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Therapeutic Effect of Magnesium Sulphate on Carbon Monoxide Toxicity-Mediated Brain Lipid Peroxidation

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Therapeutic Effect of Magnesium Sulphate on Carbon Monoxide Toxicity-Mediated Brain Lipid Peroxidation European Review for Medical and Pharmacological Sciences 2013; 17(Suppl 1): 28-33 Therapeutic effect of magnesium sulphate on carbon monoxide toxicity-mediated brain lipid peroxidation Y. YAVUZ1, H. MOLLAOGLU2, Y. YÜRÜMEZ3, K. ÜCOK4, L. DURAN1, K. TÜNAY5, L. AKGÜN6 1Department of Emergency Medicine, Ondokuz Mayis University of Medical School, Samsun, Turkey 2Department of Physiology, Sifa University of Medical School, Izmir, Turkey 3Department of Emergency Medicine, Sakarya University of Medical School, Sakarya, Turkey 4Department of Physiology, Afyon Kocatepe University of Medical School, Afyonkarahisar, Turkey 5Department of Emergency Medicine, Afyonkarahisar State Hospital, Afyonkarahisar, Turkey 6Department of Physiology, Afyonkarahisar State Hospital, Afyonkarahisar, Turkey Abstract. – BACKGROUND: Carbon monox- reaching the top level within 24th hours, significant ide (CO) toxicity primarily results from cellular hy- oxidative damage was not observed. The protective poxia caused by impedance of oxygen delivery. effect against oxidative damage of magnesium sul- Studies show that CO may cause brain lipid per- fate has been identified within the first 6 hours. oxidation and leukocyte-mediated inflammatory Key Words: changes in the brain. Carbon monoxide toxicity, Magnesium sulphate, AIM: The aim of this study was to investigate whether magnesium sulphate could prevent or Brain, Lipid peroxidation. diminish brain lipid peroxidation caused by car- bon monoxide toxicity in rats. MATERIALS AND METHODS: Fourty rats were Introduction divided into five groups of 8 rats each. Group l was not received any agent during the experiment. Carbon monoxide (CO) is a colorless, odorless Group 2 was inhaled CO gas followed by intraperi- toneally normal saline 30 minutes (min) later. and non-irritant gas produced by the incomplete Group 3 was inhaled CO gas followed by 100 combustion of carbon-containing fuels1. CO poi- mg/kg magnesium sulphate intraperitoneally 30 soning is one of the commonest public health prob- min later. Group 2 and Group 3 rats was under- lems in our country and around the world (1.2). It is gone laparotomy and craniotomy while still under the most common cause of death resulting from anesthesia at 6 hour, and tissue sample was ob- 3 tained from the cerebrum. Group 4 was inhaled poisoning in the United States . Every year, about CO gas followed by intraperitoneally normal saline 40,000 people apply to Emergency Services for CO 30 min later. Group 5 was inhaled CO gas followed poisoning in the United States1. In Turkey, CO poi- by 100 mg/kg magnesium sulphate intraperi- soning is reported the most frequent cause of death toneally 30 min later. Group 4 and Group 5 rats with a rate of approximately 31%2. CO poisoning is was undergone laparotomy and craniotomy while a toxic condition resulting from inhaling gases de- still under anesthesia at 24 hour, and tissue sam- ple was obtained from the cerebrum. veloping from any combustion reaction, car ex- RESULTS: Nitric oxide levels were no signifi- haust, improper chimney structure, industrial sub- cantly different between all groups. Malonyl- stances, or a fire in a non-aerated environment2,4,5. dialdehyde levels increased in intoxication group CO creates a reversible bind with respiratory en- (group 2) and decreased in treatment group zymes and pigments such as hemoglobin, myoglo- (group 3). Activities of superoxide dismutase de- bin, cytochrome P450 and cytochrome aa3. CO creased in intoxication group (group 2) and in- creased in treatment group (group 3). Activities of binds to hemoglobin 230-270 times more avidly catalase increased in intoxication group (group 2) than oxygen. Small concentrations such as 100 ppm and decreased in treatment group (group 3). Ac- create a COHb level of 16% approximately; this tivities of glutathione peroxidase (GSH-Px) de- level is sufficient for the occurence of clinical creased in intoxication group (group 4) and in- symptoms4,6: primary tissue hypoxia occurs and ac- creased in treatment group (group 5). CONCLUSIONS: CO poisoning caused signifi- companying damages develop. CO has been shown cant damage, detected within the first 6 hours. Due to cause brain lipid peroxidation and leukocyte-me- to antioxidant enzymes, especially GSH-Px activity diated inflammatory changes in the brain4. Increase 28 Corresponding Author: Yücel Yavuz, MD; e-mail: [email protected] Magnesium sulphate on carbon monoxide toxicity of thiobarbituric acid reactive products (TBARS) in conditions and were allowed free access to food the rat brain tissue after oxidized proteins, reduces and water. These experiments were approved by glutathione poisoning and lead to oxidative stress. the Institutional Animal Care and Use Committee Nitric Oxide (NO) may lead to elevation of glu- (IACUC) of Afyon Kocatepe University and tathione after CO poisoning. Due to the changes as- were in accordance with National Institutes of sociated with NO, extravasations of intravascular Health Guide for the Care and Use of Laboratory cells and the lipid peroxidation in brain cells occur7. Animals (NIH publication, vol 25, no. 28, 1996). Brain damage may develop if hypoxia accompa- This research was supported by Afyon Kocatepe nied with a period of loss of consciousness7. Addi- University Scientific Committee. The rats were tionally, glutamate level, an excitatory amino acid, divided into five groups as follows; increases after CO poisoning. Glutamate binds to Group 1: No test procedure was performed. N-methyl-D-aspartate receptors and leads to intra- Brain tissue was removed immediately after cellular calcium release that cause delayed neuronal sacrificing the animal (eight rats). cell death7. Central nervous system is one of the Group 2: The rats were exposed to CO gas and sensitive organs to CO. Headache, dizziness, and treated with saline. Evaluations were carried out ataxia may occur at COHb level of 15-20%. Long- at the 6th hour and the animals were sacrificed term exposure to CO may cause syncope, convul- and then brain tissue was removed (eight rats). sions, focal epileptic seizures and coma5,8. Patients Group 3: The rats were exposed to CO gas and may have acute stroke symptoms and leukoen- treated with magnesium sulfate. Evaluations cephalopathy and brain edema may develop5. were carried out at the 6th hour and the animals Treatment of CO poisoning is still controver- were sacrificed and then brain tissue was re- sial due to the confusing clinical trials5. Mankind moved (eight rats). benefits from the therapeutic effect of magne- Group 4: The rats were exposed to CO gas and sium (Mg) for centuries. Today, Mg is known to treated with saline. Evaluations were carried out have different effects on almost every system in at the 24th hour and the animals were sacrificed our body9. A sudden increase in the serum Mg and then brain tissue was removed (eight rats). concentration in the cerebral circulation leads to Group 5: The rats were exposed to CO gas and a rapid and concentration dependent vasodilata- treated with magnesium sulfate. Evaluations tion in cerebral arteries. Magnesium sulfate pro- were carried out at the 24th hour and the ani- tects the spinal cord from ischemic injury in dogs mals were sacrificed and then brain tissue was with spinal cord ischemia. Another study10 has removed (eight rats). revealed that magnesium sulfate have neuropro- tective effects on axonal function and lipid in CO Gas Exposing Protocol rats. It was also reported that magnesium sulfate Rats to be poisoned with CO were placed in an reduce neuronal apoptosis in cerebral ischemia- anesthesia chamber made of transparent glass reperfusion injury. It was suggested11 that sys- (dimensions 60 × 27 × 27 cm). Eight rats were temically administered magnesium have neuro- placed into the cup at every session. Rats were protective effects and shrink the area of stroke in randomized to a control group (N=4) and a mag- animal models of stroke. An increase of lactate nesium group (N=4). In the beginning, CO gas and MDA levels in brain tissue may cause is- exposure was set to be 1000 ppm and this chemia reperfusion injury and the magnesium process continued for 120 minutes. Then CO lev- sulfate supress this increase12. el was raised from 1000 to 2000 ppm and this To our knowledge, the effects of magnesium sul- process continued about 30 minutes. Rats were fate in CO poisoning has not been investigated yet. exposed to ambient air. Observations were made The purpose of this study is to investigate whether by the same observer throughout the experiment. magnesium sulfate have therapeutic effect on ox- idative damage due to CO poisoning in the brain. Magnesium Sulphate and Saline Administration Magnesium sulfate was administered to both Materials and Methods group 3 and group 5 in the same way. After 30- minute exposure to CO, rats were administered Preparation of Animals intraperitoneal injection of magnesium sulfate Male Sprague-Dawley rats weighing 160 to in a dose of 100 mg/kg. Intraperitoneal injec- 250 g were housed under standard laboratory tion of saline was given to control groups 29 Y. Yavuz, H. Mollaoğlu, Y. Yürümez, K. Üçok, L. Duran, K. Tünay, L. Akgün, (group 2 and group 4) after 30-minute exposure (NO2−) and subsequently to nitrate (NO3−), to CO in the same amount. which serve as index parameters of NO produc- tion. The method for determination of nitrite Biochemical Analysis and nitrate levels was based on the Griess reac- At the sixth and twenty-fourth hour of the tion. Samples were initially deproteinized with study, rats were sedated with intramuscular injec- Somogyi reagent. Total nitrite (NO2− + NO3−) tion of 50 mg/kg ketamine. Abdomen was in- was measured by spectrophotometry (Shi- cised in the midline and rats were sacrificed by madzu, UV-Pharmaspec 1700, Kyoto, Japan) at drawing blood from abdominal aorta. After inci- 545 nm after the conversion of NO2− to NO3− by sion of the skull, the brain tissue was removed as copperized cadmium (Cd) granules.
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