Central Serbia.

The concentrations of radionuclides, polycyclic aromatic hydrocarbons (PAHs) and heavy metals were measured in soil samples collected from school backyards and playgrounds in Kragujevac, one of the largest cities of Central Serbia. The activity concentrations of (226)Ra, (232)Th, (40)K and (137)Cs were determined using the HPGe semiconductor detector. The average values were 34.6, 44.7, 428.9 and 45.1 Bq kg(-1), respectively. The correlation between the activity concentrations of (226)Ra in the soil samples and the results of the previous measurement of (222)Rn concentrations in the indoor air was examined. The absorbed dose rates, the annual effective doses and excess lifetime cancer risk were also estimated. The activity concentrations of (226)Ra and (232)Th have shown normal distribution. The collected soil samples were analysed for PAHs by HPLC. All analysed soil samples contained PAHs, and their total amounts (for 15 measured compounds) were found to be between 0.038 and 3.136 mg kg(-1) of absolutely dry soil (a.d.s). In addition the concentrations of As, Cd, Co, Cr, Cu, Fe, Mn, Ni, Pb and Zn were measured in the fourteen soil samples collected from the playgrounds of kindergartens.

Oxidative stress in the rats brain capillaries in sepsis--the influence of 7-nitroindazole.

As a part of blood-brain barrier, brain capillaries participate in pathophysiological events during systemic inflammation. We investigated the effects of 7-nitroindazole (7-NI), selective neuronal nitric oxide synthase (NOS) inhibitor, to oxidative status (OS) of brain capillaries. Adult Wistar rats were randomized at groups: control group (CG) (sham operated), sepsis group (GS) (cecal ligation and perforation with inoculation of Escherichia coli (ATCC 25922), 7-NI group (G7-NI), (30 mg/kg b/w i.p.) and 7-NI + sepsis group (G7-NIS), (7-NI was applied 30 minutes before operation). Lipid peroxidation index (LPI), nitrite concentration, superoxide dismutase (SOD) activity and superoxide anion (O2*-) content were determined 3, 6, 24 and 48 hour in each group. Cerebral capillaries were separated from non-vascular brain tissue using sucrose gradient. Compared to controls, LPI, nitrite and O2*- increased at SG. In the G7-NIS, LPI reached control values at the 24th and 48th hour, while nitrite were decreased at the 3rd and 24th hour, compared to controls. In the same group, O2*- decreased at the 3rd, 6th and 24th hour, although SOD showed variable activity. The systematic nNOS inhibition with 7-NI forces OS on early terms of sepsis, but lately it contributes to the normalization of OS in cerebral capillaries.

Effects of extremely low-frequency magnetic field in the brain of rats.

An extremely low-frequency magnetic field (50 Hz, 0.5 mT) was used to investigate its possible effect on the brain of adult male Wistar rats following a 7-day exposure. The control rats were sham-exposed. Superoxide dismutase activities and production of superoxide radicals, lipid peroxidation, and nitric oxide were examined in the frontal cortex, striatum, basal forebrain, hippocampus, brainstem, and cerebellum. Significantly increased superoxide radical contents were registered in all the structures examined. Production of nitric oxide, which can oppose superoxide radical activities, was significantly increased in some structures: the frontal cortex, basal forebrain, hippocampus, and brainstem. Augmentation of lipid peroxydation was also observed, with significance only in the basal forebrain and frontal cortex, in spite of the significantly increased superoxide dismutase activities and nitric oxide production in the basal forebrain, and increased production of nitric oxide in the frontal cortex. The results obtained indicate that a 7-day exposure to extremely low-frequency magnetic field can be harmful to the brain, especially to the basal forebrain and frontal cortex due to development of lipid peroxidation. Also, high production of superoxide anion in all regions may compromise nitric oxide signaling processes, due to nitric oxide consumption in the reaction with the superoxide radical.

Cytochrome C oxidase activity and total glutathione content in experimental model of intracerebral aluminum overload.

Treatment of Wistar rats with aluminum chloride causes astroglial and neuronal cell damage in the selective brain regions of association cortex and hippocampus, seen in patients with Alzheimer's disease. Adult Wistar rats were treated with unilateral intrahippocampal injection of AlCl3 in one single dose of 3.7 g/kg b.w. Control group of animals was treated with 0.9% saline solution likewise. Animals were sacrificed by decapitation seven days after the treatment. Activity of cytochrome C oxidase (COX) and total glutathione content were measured in the ipsi- and contralateral hippocampus and forebrain cortex. Activity of COX was mutually decreased in the hippocampus (ipsi- 30%, contra- 34%), as well as in the forebrain cortex (ipsi- 44%, contra- 47%), compared to controls. These decrease could indicate a deficiency in reducing equivalents with concomitant altered proton gradient and function of electron transport chain, as well as decreased ATP synthesis. Content of glutathione, a clue antioxidative factor, was decreased for about 50% in all examined structures, primary suggesting an impaired regeneration of reduced glutathione. Such distribution of diminished antioxidative defense could be the consequence of the specific brain distribution of transferrin receptors, which was also a main protein carrier for Al. Furthermore, at the cellular level Al could impede glycolysis with consequent decreased production of reducing equivalents which were necessary for glutathione synthesis/reduction, as well as for proton gradient and functionality of electron-transport chain.

Effects of nerve growth factor on antioxidative system in the thalamus of MPTP treated Wistar rats.

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism is one of the most useful models for the study of that disease. It has been suggested that MPTP-induced neurotoxicity may involve the production of reactive oxygen species. MPTP was applied intracerebrally, unilaterally, in the striatum in single dose of 0.09 g/kg b.w. The second group was treated both with MPTP and nerve growth factor (NGF) in dose of 7 ng/ml. NGF was applied immediately after the neurotoxin. Control group was treated with 0.9% saline solution in the same manner. Animals were decapitated 7 days after the treatment. In the group treated with MPTP, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) was decreased in ipsilateral thalamus, compared to control values as well as to the contralateral thalamus. In the same structures superoxide anion production was increased, compared to controls. Following the application of both MPTP and NGF, the activity of SOD and GSH-Px remained on control values, while the superoxide anion content was decreased, compared to controls. These results indicate a temporal and spatial propagation of oxidative stress and spread protective effects of NGF on the thalamus, the structure that is distant, but very tightly connected with striatum, the place of direct neurotoxic damage.

Index of lipid peroxidation and glucose utilization in the cerebrospinal fluid in patients with cerebral infarction.

Cerebral ischemia could be observed as acute metabolic crisis, when oxygen and glucose supply is compromised and synthesis of energy is insufficient. Apart from the excitotoxicity, increased production of reactive oxygen species with consequent lipid peroxidation is also included in neuronal cell damage. Furthermore, these toxic compounds could also be produced during the process of secondary inflammation of ischemic tissue. In the early stage of ischemia, as a systemic response to acute stress, there is an increase in glucose level in cerebrospinal fluid (CSF) and peripheral blood. According to the metabolic crisis and acidosis in ischemic brain tissue we investigated index of lipid peroxidation (ILP) and glucose utilization (IGU) in CSF of 53 patients of both sexes, aged 55-70 years with cerebral infarction. Control group comprised 15 patients with sudden onset of motor deficit subjected to diagnostic lumbar radiculography and suspected on discal genesis. ILP in CSF, as the indicator and sequela of neuronal cell membranes damage, was two fold increased in the acute period of cerebral infarction and maximal values (3.5 times) were noticed 24 hours after the ischemic episode compared to controls. Besides the increase in glucose concentration in peripheral blood and CSF of patients with cerebral infarction, IGU was decreased (37%) with minimal values (32%) 24 hours after the ischemia. These changes indicate that glucose is available but cells are incapable to metabolize it. We concluded that ILP and IGU in CSF of patients with cerebral infarction could be indicators of metabolic dysfunction and neuronal cell damage. Also, these results suggest the significance of polyvalent therapy including antioxidative and antiinflammatory agents in acute phase of cerebral ischemia.

Oxidative stress in the thalamus of Wistar rats treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

Experimental parkinsonism was induced in adult Wistar rats by selective nigrostriatal neurotoxine, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in a single dose of 0.09 g/kg, by unilateral intrastriatal application using stereotaxic instrument. Control group included rats treated with 0.9% saline solution in the same manner. Animals were sacrificed by decapitation seven days after the treatment. Total glutathione was measured in the crude mitochondrial fraction of thalamus and striatum. Total glutathione content, as a measure of reduced cell atmosphere, was mutually decreased in the thalamus and striatum of MPTP-treated animals, compared to controls: thalamus ipsi- = 24.8 +/- 3.11, contralateral = 26.81 +/- 5.31; striatum ipsi- = 19.96 +/- 4.13, contralateral = 17.3 +/- 4.09 nmol/mg prot. Mutually depleted glutathione content in the thalamus and contralateral striatum, the structures distant from ipsilateral treated striatum, could indicate on spatial propagation of oxidative stress, not only in the selective vulnerable dopaminergic nigrostriatal neurons, but in the structures included in the motor and cognitive loops of basal ganglia.