Toxic copper level increases erythrocyte glycolytic rate,glutathione production and alters electrolyte balance in male Wistar rats |
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| Affiliation: | 1. Applied and Environmental Physiology Unit, Department of Physiology, University of Ibadan, Nigeria;2. Department of Human Physiology, College of Health Sciences, Nnamdi Azikiwe University, Nnewi Campus, Nigeria;1. Department of Biomedical Engineering, Iskenderun Technical University, Hatay 31200, Turkey;2. Department of Genetics, Inonu University School of Medicine, Malatya 44280, Turkey;3. Department of Molecular Biology and Genetics, Izmir Institute of Technology, Izmir 35430, Turkey;1. Laboratory Medicine Department, Faculty of Applied Medical Sciences, Umm Al-Qura University, Al Abdeyah, PO Box 7607, Makkah, Saudi Arabia;2. Biochemistry Department, Faculty of Medicine, Umm Al-Qura University, Al Abdeyah, PO Box 7607, Makkah, Saudi Arabia;3. Clinical Pathology Department, Faculty of Veterinary Medicine, Mansoura University, Mansoura, Egypt;4. Biochemistry Department, Faculty of Pharmacy, Al-Azhar University, Assuit 71524, Egypt;1. Department of Restorative Dentistry, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran;2. Department of Radiopharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran;3. Iranian National Center for Addiction Studies (INCAS), Tehran University of Medical Sciences, Tehran, Iran;4. School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran;5. Department of Community Oral Health, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran;6. Research Center for Caries Prevention, Dentistry Research Institute, Tehran University of Medical Sciences, Tehran, Iran;7. Department of Cariology, Operative Dentistry and Dental Public Health, Oral Health Research Institute, Indiana University School of Dentistry, Indianapolis, IN, USA;1. Department of Animal and Poultry Nutrition, Faculty of Animal Science, Gorgan University of Agricultural Science and Natural Resources, Iran;2. Department of Animal Science, faculty of Agriculture, University of Tabriz, Iran;1. Department of Thoracic Surgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, PR China;2. Department of Clinical Laboratory, Binzhou Medical University Hospital, Binzhou 256603, PR China;3. National Center for Orthopaedics, Department of Molecular Orthopaedics, Beijing Research Institute of Traumatology and Orthopaedics, Beijing Jishuitan Hospital, Beijing 100035, PR China;4. State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, PR China;5. College of Veterinary Medicine, China Agricultural University, Beijing 100083, PR China;6. State Key Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medicine Sciences & School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100005, PR China;1. Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha 410078, China;2. Center of Clinical Pharmacology, the Third Xiangya Hospital, Central South University, Changsha 410013, China;3. Environmental Science and Engineering, College of Resource and Environment, Hunan Agricultural University, Changsha 410128, China |
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| Abstract: | BackgroundCopper is a micronutrient vital to several cellular energy metabolic processes and drives erythropoiesis. However, it disrupts cellular biological activities and causes oxidative damage when in excess of cellular needs. This study investigated the effects of copper toxicity on erythrocyte energy metabolism in male Wistar rats.MethodsTen Wistar rats (150–170 g) were randomly divided into 2 groups: control (given 0.1 ml distilled water) and copper toxic (given 100 mg/kg copper sulphate). Rats were orally treated for 30 days. Blood, collected retro-orbitally after sodium thiopentone anaesthesia (50 mg/kg i.p.) into fluoride oxalate and EDTA bottles, was subjected to blood lactate assay and extraction of red blood cell respectively. Red blood cell nitric oxide (RBC NO), glutathione (RBC GSH), adenosine triphosphate (RBC ATP) levels, RBC hexokinase, glucose-6-phosphate (RBC G6P), glucose-6-phosphate dehydrogenase (RBC G6PDH), and lactate dehydrogenase (RBC LDH) activity was estimated spectrophotometrically. Values (Mean±SEM, n = 5) were compared by Student’s unpaired T-test at p < 0.05.Results and conclusionCopper toxicity significantly increased RBC hexokinase (23.41 ± 2.80 µM), G6P (0.48 ± 0.03 µM), G6PDH (71.03 ± 4.76nmol/min/ml) activities, ATP (624.70 ± 57.36 µmol/gHb) and GSH (3.08 ± 0.37 µM) level compared to control (15.28 ± 1.37 µM, 0.35 ± 0.02 µM, 330.30 ± 49.58 µmol/gHb, 54.41 ± 3.01nmol/min/ml and 2.05 ± 0.14 µM respectively, p < 0.05). Also, RBC LDH activity (145.00 ± 19.88mU/ml), NO (3.45 ± 0.25 µM) and blood lactate (31.64 ± 0.91 mg/dl) level were lowered significantly compared to control (467.90 ± 94.23mU/ml, 4.48 ± 0.18 µM and 36.12 ± 1.06 mg/dl respectively). This study shows that copper toxicity increases erythrocyte glycolytic rate and glutathione production. This increase could be connected to a compensatory mechanism for cellular hypoxia and increased free radical generation. |
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| Keywords: | Copper Erythrocyte Glycolytic rate Adenosine triphosphate Glutathione Nitric oxide |
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