Ivana Vasiljevic

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.

7-nitroindazole reduces nitrite concentration in rat brain after intrahippocampal kainate-induced seizure.

Kainic acid is an endogenous excitotoxin acting on glutamate receptors, that leads to neurotoxic damage resembling the alterations observed in some neurological disorders. Stimulation of glutamate receptors induces neuronal nitric oxide (NO) release, which in turn modulates glutamate transmission. NO may be a key mediator of excitotoxic neuronal injury in the central nervous system. We investigated the effects of 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor in vivo, on nitrite concentration after kainic acid injection (0.6 mg/ml, pH 7.2) unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times (5 min, 15 min, 2 h, 48 h and 7 days) following kainate injection in the ipsilateral and contralateral hippocampus, forebrain cortex, striatum and cerebellum homogenates. 7-Nitroindazole (100 microM) can effectively inhibit NO synthesis in rat brain after kainate-induced intrahippocampal neurotoxicity and suppressed nitrite accumulation. The present results suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases where excitotoxic mechanisms play a role.

Oxidative stress in rat kidneys due to 3,4-methylenedioxymetamphetamine (ecstasy) toxicity

Aim:  The mechanism of MDMA (3,4‐methylenedioxymethamphetamine)‐induced toxicity is believed to be, in part, due to enhanced oxidative stress. As MDMA is eliminated via the kidney, the aim of this study was to investigate whether MDMA created conditions of oxidative stress within rat kidney.

The effects of exposure to extremely low-frequency magnetic field and amphetamine on the reduced glutathione in the brain.

Abstract: Continuous exposure to extremely low‐frequency magnetic field (ELF‐MF, 50 Hz, 0.5 mT) alone and combined with D‐amphetamine (1.5/mg/kg) affected the reduced glutathione content in brain regions of rats. Compared to sham‐exposed rats, the glutathione content in the forebrain cortex of the ELF‐MF‐exposed rats decreased (P < 0.001), but this reverted after giving amphetamine upon ELF‐MF exposure. In this group, the glutathione content was increased in the brain stem and cerebellum (P < 0.05 compared to the sham‐exposed, ELM‐MF‐exposed, and amphetamine‐treated groups). It is suggested that biogenic monoamines are involved in the reduced glutathione changes observed. The changes are not uniform in the brain regions examined.

Spermine and L-Name Pretreatment Effects on Polyamine and Nitric Oxide Metabolism in Rat Brain During Seizures

Spermine and L-Name Pretreatment Effects on Polyamine and Nitric Oxide Metabolism in Rat Brain During Seizures In the CNS polyamines can exert opposite effects, depending on the concentration and conditions in the cell. Protective or neurotoxic polyamine effects were documented during seizures and repeated CNS excitation. Intensive research of exogenous polyamines effects during seizures induced by numerous agents did not clear up confusions about the duality of effects and the role of polyamines in seizures. In order to understand polyamine modulatory effects in seizures, the importance of NO and polyamine metabolism interdependence and the possible implication of changes of postulated NO and polyamine equillibrium in seizures, the effects of spermine alone and in combination with L-NAME (NOS inhibitor) on seizures induced by pentazol (PTZ) were investigated. To compare the obtained results, the effects of anticonvulsant midazolam on NO production during seizures were also investigated. Seizures were induced by i.p. application of pentazol (100 mg/kg b.w.). Spermine and L-NAME were administered i.p. before PTZ. In the striatum and hippocampus, spermine induced increased NO production (p<0.001) related to values in the group treated by PTZ. Application of L-NAME before spermine and PTZ caused decrease of NO production in comparison with animals treated only by PTZ or spermine and PTZ. L-NAME given before spermine exerts protective effects related to seizures induced by PTZ and to the group treated by spermine, extending the time of seizure symptoms appearance, thus confirming the NO signaling system involvement in spermine effects during seizures. Highly significant PAO activity increase caused by spermine points out the intensified interconversion of spermine into putrescine, in order to maintain the intracellular putrescine concentration. The obtained results prove a strong relationship between the NO signaling system and polyamine metabolism in the brain during seizures and the importance of their changes in this kind of CNS injury.