Role of Exogenous Melatonin on Cell Proliferation and Oxidant/Antioxidant System in Aluminum-Induced Renal Toxicity
Aluminum has toxic potential on humans and animals when it accumulates in various tissues. It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous stu...
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| Veröffentlicht in: | Biological trace element research 2015-11, Vol.168 (1), p.141-149 |
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| description | Aluminum has toxic potential on humans and animals when it accumulates in various tissues. It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity. |
| doi_str_mv | 10.1007/s12011-015-0320-9 |
| format | Article |
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It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity.</description><identifier>ISSN: 0163-4984</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-015-0320-9</identifier><identifier>PMID: 25855374</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Alum Compounds - toxicity ; Aluminum ; Aluminum sulfate ; Animals ; Antioxidants ; Antioxidants - metabolism ; Antioxidants - pharmacology ; Biochemistry ; Biomedical and Life Sciences ; Biotechnology ; Cell growth ; Cell Proliferation - drug effects ; Ethanol ; Kidney - pathology ; Kidney Diseases - chemically induced ; Kidney Diseases - drug therapy ; Kidney Diseases - pathology ; Kidney Function Tests ; Kidneys ; Life Sciences ; Male ; Melatonin ; Melatonin - therapeutic use ; Nutrition ; Oncology ; Oxidants - toxicity ; Oxidative stress ; Oxidizing agents ; Peroxidation ; Physiology ; Rats ; Rats, Wistar ; Rodents ; Sulfates ; Toxicity ; Trace elements</subject><ispartof>Biological trace element research, 2015-11, Vol.168 (1), p.141-149</ispartof><rights>Springer Science+Business Media New York 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-597ac13089bb66b26b87e24bcf8dc3147c4654619f74b23f70fe9e3e19618f4d3</citedby><cites>FETCH-LOGICAL-c442t-597ac13089bb66b26b87e24bcf8dc3147c4654619f74b23f70fe9e3e19618f4d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12011-015-0320-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12011-015-0320-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25855374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Karabulut-Bulan, Omur</creatorcontrib><creatorcontrib>Bayrak, Bertan Boran</creatorcontrib><creatorcontrib>Arda-Pirincci, Pelin</creatorcontrib><creatorcontrib>Sarikaya-Unal, Guner</creatorcontrib><creatorcontrib>Us, Huseyin</creatorcontrib><creatorcontrib>Yanardag, Refiye</creatorcontrib><title>Role of Exogenous Melatonin on Cell Proliferation and Oxidant/Antioxidant System in Aluminum-Induced Renal Toxicity</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>Aluminum has toxic potential on humans and animals when it accumulates in various tissues. It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity.</description><subject>Alum Compounds - toxicity</subject><subject>Aluminum</subject><subject>Aluminum sulfate</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>Cell growth</subject><subject>Cell Proliferation - drug effects</subject><subject>Ethanol</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - drug therapy</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Function Tests</subject><subject>Kidneys</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Melatonin</subject><subject>Melatonin - therapeutic 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of Exogenous Melatonin on Cell Proliferation and Oxidant/Antioxidant System in Aluminum-Induced Renal Toxicity</title><author>Karabulut-Bulan, Omur ; Bayrak, Bertan Boran ; Arda-Pirincci, Pelin ; Sarikaya-Unal, Guner ; Us, Huseyin ; Yanardag, Refiye</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-597ac13089bb66b26b87e24bcf8dc3147c4654619f74b23f70fe9e3e19618f4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Alum Compounds - toxicity</topic><topic>Aluminum</topic><topic>Aluminum sulfate</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>Antioxidants - pharmacology</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biotechnology</topic><topic>Cell growth</topic><topic>Cell Proliferation - drug effects</topic><topic>Ethanol</topic><topic>Kidney - pathology</topic><topic>Kidney 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It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>25855374</pmid><doi>10.1007/s12011-015-0320-9</doi><tpages>9</tpages></addata></record> |
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| subjects | Alum Compounds - toxicity Aluminum Aluminum sulfate Animals Antioxidants Antioxidants - metabolism Antioxidants - pharmacology Biochemistry Biomedical and Life Sciences Biotechnology Cell growth Cell Proliferation - drug effects Ethanol Kidney - pathology Kidney Diseases - chemically induced Kidney Diseases - drug therapy Kidney Diseases - pathology Kidney Function Tests Kidneys Life Sciences Male Melatonin Melatonin - therapeutic use Nutrition Oncology Oxidants - toxicity Oxidative stress Oxidizing agents Peroxidation Physiology Rats Rats, Wistar Rodents Sulfates Toxicity Trace elements |
| title | Role of Exogenous Melatonin on Cell Proliferation and Oxidant/Antioxidant System in Aluminum-Induced Renal Toxicity |
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