The effect of vitamin E supplementation on brain tissue element levels in epileptic rats.

The aim of this study was to investigate how the application of vitamin E affected the levels of chemical elements in the brain tissues of epilepsy-induced rats. The sample of 40 adult male rats was separated into 4 equal groups: Group 1: control, Group 2: vitamin E; Group 3: penicillin to promote epileptic form activity and Group 4: penicillin + vitamin E. After three months of treatment, an Atomic Absorption Spectrophotometer was used to analyze the presence of the elements in brain tissue sections (brain, brainstem, cerebellum) of the decapitated animals. The levels of magnesium in the groups that received vitamin E (G2 and 4) were significantly higher than in the control group (G1) and the first epilepsy group (G3) (p.05).Chrome and zinc levels in brain, brainstem, and cerebellum tissue of the two epilepsy groups (G3-4) decreased significantly compared to the control group (G1) and the vitamin E group (G2) (p.05). The levels of copper in the brainstem and lead in the cerebellum of the first epilepsy group (G3) were higher than in all other groups (p.05). The findings showed that the application of vitamin E in experimental epilepsy may have a limited effect on element metabolism in brain tissue. A decline in zinc levels in the brain, brainstem and cerebellum tissues in epilepsy groups constitutes another result of our study. This should be examined further to determine whether decreased levels of zinc play a role in epilepsy pathogenesis.

Hemopressin increases penicillin-induced epileptiform activity in rats.

OBJECTIVE: Hemopressin (Hp) is the first peptide ligand described for the CB1 cannabinoid receptor. Therefore, we aimed to investigate the effect of hemopressin on pencillin-induced epileptiform activity by using electrophysiological recording (ECoG) technique. METHODS: Male Wistar rats were anesthetized with urethane (1.25 g/kg), and epileptiform activity was induced by intracortical injection of penicillin (500 IU). Animals were randomly divided into eight groups. Subsequently, the rats were administered with saline or hemopressin as follows: saline control group (Group I: 2 µl/i.c.v/saline), hemopressin groups (Group II: 0.025 µg/i.c.v; Group III: 0.075 µg/i.c.v; Group IV: 0.15 µg/i.c.v; Group V: 0.3 µg/i.c.v; Group VI: 0.6 µg/i.c.v; Group VII: 1.2 µg/i.c.v; Group VIII: 2.4 µg/i.c.v). The various doses of hemopressin were injected intracerebroventricularly (i.c.v) 30 minutes after penicillin (2.5µl) injection. After hemopressin injection, ECoGs were recorded for three hours. RESULTS: Hp at doses of 0.075, 0.15, 0.3, 0.6, 1.2 and 2.4 µg/kg significantly increased the frequency of epileptiform ECoG activity compared to penicillin-injected group without changing the amplitude. The 0.6 µg hemopressin was the most effective dose to increase the epileptiform activity (p 0.05). CONCLUSIONS: The results of this study provided electrophysiological evidence for hemopressin to be modulating penicillin-induced epileptiform activity by acting as CB1 receptor antagonist. Further studies are required to elucidate the involved mechanism underlying this effect (Fig. 3, Ref. 40).

Lipid peroxidation in kidney and testis tissues in experimental hypothyroidism: the role of zinc.

The aim of the present study was to determine the effect of zinc supplementation and zinc deficiency on the lipid peroxidation in the testis and kidney tissues of rats with experimentally induced hypothyroidism. The experimental Groups were formed as follows: 1 - Control; 2 - Sham-Hypothyroidism; 3 - Hypothyroidism (intraperitoneal administration of 10 mg/kg/day PTU for 4 weeks); 4 - Hypothyroidism + 3 mg/kg/day zinc supplementation (4 weeks); 5 - Hypothyroidism + zinc deficiency (4 weeks). The examination of the study results revealed that hypothyroidism in testis and kidney tissues increased MDA levels and decreased GSH levels (p<0.001). Zinc supplementation in addition to hypothyroidism, however, reduced the increased MDA amount and elevated GSH levels (p<0.001). Zinc deficiency together with hypothyroidism, on the other hand, was found to produce the opposite results (p<0.001). The results of the study indicated that experimental hypothyroidism caused lipid peroxidation in kidney and testis tissues. Zinc deficiency together with hypothyroidism made lipid peroxidation more evident, while zinc supplementation significantly inhibited the increased oxidative stress by activating the antioxidant system (Tab. 1, Ref. 24).

Effects of high fat diet induced obesity on peripheral nerve regeneration and levels of GAP 43 and TGF-ß in rats.

The increasing frequency of obesity is important because of its accompanying related health problems. The effects of obesity on peripheral nerves have not been elucidated. We investigated the effects of obesity on sciatic nerve regeneration using electrophysiology, stereology, immunohistochemistry, histopathology and functional tests. We used control, obese, control injured and obese injured groups of rats. Electrophysiological results showed that nerve conduction velocity and EMG were same in the experimental groups, but the amplitude of the compound action potential of the control group was significantly higher than that of the obese group. Examination of the nerves showed that the control and obese groups had both larger axon diameters and thicker myelin sheaths. The number of myelinated axons was decreased in both of the injured groups. Axon diameters and myelin sheath thicknesses of the control injured group were significantly greater those of the obese injured group. There were no significant differences in functional tests among the groups. Although growth associated protein 43 immunostaining in the control injured group was significantly greater than that of the obese injured group, no significant difference was observed between the control and obese groups. There was no significant difference in immunohistochemical staining for transforming growth factor beta 3 between the control injured and obese injured groups. Our results suggest that obesity may affect peripheral nerve regeneration negatively after crush injury.

The involvement of iNOS activity in the anticonvulsant effect of grape seed extract on the penicillin-induced epileptiform activity in rats.

Grape seed extract (GSE) has been known as being neuroprotective due to its antioxidant properties. The aim of the present study was to examine both the effect of GSE on the penicillin-induced epileptiform activity in rat and the role of nitric oxide (NO) pathway in the effect of GSE. GSE, at doses of 50, 100, 200 mg/kg, significantly decreased the mean frequency of epileptiform activity. GSE, at the highest dose (400 mg/kg), did not change either the frequency or amplitude of epileptiform activity. GSE, at a dose of 200 mg/kg, was the most effective in changing the frequency of epileptiform activity. The occurrence of anticonvulsant activity of GSE was significantly delayed in the presence of selective inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (60 mg/kg), which was inhibited by the NO precursor, L-arginine (500 mg/kg). The administration of a non-selective NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) partially reversed the anticonvulsant activity of GSE. Selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) and L-arginine showed a similar anticonvulsant activity in the presence of GSE. The electrophysiological evidence of the present study indicates that GSE decreases the mean frequency of penicillin-induced epileptiform activity, suggesting an anticonvulsant role. iNOS/NO pathway could be involved in mediating anticonvulsant effect of GSE on the epileptiform activity.

An optoelectromechanical tactile sensor for detection of breast lumps.

We developed a compact tactile imaging (TI) system to guide the clinician or the self-user for noninvasive detection of breast tumors. Our system measures the force distribution based on the difference in stiffness between a palpated object and an abnormality within. The average force resolution, force range, and the spatial resolution of the device are 0.02 N, 0-4 N, and 2.8 mm, respectively. To evaluate the performance of the proposed TI system, compression experiments were performed to measure the sensitivity and specificity of the system in detecting tumor-like inclusions embedded in tissue-like cylindrical silicon samples. Based on the experiments performed with 11 inclusions, having two different sizes and two different stiffnesses located at three different depths, our TI system showed an average sensitivity of 90.8 ± 8.1 percent and an average specificity of 89.8 ± 12.7 percent. Finally, manual palpation experiments were performed with 12 human subjects on the same silicon samples and the results were compared to that of the TI system. The performance of the TI system was significantly better than that of the human subjects in detecting deep inclusions while the human subjects performed slightly better in detecting shallow inclusions close to the contact surface.

The effects of albendazole solution at scolocidal concentration in the rat brain.

Intra-operative cyst rupture is a catastrophic event in the intracranial hydatid cyst disease. Dissemination of the cyst contents may lead to severe anaphylactic reactions and an increased risk of recurrence. Several scolicidal agents have been used to eradicate the infective scolices but recurrences occur and no solution has been evaluated for its adverse effects to the brain tissue. Being a specific scolocidal agent albendazole has been shown to be 100% scolicidal in vitro. In this study, we present the electrophysiological and histopathological effects of intracerebral 2% albendazole injection in the rat brain. Vascular, neuronal and glial as well as inflammatory changes were evaluated in order to detect any adverse pharmacological effects. Electrophysiological and most microscopic parameters showed no significant effects attributable to albendazole but in 25% of the albendazole group cerebral gliosis was detected whereas no gliosis was present in the control group. It is concluded that being a specific scolicidal agent albendazole offers an efficient alternative for ruptured cerebral hydatid disease, but the significance and clinical importance of the gliosis should be further investigated.

The effect of ethanol on lipid peroxidation and glutathione level in the brain stem of rat.

The effects of ethanol consumption on the levels of lipid peroxidation (TBARS) and reduced glutathione (GSH) in the brain stem of male rats were investigated. The rats randomly divided into eight groups: control, 10%, 25%, 35% ethanol-consuming groups and four groups given vitamin E. Brain stem GSH levels were significantly decreased by 39.74%, 61.57%, 78.23% in rats consuming 10%, 25% and 35% ethanol, respectively. The level of TBARS was increased six-fold, 12-fold and 17-fold in these groups when compared with the control group. The administration of vitamin E (100 mg/kg/day, i.p) to ethanol-consuming rats for 20 days caused a significant increase in glutathione levels and a significant decrease in lipid peroxidation.

Do cochlear nuclei contribute to auditory lateralization? A stereological evaluation of neuron numbers.

The aim of this study was to estimate the total number of cells in the subdivisions of the cochlear nucleus (CN) of the rat with unbiased stereological methods. The total number of neurons was determined in both the ventral cochlear nucleus (VCN) and the dorsal cochlear nucleus (DCN) to compare the right and left sides. The total cell numbers were 15,280 in the left VCN, 15,400 in the right VCN, 10,260 in the left DCN, and 10,860 in the right DCN. Comparison of the right and left major subdivisions of the CN of the rat showed that there was no significant difference between the right and left sides of the rat CN. This result indicates that the CNs do not contribute to auditory lateralization in the rat in regard to cell numbers.

Effect of oral pyridoxine hydrochloride supplementation on arterial blood pressure in patients with essential hypertension.

The purpose of this study was to test the effect of vitamin B6 (pyridoxine-HCl, CAS 58-56-0) supplementation on arterial blood pressure in essential hypertension. The trial comprised 9 normotensive subjects (7 men and 2 women, aged between 32-58 years; mean +/- SD, 48 +/- 11) and 20 patients with essential hypertension (16 men and 4 women, aged between 32-69 years; mean +/- SD, 56 +/- 12). The patients were treated during 4 weeks with a single oral dose of pyridoxine (5 mg/kg body weight/day). After a 5-min rest, measurements were made in the supine position. When compared with the normotensive subjects, the hypertensive subject group had a significantly higher systolic and diastolic blood pressure (p < 0.001) and higher level of plasma norepinephrine (NE) (p < 0.01) before pyridoxine treatment. On the other hand, there were no significant differences in plasma epinephrine (E) and heart rates. Treatment of hypertensive patients with pyridoxine significantly reduced systolic (p < 0.01) and diastolic blood pressure (p < 0.005), plasma NE (p < 0.005) and E (p < 0.05) within 4 weeks. However, there was no significant difference in heart rate at the end of pyridoxine treatment. These results indicate a relationship between pyridoxine status and arterial blood pressure in the essential hypertensive patients.

Evidence that sodium nitroprusside possesses anticonvulsant effects mediated through nitric oxide.

The effect of sodium nitroprusside (SNP) on epileptiform activity elicited by administration of penicillin (500 units) into the somatomotor cortex was studied in anaesthetized rats. No epileptiform activity was observed after intracortical microinjection of SNP (5 and 20 nM). Microinjection of penicillin into the somatomotor cortex induced epileptiform activity in electrocorticograms (ECoG). Epileptiform discharges elicited by penicillin were significantly decreased by SNP. The effect of SNP appeared within 1 min of application and lasted for 2-5 min. The inhibitory effect of SNP on epileptiform activity could be prevented by pretreatment with methylene blue (20 nM), a soluble guanylate cyclase inhibitor. Prior injection of haemoglobin (5 microliter), a nitric oxide (NO) scavenger, prevented the anticonvulsant effect of SNP. These results suggest that NO may be an endogenous anticonvulsant substance.

The effects of the purinergic system on digitalis-induced epileptiform activity.

It has been suggested that endogenous chemical substances, such as adenosine, released during a seizure attack, may act as anticonvulsants in vivo. We have investigated electrophysiologically the effects of purinoceptor agonists and antagonists on the epileptiform activity induced by intracortical digitalis in anesthetized rats. Intracortical injections of 1, 2, or 4 micrograms digitalis (desacetyl lanatocid C) caused an epileptiform electrocorticogram (ECoG). The application of adenosine (25 or 100 microM) or adenosine triphosphate (ATP) (3 mM) after desacetyl lanatocid C blocked the epileptiform activity. beta, gamma-Methylene ATP (0.1-0.8 mM), a stable analog of ATP, produced inhibition and then death. The epileptogenic effect of desacetyl lanatocid C was enhanced by theophylline (1 mM); however, suramin (1 mM) changed the pattern of epilepsy. These results indicate that the purinergic system may be involved in the mechanism of action of digitalis glycosides.