The role of allopurinol on oxidative stress in experimental hyperthyroidism
Aim : During hyperthyroidism, production of free oxygen radicals derives, where xanthine oxidase may also play an important role. Allopurinol, a xanthine oxidase inhibitor, has a significant effect on thyrotoxicosis-related oxidative stress. However, the relationship between thyroid hormones, oxidat...
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| Veröffentlicht in: | Journal of endocrinological investigation 2009-09, Vol.32 (8), p.641-646 |
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| container_title | Journal of endocrinological investigation |
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| creator | Makay, O. Yenisey, C. Icoz, G. Simsek, N. Genc Ozgen, G. Akyildiz, M. Yetkin, E. |
| description | Aim
: During hyperthyroidism, production of free oxygen radicals derives, where xanthine oxidase may also play an important role. Allopurinol, a xanthine oxidase inhibitor, has a significant effect on thyrotoxicosis-related oxidative stress. However, the relationship between thyroid hormones, oxidative stress parameters and allopurinol remains to be explored.
Methods
: Forty-two Wistar albino rats were divided into three groups. Rats in group A served as negative controls, while group B had untreated thyrotoxicosis and group C received allopurinol. Hyperthyroidism was induced by daily 0.2 mg/kg L-thyroxine intraperitoneally in groups B and C; 40 mg/kg allopurinol were given daily intraperitoneally. Efficacy of the treatment was assessed after 72 h and 21 days, by measuring serum xanthine oxidase (XO), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx) and nitric oxide derivates (NO·x).
Results
: In both time periods, serum XO, MDA, GSH and NO·x levels were significantly increased after thyroid hormone induction (
p |
| doi_str_mv | 10.1007/BF03345734 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1007_BF03345734</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19942821</sourcerecordid><originalsourceid>FETCH-LOGICAL-c322t-e8e7d7f1129925df659a10bc3bf6b2781897c6b21a1188ddd54181376506a9a33</originalsourceid><addsrcrecordid>eNptkMFOwzAMhiMEYmNw4QFQzqBCnLRNcoRpA8QkLuNcpU1KM3VNlXRoe3uCOmkXTrblT7_sD6FbII9ACH96WRLG0oyz9AxNgVOSCCbyczQlTEKSEskn6CqEDSGMM8Ev0QSkTKmgMEUf68Zg71qDXY1V27p-523nWuw67PZWq8H-GBwGb0LAtsNm3xtvt6YbVIubQxyG5uCd1TZsr9FFrdpgbo51hr6Wi_X8LVl9vr7Pn1dJxSgdEiMM17wGoFLSTNd5JhWQsmJlnZeUCxCSV7EDBSCE1jpLQQDjeUZyJRVjM3Q_5lbeheBNXfTxJOUPBZDiz0hxMhLhuxHud-XW6BN6VBCBhxEIcdV9G19s3M538YH_4n4BCl5pDQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>The role of allopurinol on oxidative stress in experimental hyperthyroidism</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Makay, O. ; Yenisey, C. ; Icoz, G. ; Simsek, N. Genc ; Ozgen, G. ; Akyildiz, M. ; Yetkin, E.</creator><creatorcontrib>Makay, O. ; Yenisey, C. ; Icoz, G. ; Simsek, N. Genc ; Ozgen, G. ; Akyildiz, M. ; Yetkin, E.</creatorcontrib><description>Aim
: During hyperthyroidism, production of free oxygen radicals derives, where xanthine oxidase may also play an important role. Allopurinol, a xanthine oxidase inhibitor, has a significant effect on thyrotoxicosis-related oxidative stress. However, the relationship between thyroid hormones, oxidative stress parameters and allopurinol remains to be explored.
Methods
: Forty-two Wistar albino rats were divided into three groups. Rats in group A served as negative controls, while group B had untreated thyrotoxicosis and group C received allopurinol. Hyperthyroidism was induced by daily 0.2 mg/kg L-thyroxine intraperitoneally in groups B and C; 40 mg/kg allopurinol were given daily intraperitoneally. Efficacy of the treatment was assessed after 72 h and 21 days, by measuring serum xanthine oxidase (XO), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx) and nitric oxide derivates (NO·x).
Results
: In both time periods, serum XO, MDA, GSH and NO·x levels were significantly increased after thyroid hormone induction (
p
<0.05). Levels of XO, MDA and NO·x decreased with allopurinol treatment (
p
<0.05). There was a remarkable decrease in triiodothyronine levels in group C after 72 h (
p
<0.05), and in both triiodothyronine and thyroxine levels in group C after 21 days (
p
<0.05). There was no difference between groups B and C in means of serum GSH, GR and GPx levels (
p
>0.05).
Conclusions
: This study suggests an association between allopurinol and the biosynthesis of thyroid hormones. Allopurinol prevents the hyperthyroid state, which is mediated predominantly by triiodothyronine and not by XO. This issue has to be questioned in further studies where allopurinol is administered in control subjects.</description><identifier>ISSN: 0391-4097</identifier><identifier>EISSN: 1720-8386</identifier><identifier>DOI: 10.1007/BF03345734</identifier><identifier>PMID: 19942821</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allopurinol - pharmacology ; Animals ; Endocrinology ; Glutathione - blood ; Glutathione Peroxidase - blood ; Glutathione Reductase - blood ; Hyperthyroidism - drug therapy ; Hyperthyroidism - etiology ; Hyperthyroidism - prevention & control ; Male ; Malondialdehyde - blood ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Nitric Oxide - blood ; Original Articles ; Oxidative Stress - drug effects ; Rats ; Rats, Wistar ; Thyroxine ; Xanthine Oxidase - blood</subject><ispartof>Journal of endocrinological investigation, 2009-09, Vol.32 (8), p.641-646</ispartof><rights>Italian Society of Endocrinology (SIE) 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c322t-e8e7d7f1129925df659a10bc3bf6b2781897c6b21a1188ddd54181376506a9a33</citedby><cites>FETCH-LOGICAL-c322t-e8e7d7f1129925df659a10bc3bf6b2781897c6b21a1188ddd54181376506a9a33</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/BF03345734$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/BF03345734$$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/19942821$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Makay, O.</creatorcontrib><creatorcontrib>Yenisey, C.</creatorcontrib><creatorcontrib>Icoz, G.</creatorcontrib><creatorcontrib>Simsek, N. Genc</creatorcontrib><creatorcontrib>Ozgen, G.</creatorcontrib><creatorcontrib>Akyildiz, M.</creatorcontrib><creatorcontrib>Yetkin, E.</creatorcontrib><title>The role of allopurinol on oxidative stress in experimental hyperthyroidism</title><title>Journal of endocrinological investigation</title><addtitle>J Endocrinol Invest</addtitle><addtitle>J Endocrinol Invest</addtitle><description>Aim
: During hyperthyroidism, production of free oxygen radicals derives, where xanthine oxidase may also play an important role. Allopurinol, a xanthine oxidase inhibitor, has a significant effect on thyrotoxicosis-related oxidative stress. However, the relationship between thyroid hormones, oxidative stress parameters and allopurinol remains to be explored.
Methods
: Forty-two Wistar albino rats were divided into three groups. Rats in group A served as negative controls, while group B had untreated thyrotoxicosis and group C received allopurinol. Hyperthyroidism was induced by daily 0.2 mg/kg L-thyroxine intraperitoneally in groups B and C; 40 mg/kg allopurinol were given daily intraperitoneally. Efficacy of the treatment was assessed after 72 h and 21 days, by measuring serum xanthine oxidase (XO), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx) and nitric oxide derivates (NO·x).
Results
: In both time periods, serum XO, MDA, GSH and NO·x levels were significantly increased after thyroid hormone induction (
p
<0.05). Levels of XO, MDA and NO·x decreased with allopurinol treatment (
p
<0.05). There was a remarkable decrease in triiodothyronine levels in group C after 72 h (
p
<0.05), and in both triiodothyronine and thyroxine levels in group C after 21 days (
p
<0.05). There was no difference between groups B and C in means of serum GSH, GR and GPx levels (
p
>0.05).
Conclusions
: This study suggests an association between allopurinol and the biosynthesis of thyroid hormones. Allopurinol prevents the hyperthyroid state, which is mediated predominantly by triiodothyronine and not by XO. This issue has to be questioned in further studies where allopurinol is administered in control subjects.</description><subject>Allopurinol - pharmacology</subject><subject>Animals</subject><subject>Endocrinology</subject><subject>Glutathione - blood</subject><subject>Glutathione Peroxidase - blood</subject><subject>Glutathione Reductase - blood</subject><subject>Hyperthyroidism - drug therapy</subject><subject>Hyperthyroidism - etiology</subject><subject>Hyperthyroidism - prevention & control</subject><subject>Male</subject><subject>Malondialdehyde - blood</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Nitric Oxide - blood</subject><subject>Original Articles</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Thyroxine</subject><subject>Xanthine Oxidase - blood</subject><issn>0391-4097</issn><issn>1720-8386</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkMFOwzAMhiMEYmNw4QFQzqBCnLRNcoRpA8QkLuNcpU1KM3VNlXRoe3uCOmkXTrblT7_sD6FbII9ACH96WRLG0oyz9AxNgVOSCCbyczQlTEKSEskn6CqEDSGMM8Ev0QSkTKmgMEUf68Zg71qDXY1V27p-523nWuw67PZWq8H-GBwGb0LAtsNm3xtvt6YbVIubQxyG5uCd1TZsr9FFrdpgbo51hr6Wi_X8LVl9vr7Pn1dJxSgdEiMM17wGoFLSTNd5JhWQsmJlnZeUCxCSV7EDBSCE1jpLQQDjeUZyJRVjM3Q_5lbeheBNXfTxJOUPBZDiz0hxMhLhuxHud-XW6BN6VBCBhxEIcdV9G19s3M538YH_4n4BCl5pDQ</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Makay, O.</creator><creator>Yenisey, C.</creator><creator>Icoz, G.</creator><creator>Simsek, N. Genc</creator><creator>Ozgen, G.</creator><creator>Akyildiz, M.</creator><creator>Yetkin, E.</creator><general>Springer International Publishing</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></search><sort><creationdate>20090901</creationdate><title>The role of allopurinol on oxidative stress in experimental hyperthyroidism</title><author>Makay, O. ; Yenisey, C. ; Icoz, G. ; Simsek, N. Genc ; Ozgen, G. ; Akyildiz, M. ; Yetkin, E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c322t-e8e7d7f1129925df659a10bc3bf6b2781897c6b21a1188ddd54181376506a9a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Allopurinol - pharmacology</topic><topic>Animals</topic><topic>Endocrinology</topic><topic>Glutathione - blood</topic><topic>Glutathione Peroxidase - blood</topic><topic>Glutathione Reductase - blood</topic><topic>Hyperthyroidism - drug therapy</topic><topic>Hyperthyroidism - etiology</topic><topic>Hyperthyroidism - prevention & control</topic><topic>Male</topic><topic>Malondialdehyde - blood</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Nitric Oxide - blood</topic><topic>Original Articles</topic><topic>Oxidative Stress - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Thyroxine</topic><topic>Xanthine Oxidase - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Makay, O.</creatorcontrib><creatorcontrib>Yenisey, C.</creatorcontrib><creatorcontrib>Icoz, G.</creatorcontrib><creatorcontrib>Simsek, N. Genc</creatorcontrib><creatorcontrib>Ozgen, G.</creatorcontrib><creatorcontrib>Akyildiz, M.</creatorcontrib><creatorcontrib>Yetkin, E.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Journal of endocrinological investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Makay, O.</au><au>Yenisey, C.</au><au>Icoz, G.</au><au>Simsek, N. Genc</au><au>Ozgen, G.</au><au>Akyildiz, M.</au><au>Yetkin, E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of allopurinol on oxidative stress in experimental hyperthyroidism</atitle><jtitle>Journal of endocrinological investigation</jtitle><stitle>J Endocrinol Invest</stitle><addtitle>J Endocrinol Invest</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>32</volume><issue>8</issue><spage>641</spage><epage>646</epage><pages>641-646</pages><issn>0391-4097</issn><eissn>1720-8386</eissn><abstract>Aim
: During hyperthyroidism, production of free oxygen radicals derives, where xanthine oxidase may also play an important role. Allopurinol, a xanthine oxidase inhibitor, has a significant effect on thyrotoxicosis-related oxidative stress. However, the relationship between thyroid hormones, oxidative stress parameters and allopurinol remains to be explored.
Methods
: Forty-two Wistar albino rats were divided into three groups. Rats in group A served as negative controls, while group B had untreated thyrotoxicosis and group C received allopurinol. Hyperthyroidism was induced by daily 0.2 mg/kg L-thyroxine intraperitoneally in groups B and C; 40 mg/kg allopurinol were given daily intraperitoneally. Efficacy of the treatment was assessed after 72 h and 21 days, by measuring serum xanthine oxidase (XO), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx) and nitric oxide derivates (NO·x).
Results
: In both time periods, serum XO, MDA, GSH and NO·x levels were significantly increased after thyroid hormone induction (
p
<0.05). Levels of XO, MDA and NO·x decreased with allopurinol treatment (
p
<0.05). There was a remarkable decrease in triiodothyronine levels in group C after 72 h (
p
<0.05), and in both triiodothyronine and thyroxine levels in group C after 21 days (
p
<0.05). There was no difference between groups B and C in means of serum GSH, GR and GPx levels (
p
>0.05).
Conclusions
: This study suggests an association between allopurinol and the biosynthesis of thyroid hormones. Allopurinol prevents the hyperthyroid state, which is mediated predominantly by triiodothyronine and not by XO. This issue has to be questioned in further studies where allopurinol is administered in control subjects.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>19942821</pmid><doi>10.1007/BF03345734</doi><tpages>6</tpages></addata></record> |
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| identifier | ISSN: 0391-4097 |
| ispartof | Journal of endocrinological investigation, 2009-09, Vol.32 (8), p.641-646 |
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| language | eng |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Allopurinol - pharmacology Animals Endocrinology Glutathione - blood Glutathione Peroxidase - blood Glutathione Reductase - blood Hyperthyroidism - drug therapy Hyperthyroidism - etiology Hyperthyroidism - prevention & control Male Malondialdehyde - blood Medicine Medicine & Public Health Metabolic Diseases Nitric Oxide - blood Original Articles Oxidative Stress - drug effects Rats Rats, Wistar Thyroxine Xanthine Oxidase - blood |
| title | The role of allopurinol on oxidative stress in experimental hyperthyroidism |
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