Changes in renal function and oxidative damage in methamphetamine-treated rat
In this study, we observed renal damage and peroxidative injury as the acute or sub-acute effect of methamphetamine (MA) to determine whether MA intoxication can be diagnosed from immunohistochemical changes in the kidney. In addition, renal function was investigated in relation to the immunohistoch...
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| Veröffentlicht in: | Legal medicine (Tokyo, Japan) Japan), 2006, Vol.8 (1), p.16-21 |
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| creator | Tokunaga, Itsuo Kubo, Shin-ichi Ishigami, Akiko Gotohda, Takako Kitamura, Osamu |
| description | In this study, we observed renal damage and peroxidative injury as the acute or sub-acute effect of methamphetamine (MA) to determine whether MA intoxication can be diagnosed from immunohistochemical changes in the kidney. In addition, renal function was investigated in relation to the immunohistochemical changes. A single administration of MA (group I) (50
mg/kg/ (i.p.)) and repeated administration (group II) (10
mg/kg/day (i.p.) for 5 days) were designed as an acute model and a sub-acute or chronic model. Immunohistochemically, cell damage markers were observed. Then, renal function markers and minerals in blood were measured. Myoglobin and creatinine phosphokinase (CPK) in blood were also analyzed. In group I, ubiquitin immunoreactivity was enhanced only in the renal tubules. Creatinine increased, while K, Ca, and P decreased (
P |
| doi_str_mv | 10.1016/j.legalmed.2005.07.003 |
| format | Article |
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mg/kg/ (i.p.)) and repeated administration (group II) (10
mg/kg/day (i.p.) for 5 days) were designed as an acute model and a sub-acute or chronic model. Immunohistochemically, cell damage markers were observed. Then, renal function markers and minerals in blood were measured. Myoglobin and creatinine phosphokinase (CPK) in blood were also analyzed. In group I, ubiquitin immunoreactivity was enhanced only in the renal tubules. Creatinine increased, while K, Ca, and P decreased (
P<0.01). CPK increased significantly (
P<0.01). Therefore, it was suspected that MA might induce renal dysfunction with renal tubule damage. This damage might be related to leakage of CPK from muscle. In group II, 8-hydroxy-2′-deoxyguanosine (8-OH-dG) increased immunohistochemically and quantitatively (
P<0.01). It was considered that oxidative DNA damage might be induced by repeated administration. It was considered that this study offers basic information for the evaluation of pathological changes in the kidney in MA-related autopsy cases.</description><identifier>ISSN: 1344-6223</identifier><identifier>EISSN: 1873-4162</identifier><identifier>DOI: 10.1016/j.legalmed.2005.07.003</identifier><identifier>PMID: 16157497</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>8-OH-dG ; Animals ; Biomarkers - blood ; Body Temperature ; Body Weight ; Calcium - blood ; Cause of death ; Central Nervous System Stimulants - administration & dosage ; Central Nervous System Stimulants - toxicity ; Creatinine - blood ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - metabolism ; Disease Models, Animal ; Immunohistochemistry ; Kidney - drug effects ; Kidney - metabolism ; Male ; Methamphetamine ; Methamphetamine - administration & dosage ; Methamphetamine - toxicity ; Myoglobin - blood ; Oxidative damage ; Phosphorus - blood ; Potassium - blood ; Rats ; Rats, Wistar ; Renal function ; Ubiquitin - metabolism</subject><ispartof>Legal medicine (Tokyo, Japan), 2006, Vol.8 (1), p.16-21</ispartof><rights>2005 Elsevier Ireland Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c431t-5337bf272648ecbbe896d4cae4ee2be7d88e638148949abd861de3066a396d8f3</citedby><cites>FETCH-LOGICAL-c431t-5337bf272648ecbbe896d4cae4ee2be7d88e638148949abd861de3066a396d8f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1344622305000787$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16157497$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tokunaga, Itsuo</creatorcontrib><creatorcontrib>Kubo, Shin-ichi</creatorcontrib><creatorcontrib>Ishigami, Akiko</creatorcontrib><creatorcontrib>Gotohda, Takako</creatorcontrib><creatorcontrib>Kitamura, Osamu</creatorcontrib><title>Changes in renal function and oxidative damage in methamphetamine-treated rat</title><title>Legal medicine (Tokyo, Japan)</title><addtitle>Leg Med (Tokyo)</addtitle><description>In this study, we observed renal damage and peroxidative injury as the acute or sub-acute effect of methamphetamine (MA) to determine whether MA intoxication can be diagnosed from immunohistochemical changes in the kidney. In addition, renal function was investigated in relation to the immunohistochemical changes. A single administration of MA (group I) (50
mg/kg/ (i.p.)) and repeated administration (group II) (10
mg/kg/day (i.p.) for 5 days) were designed as an acute model and a sub-acute or chronic model. Immunohistochemically, cell damage markers were observed. Then, renal function markers and minerals in blood were measured. Myoglobin and creatinine phosphokinase (CPK) in blood were also analyzed. In group I, ubiquitin immunoreactivity was enhanced only in the renal tubules. Creatinine increased, while K, Ca, and P decreased (
P<0.01). CPK increased significantly (
P<0.01). Therefore, it was suspected that MA might induce renal dysfunction with renal tubule damage. This damage might be related to leakage of CPK from muscle. In group II, 8-hydroxy-2′-deoxyguanosine (8-OH-dG) increased immunohistochemically and quantitatively (
P<0.01). It was considered that oxidative DNA damage might be induced by repeated administration. It was considered that this study offers basic information for the evaluation of pathological changes in the kidney in MA-related autopsy cases.</description><subject>8-OH-dG</subject><subject>Animals</subject><subject>Biomarkers - blood</subject><subject>Body Temperature</subject><subject>Body Weight</subject><subject>Calcium - blood</subject><subject>Cause of death</subject><subject>Central Nervous System Stimulants - administration & dosage</subject><subject>Central Nervous System Stimulants - toxicity</subject><subject>Creatinine - blood</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - metabolism</subject><subject>Disease Models, Animal</subject><subject>Immunohistochemistry</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Methamphetamine</subject><subject>Methamphetamine - administration & dosage</subject><subject>Methamphetamine - toxicity</subject><subject>Myoglobin - blood</subject><subject>Oxidative damage</subject><subject>Phosphorus - blood</subject><subject>Potassium - blood</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renal function</subject><subject>Ubiquitin - metabolism</subject><issn>1344-6223</issn><issn>1873-4162</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtP6zAQRi0E4lH4Cyiru0uwY9d2dveq4iWB2MDamtiT1lXiFNtF8O9J1V62rGakOd-M5hByzWjFKJM366rHJfQDuqqmdF5RVVHKj8g504qXgsn6eOq5EKWsa35GLlJaU8oUo-qUnDHJ5ko06pw8L1YQlpgKH4qIAfqi2wab_RgKCK4YP72D7D-wcDDAEnfYgHkFw2aFGQYfsMwRIaMrIuRLctJBn_DqUGfk7e72dfFQPr3cPy7-PZVWcJbLOeeq7WpVS6HRti3qRjphAQVi3aJyWqPkmgndiAZapyVzyKmUwCdQd3xG_uz3buL4vsWUzeCTxb6HgOM2mZpRIVmjJlDuQRvHlCJ2ZhP9APHLMGp2Is3a_BdpdiINVWYSOQWvDxe27W72EzuYm4C_ewCnPz88RpOsx2DR-Yg2Gzf63258A0efiEQ</recordid><startdate>2006</startdate><enddate>2006</enddate><creator>Tokunaga, Itsuo</creator><creator>Kubo, Shin-ichi</creator><creator>Ishigami, Akiko</creator><creator>Gotohda, Takako</creator><creator>Kitamura, Osamu</creator><general>Elsevier Ireland Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>2006</creationdate><title>Changes in renal function and oxidative damage in methamphetamine-treated rat</title><author>Tokunaga, Itsuo ; Kubo, Shin-ichi ; Ishigami, Akiko ; Gotohda, Takako ; Kitamura, Osamu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c431t-5337bf272648ecbbe896d4cae4ee2be7d88e638148949abd861de3066a396d8f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>8-OH-dG</topic><topic>Animals</topic><topic>Biomarkers - blood</topic><topic>Body Temperature</topic><topic>Body Weight</topic><topic>Calcium - blood</topic><topic>Cause of death</topic><topic>Central Nervous System Stimulants - administration & dosage</topic><topic>Central Nervous System Stimulants - toxicity</topic><topic>Creatinine - blood</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - metabolism</topic><topic>Disease Models, Animal</topic><topic>Immunohistochemistry</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Methamphetamine</topic><topic>Methamphetamine - administration & dosage</topic><topic>Methamphetamine - toxicity</topic><topic>Myoglobin - blood</topic><topic>Oxidative damage</topic><topic>Phosphorus - blood</topic><topic>Potassium - blood</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renal function</topic><topic>Ubiquitin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tokunaga, Itsuo</creatorcontrib><creatorcontrib>Kubo, Shin-ichi</creatorcontrib><creatorcontrib>Ishigami, Akiko</creatorcontrib><creatorcontrib>Gotohda, Takako</creatorcontrib><creatorcontrib>Kitamura, Osamu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Legal medicine (Tokyo, Japan)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tokunaga, Itsuo</au><au>Kubo, Shin-ichi</au><au>Ishigami, Akiko</au><au>Gotohda, Takako</au><au>Kitamura, Osamu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in renal function and oxidative damage in methamphetamine-treated rat</atitle><jtitle>Legal medicine (Tokyo, Japan)</jtitle><addtitle>Leg Med (Tokyo)</addtitle><date>2006</date><risdate>2006</risdate><volume>8</volume><issue>1</issue><spage>16</spage><epage>21</epage><pages>16-21</pages><issn>1344-6223</issn><eissn>1873-4162</eissn><abstract>In this study, we observed renal damage and peroxidative injury as the acute or sub-acute effect of methamphetamine (MA) to determine whether MA intoxication can be diagnosed from immunohistochemical changes in the kidney. In addition, renal function was investigated in relation to the immunohistochemical changes. A single administration of MA (group I) (50
mg/kg/ (i.p.)) and repeated administration (group II) (10
mg/kg/day (i.p.) for 5 days) were designed as an acute model and a sub-acute or chronic model. Immunohistochemically, cell damage markers were observed. Then, renal function markers and minerals in blood were measured. Myoglobin and creatinine phosphokinase (CPK) in blood were also analyzed. In group I, ubiquitin immunoreactivity was enhanced only in the renal tubules. Creatinine increased, while K, Ca, and P decreased (
P<0.01). CPK increased significantly (
P<0.01). Therefore, it was suspected that MA might induce renal dysfunction with renal tubule damage. This damage might be related to leakage of CPK from muscle. In group II, 8-hydroxy-2′-deoxyguanosine (8-OH-dG) increased immunohistochemically and quantitatively (
P<0.01). It was considered that oxidative DNA damage might be induced by repeated administration. It was considered that this study offers basic information for the evaluation of pathological changes in the kidney in MA-related autopsy cases.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>16157497</pmid><doi>10.1016/j.legalmed.2005.07.003</doi><tpages>6</tpages></addata></record> |
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| subjects | 8-OH-dG Animals Biomarkers - blood Body Temperature Body Weight Calcium - blood Cause of death Central Nervous System Stimulants - administration & dosage Central Nervous System Stimulants - toxicity Creatinine - blood Deoxyguanosine - analogs & derivatives Deoxyguanosine - metabolism Disease Models, Animal Immunohistochemistry Kidney - drug effects Kidney - metabolism Male Methamphetamine Methamphetamine - administration & dosage Methamphetamine - toxicity Myoglobin - blood Oxidative damage Phosphorus - blood Potassium - blood Rats Rats, Wistar Renal function Ubiquitin - metabolism |
| title | Changes in renal function and oxidative damage in methamphetamine-treated rat |
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