Effects of extremely low-frequency electric fields at different intensities and exposure durations on mismatch negativity.

The effects of extremely low-frequency electric fields (ELF-EFs, 3-300Hz) on lipid peroxidation levels and antioxidant enzyme activities have been shown in many tissues and plasma after exposure to 50-Hz alternating current (AC) electric fields. However, similar studies investigating brain lipid peroxidation status are limited. Moreover and as far as we know, no study has been conducted to examine mismatch negativity (MMN) response in rats following exposure to a 50-Hz AC electric field. Therefore, the purpose of the study was to investigate different intensities and exposure durations of ELF-EFs on MMN component of event-related potentials (ERPs) as well as apoptosis and oxidative brain damage in rats. Ninety male rats, aged 3months were used in our study. A total of six groups, composed of 15 animals each, was formed as follows: sham-exposed rats for 2weeks (C2), sham-exposed rats for 4weeks (C4), rats exposed to 12-kV/m and 18-kV/m electric fields for 2weeks (E12-2 and E18-2), rats exposed to 12- and 18-kV/m electric fields for 4weeks (E12-4 and E18-4). At the end of the experimental period, MMN responses were recorded in urethane-anesthetized rats by electrodes positioned stereotaxically to the surface of the dura. After MMN recordings, animals were killed by exsanguination and their brain tissues were removed for 4-hydroxy-2-nonenal (4-HNE), protein carbonyl and TUNEL analysis. In the current study, different change patterns in ERP parameters were observed dependent on the intensity and exposure duration of ELF-EFs. There were differences in the amplitudes of ERP between the responses to the standard and the deviant tones in all groups. When peak-to-peak amplitude of the difference curves was evaluated, MMN amplitude was significantly decreased in the E18-4 group compared with the C4 group. Additionally, the amount of 4-HNE was increased in all experimental groups compared with the control group. Consequently, it could be concluded that electric field decreased MMN amplitudes possibly induced by lipid peroxidation.

Overview of the critical disaster management challenges faced during Van 2011 earthquakes.

On October 23, 2011, a M7.2 earthquake caused damage in a widespread area in the Van province located in eastern Turkey. This strong earthquake was followed by a M5.7 earthquake on November 9, 2011. This sequence of damaging earthquakes led to 644 fatalities. The management during and after these earthquake disaster imposed many critical challenges. In this article, an overview of these challenges is presented based on the observations by the authors in the aftermath of this disaster. This article presents the characteristics of 2011 Van earthquakes. Afterward, the key information related to the four main phases (ie, preparedness, mitigation, response, and recovery) of the disaster in Van is presented. The potential strategies that can be taken to improve the disaster management practice are identified, and a set of recommendations are proposed to improve the existing situation.

The effect of lipoic acid on antioxidant status and lipid peroxidation in rats exposed to chronic restraint stress.

This study was designed to investigate effect of alpha-lipoic acid (LA) on lipid peroxidation, nitric oxide production and antioxidant systems in rats exposed to chronic restraint stress. Twenty four male Wistar rats, aged three months, were divided into four groups: control (C), the group treated with LA (L), the group exposed to restraint stress (S) and the group exposed to stress and treated with LA (LS). Restraint stress was applied for 21 days (1 h/day) and LA (100 mg/kg/day) was injected intraperitonally to the L and LS groups for the same period. Restraint stress significantly decreased brain copper/zinc superoxide dismutase (Cu,Zn-SOD) and brain and retina glutathione peroxidase (GSH-Px) and catalase (CAT) activities compared with the control group. Thiobarbituric acid reactive substances (TBARS), nitrite and nitrate levels were significantly increased in the tissues of the S group compared with the C group. LA produced a significant decrease in brain and retina TBARS, nitrite and nitrate levels of the L and LS groups compared to their corresponding control groups. LA increased all enzyme activities in the tissues of the LS group compared to the S group. Our study indicated that LA is an ideal antioxidant candidate for the prevention of stress-induced lipid peroxidation.

L-carnitine protects gastric mucosa by decreasing ischemia-reperfusion induced lipid peroxidation.

Studies have shown that reactive oxygen metabolites and lipid peroxidation play important roles in ischemia-reperfusion injury in many organs such as heart, brain and stomach. The aim of this study is to evaluate the antioxidant effect of L-carnitine on gastric mucosal barrier, lipid peroxidation and the activities of antioxidant enzymes in rat gastric mucosa subjected to ischemia-reperfusion injury. Rats were subjected to 30 min of ischemia followed by 60 min of reperfusion. L-carnitine (100 mg/kg), was given to rats intravenously five minutes before the ischemia. In our experiment, lesion index, thiobarbituric acid reactive substances, prostaglandin E2 and mucus content in gastric tissue were measured. The results indicated that the lesion index and the formation of thiobarbituric acid reactive substances increased significantly with the ischemia-reperfusion injury in the gastric mucosa. L-carnitine treatment reduced these parameters to the values of sham operated rats. The tissue catalase and superoxide dismutase activities and prostaglandin E2 production decreased significantly in the gastric mucosa of rats exposed to ischemia-reperfusion. L-carnitine pretreatment increased the tissue catalase activity and prostaglandin E2 to the levels of sham-operated rats but did not change superoxide dismutase activity. There were no significant difference in glutathione peroxidase activity and mucus content between the groups in the gastric mucosa. In summary, L-carnitine pretreatment protected gastric mucosa from ischemia-reperfusion injury by its decreasing effect on lipid peroxidation and by preventing the decrease in prostaglandin E2 content of gastric mucosa.

The effects of L-carnitine on presbyacusis in the rat model.

Reactive oxygen metabolites are products of oxidative metabolism that are continuously generated in vivo, and are known to produce serious cellular, tissue and genomic damage. l-carnitine is an endogenous amine that has been shown to have an effect on the synthesis of reactive oxygen metabolites. Twenty Wistar rats, 24 months of age, were randomly assigned to two groups as control and l-carnitine treatment groups. One millilitre of distilled water was administered to control rats and 50 mg/kg l-carnitine to rats of l-carnitine treatment groups by intragastric gavage once a day for 30 days. At the end of 30 days, all groups underwent auditory brainstem response testing after administration of intraperitoneal urethane anaesthesia. l-carnitine treatment reduced III, V latencies and I-III, III-V and I-V interpeak latencies (IPL) significantly compared with the control group. l-carnitine treatment improved age-related deterioration in auditory pathways and hence may be a new alternative for the treatment of presbyacusis.

Protective effect of L-carnitine on gastric mucosal barrier in rats exposed to cold-restraint stress.

AIM: The protective effect of L-carnitine on stress-induced gastric mucosal injury was investigated in rats exposed to cold-restraint stress (CRS). METHODS: The animals were divided into four groups. Groups 1 and 3 received saline by intragastric gavage for 10 days. Groups 2 and 4 received L-carnitine (50 mg/Kg/day) in the same manner. Groups 3 and 4 were exposed to CRS in the form of immobilization at 4 degrees C for 4 h on day 10. Ulcer index, gastric acid secretion and hemoglobin leakage, and gastric mucosal mucin and PGE2 content were measured. RESULTS: In rats exposed to CRS, as compared to control rats (group 1), ulcer index was higher, gastric acid production was lower, hemoglobin leakage into the gastric lumen was increased, and gastric mucosal mucin and PGE content were reduced. L-carnitine treatment prior to CRS led to attenuation of changes in ulcer index, gastric acid secretion, amount of hemoglobin leakage into the gastric lumen and gastric PGE2 content. In rats receiving L-carnitine but not exposed to CRS, gastric acid secretion, mucin and PGE2 content of gastric mucosa were similar to those in control rats. CONCLUSION: L-carnitine decreases CRS-induced gastric mucosal injury.

Effect of carnitine on stress-induced lipid peroxidation in rat gastric mucosa.

PURPOSE: Carnitine is an essential cofactor in the mitochondrial transfer of fatty acids, but is also a scavenger of oxygen free radicals in mammalian tissues. It has been shown that cold-restraint stress (CRS) produces gastric mucosal injury due to oxygen free radicals. The aim of this study was to determine the effect of L-carnitine on lipid peroxidation induced by CRS in rat stomachs. METHODS: Rats pretreated with L-carnitine (50 mg/kg per day for 10 days) were restrained in a wire cage for 4 h at 4 degrees C. At the end of the experimental period, the lesion index in gastric mucosa was determined. In blood and gastric mucosa samples, the content of mucin, prostaglandin (PG)E2, the products of lipid peroxidation, and catalase activity were measured. RESULTS: CRS caused a significant decrease in gastric mucin and PGE2 content, while in the gastric mucosa of rats pretreated with L-carnitine, the changes in gastric mucin and PGE2 content, as well as gastric lesion development and enhanced lipid peroxide formation due to stress, were prevented. On the other hand, catalase activity in blood increased in the CRS group, while its value in gastric mucosa was not different from that in the control rats. L-Carnitine treatment increased catalase activity in both blood and gastric mucosa in control animals. Following stress, increased catalase activity of blood was associated with decreased mucosal catalase activity in rats that received L-carnitine. CONCLUSIONS: L-Carnitine prevents the occurrence of mucosal lesions by strengthening the gastric mucosal barrier and by reducing the products of lipid peroxidation against noxious factors that cause elevation of lipid peroxidation, such as CRS.

Effect of nitric oxide synthase inhibition on the gastric mucosal barrier in rats.

The aim of this study was to investigate the effect of N-G-nitro-L-arginine-methyl ester (L-NAME), a nitric oxide synthase inhibitor, on the gastric mucosal barrier in rats. A group of Swiss albino rats received L-NAME (60 mg/kg/d) in their drinking water daily for 21 d. The mucin and prostaglandin E2 (PGE2) contents of the gastric mucosa were measured in gastric tissue samples. L-NAME intake did not affect gastric mucin, but it significantly reduced PGE2, a component of the gastric mucosal barrier. The results of this study imply that nitric oxide plays an important mediatory role in maintaining the gastric mucosal barrier. The inhibition of nitric oxide may be involved in the increased vulnerability of the gastric mucosa to injurious stimuli in rats.

Effect of cold-restraint stress on the distribution of trace elements in rat tissues.

The aim of this study was to assess the effects of cold-restraint stress on blood and the other tissue levels of trace elements. The experiment was performed on male Swiss albino rats. The animals were divided to two groups: control and stressed groups. In the stressed group, the rats were subjected to immobilization for 4 h at 4 degrees C. At the end of the experimental period, blood and tissue samples were collected from all of the animals. The levels of zinc, copper, magnesium, and manganese were measured using flame and graphite furnace atomic absorption spectrometry. In rats subjected to stress, the zinc levels of serum were increased, whereas in the duodenum and brain, zinc was found to decrease when compared to the control. The magnesium content of both the stomach and duodenum were reduced, but the manganese levels of the liver, kidneys, and brain significantly increased because of stress. In conclusion, cold-restraint stress may affect the metabolic process by changing the distributions of zinc, magnesium, and manganese in tissues.