Morphine enhances purine nucleotide catabolism in vivo and in vitro

Aim: To investigate the effect and mechanism of morphine on purine nucleotide catabolism. Methods: The rat model of morphine dependence and withdrawal and rat C6 glioma cells in culture were used. Concentrations of uric acid in the plasma were measured by the uricase‐rap method, adenosine deaminase...

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Veröffentlicht in:Acta pharmacologica Sinica 2007-08, Vol.28 (8), p.1105-1115
Hauptverfasser: LIU, Chang, LIU, Jian‐kai, KAN, Mu‐jie, GAO, Lin, FU, Hai‐ying, ZHOU, Hang, HONG, Min
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container_title Acta pharmacologica Sinica
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creator LIU, Chang
LIU, Jian‐kai
KAN, Mu‐jie
GAO, Lin
FU, Hai‐ying
ZHOU, Hang
HONG, Min
description Aim: To investigate the effect and mechanism of morphine on purine nucleotide catabolism. Methods: The rat model of morphine dependence and withdrawal and rat C6 glioma cells in culture were used. Concentrations of uric acid in the plasma were measured by the uricase‐rap method, adenosine deaminase (ADA) and xanthine oxidase (XO) in the plasma and tissues were measured by the ADA and XO test kit. RT‐PCR and RT‐PCR‐Southern blotting were used to examine the relative amount of ADA and XO gene transcripts in tissues and C6 cells. Results: (i) the concentration of plasma uric acid in the morphine‐administered group was significantly higher (P < 0.05) than the control group; (ii) during morphine administration and withdrawal periods, the ADA and XO concentrations in the plasma increased significantly (P < 0.05); (iii) the amount of ADA and XO in the parietal lobe, liver, small intestine, and skeletal muscles of the morphine‐administered groups increased, while the level of ADA and XO in those tissues of the withdrawal groups decreased; (iv) the transcripts of the ADA and XO genes in the parietal lobe, liver, small intestine, and skeletal muscles were higher in the morphine‐administered group. The expression of the ADA and XO genes in those tissues returned to the control level during morphine withdrawal, with the exception of the skeletal muscles; and (v) the upregulation of the expression of the ADA and XO genes induced by morphine treatment could be reversed by naloxone. Conclusion: The effects of morphine on purine nucleotide metabolism might be an important, new biochemical pharmacological mechanism of morphine action.
doi_str_mv 10.1111/j.1745-7254.2007.00592.x
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Methods: The rat model of morphine dependence and withdrawal and rat C6 glioma cells in culture were used. Concentrations of uric acid in the plasma were measured by the uricase‐rap method, adenosine deaminase (ADA) and xanthine oxidase (XO) in the plasma and tissues were measured by the ADA and XO test kit. RT‐PCR and RT‐PCR‐Southern blotting were used to examine the relative amount of ADA and XO gene transcripts in tissues and C6 cells. Results: (i) the concentration of plasma uric acid in the morphine‐administered group was significantly higher (P &lt; 0.05) than the control group; (ii) during morphine administration and withdrawal periods, the ADA and XO concentrations in the plasma increased significantly (P &lt; 0.05); (iii) the amount of ADA and XO in the parietal lobe, liver, small intestine, and skeletal muscles of the morphine‐administered groups increased, while the level of ADA and XO in those tissues of the withdrawal groups decreased; (iv) the transcripts of the ADA and XO genes in the parietal lobe, liver, small intestine, and skeletal muscles were higher in the morphine‐administered group. The expression of the ADA and XO genes in those tissues returned to the control level during morphine withdrawal, with the exception of the skeletal muscles; and (v) the upregulation of the expression of the ADA and XO genes induced by morphine treatment could be reversed by naloxone. Conclusion: The effects of morphine on purine nucleotide metabolism might be an important, new biochemical pharmacological mechanism of morphine action.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1111/j.1745-7254.2007.00592.x</identifier><identifier>PMID: 17640470</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>adenosine deaminase ; Adenosine Deaminase - analysis ; Adenosine Deaminase - genetics ; Animals ; Blood Urea Nitrogen ; Cell Line, Tumor ; Female ; morphine ; Morphine - pharmacology ; purine nucleotide ; Purine Nucleotides - metabolism ; Rats ; Rats, Wistar ; RNA, Messenger - analysis ; uric acid ; Uric Acid - blood ; xanthine oxidase ; Xanthine Oxidase - analysis ; Xanthine Oxidase - genetics</subject><ispartof>Acta pharmacologica Sinica, 2007-08, Vol.28 (8), p.1105-1115</ispartof><rights>Copyright Nature Publishing Group Aug 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4752-747bf844bb3249c9d73702a77e4fadf9e5a0f7aa28f3233c2af4dd391daa4d1f3</citedby><cites>FETCH-LOGICAL-c4752-747bf844bb3249c9d73702a77e4fadf9e5a0f7aa28f3233c2af4dd391daa4d1f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1745-7254.2007.00592.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1745-7254.2007.00592.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17640470$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LIU, Chang</creatorcontrib><creatorcontrib>LIU, Jian‐kai</creatorcontrib><creatorcontrib>KAN, Mu‐jie</creatorcontrib><creatorcontrib>GAO, Lin</creatorcontrib><creatorcontrib>FU, Hai‐ying</creatorcontrib><creatorcontrib>ZHOU, Hang</creatorcontrib><creatorcontrib>HONG, Min</creatorcontrib><title>Morphine enhances purine nucleotide catabolism in vivo and in vitro</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><description>Aim: To investigate the effect and mechanism of morphine on purine nucleotide catabolism. Methods: The rat model of morphine dependence and withdrawal and rat C6 glioma cells in culture were used. Concentrations of uric acid in the plasma were measured by the uricase‐rap method, adenosine deaminase (ADA) and xanthine oxidase (XO) in the plasma and tissues were measured by the ADA and XO test kit. RT‐PCR and RT‐PCR‐Southern blotting were used to examine the relative amount of ADA and XO gene transcripts in tissues and C6 cells. Results: (i) the concentration of plasma uric acid in the morphine‐administered group was significantly higher (P &lt; 0.05) than the control group; (ii) during morphine administration and withdrawal periods, the ADA and XO concentrations in the plasma increased significantly (P &lt; 0.05); (iii) the amount of ADA and XO in the parietal lobe, liver, small intestine, and skeletal muscles of the morphine‐administered groups increased, while the level of ADA and XO in those tissues of the withdrawal groups decreased; (iv) the transcripts of the ADA and XO genes in the parietal lobe, liver, small intestine, and skeletal muscles were higher in the morphine‐administered group. The expression of the ADA and XO genes in those tissues returned to the control level during morphine withdrawal, with the exception of the skeletal muscles; and (v) the upregulation of the expression of the ADA and XO genes induced by morphine treatment could be reversed by naloxone. 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Methods: The rat model of morphine dependence and withdrawal and rat C6 glioma cells in culture were used. Concentrations of uric acid in the plasma were measured by the uricase‐rap method, adenosine deaminase (ADA) and xanthine oxidase (XO) in the plasma and tissues were measured by the ADA and XO test kit. RT‐PCR and RT‐PCR‐Southern blotting were used to examine the relative amount of ADA and XO gene transcripts in tissues and C6 cells. Results: (i) the concentration of plasma uric acid in the morphine‐administered group was significantly higher (P &lt; 0.05) than the control group; (ii) during morphine administration and withdrawal periods, the ADA and XO concentrations in the plasma increased significantly (P &lt; 0.05); (iii) the amount of ADA and XO in the parietal lobe, liver, small intestine, and skeletal muscles of the morphine‐administered groups increased, while the level of ADA and XO in those tissues of the withdrawal groups decreased; (iv) the transcripts of the ADA and XO genes in the parietal lobe, liver, small intestine, and skeletal muscles were higher in the morphine‐administered group. The expression of the ADA and XO genes in those tissues returned to the control level during morphine withdrawal, with the exception of the skeletal muscles; and (v) the upregulation of the expression of the ADA and XO genes induced by morphine treatment could be reversed by naloxone. Conclusion: The effects of morphine on purine nucleotide metabolism might be an important, new biochemical pharmacological mechanism of morphine action.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17640470</pmid><doi>10.1111/j.1745-7254.2007.00592.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects adenosine deaminase
Adenosine Deaminase - analysis
Adenosine Deaminase - genetics
Animals
Blood Urea Nitrogen
Cell Line, Tumor
Female
morphine
Morphine - pharmacology
purine nucleotide
Purine Nucleotides - metabolism
Rats
Rats, Wistar
RNA, Messenger - analysis
uric acid
Uric Acid - blood
xanthine oxidase
Xanthine Oxidase - analysis
Xanthine Oxidase - genetics
title Morphine enhances purine nucleotide catabolism in vivo and in vitro
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