Amelioration of thioacetamide-induced hepatic encephalopathy in rats by low-dose gamma irradiation
Brain affection is a common symptom of liver insufficiency. This study aimed to evaluate the role of low-dose γ irradiation (LDR) as a potential therapeutic agent in thioacetamide (TAA)-induced hepatic encephalopathy (HE) in rats. Effects of local and whole-body irradiation (0.5 Gy) on rat brain/liv...
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| Veröffentlicht in: | Environmental science and pollution research international 2020-01, Vol.27 (1), p.334-343 |
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| creator | El-Latif El-Ghazaly, Mona Abd Rashed, Engy Refaat Shafey, Ghada Mahmoud Zaki, Hala Fahmy Attia, Amina Salem |
| description | Brain affection is a common symptom of liver insufficiency. This study aimed to evaluate the role of low-dose γ irradiation (LDR) as a potential therapeutic agent in thioacetamide (TAA)-induced hepatic encephalopathy (HE) in rats. Effects of local and whole-body irradiation (0.5 Gy) on rat brain/liver were evaluated following the induction of HE by TAA (200 mg/kg/day/for 3 successive days). Serum activities of aspartate transaminase (AST) and alanine transaminase (ALT) and ammonia level were assessed. The effect of HE on brain was evaluated through the determination of brain contents of malondialdehyde (MDA), reduced glutathione (GSH), tumor necrosis factor-alpha (TNF-α), and interleukin-1beta (IL-1β) and glutathione peroxidase (GPx) activity. Moreover, apoptotic and inflammatory changes in brain and liver tissues were assessed together with alpha-smooth muscle actin (α-SMA); fibrosis marker. Results showed correction of the biochemical parameters which was supported by the results of the immunohistochemical examinations. LDR is a promising hepato- and neurotherapy against HE. |
| doi_str_mv | 10.1007/s11356-019-06934-w |
| format | Article |
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This study aimed to evaluate the role of low-dose γ irradiation (LDR) as a potential therapeutic agent in thioacetamide (TAA)-induced hepatic encephalopathy (HE) in rats. Effects of local and whole-body irradiation (0.5 Gy) on rat brain/liver were evaluated following the induction of HE by TAA (200 mg/kg/day/for 3 successive days). Serum activities of aspartate transaminase (AST) and alanine transaminase (ALT) and ammonia level were assessed. The effect of HE on brain was evaluated through the determination of brain contents of malondialdehyde (MDA), reduced glutathione (GSH), tumor necrosis factor-alpha (TNF-α), and interleukin-1beta (IL-1β) and glutathione peroxidase (GPx) activity. Moreover, apoptotic and inflammatory changes in brain and liver tissues were assessed together with alpha-smooth muscle actin (α-SMA); fibrosis marker. Results showed correction of the biochemical parameters which was supported by the results of the immunohistochemical examinations. LDR is a promising hepato- and neurotherapy against HE.</description><identifier>ISSN: 0944-1344</identifier><identifier>ISSN: 1614-7499</identifier><identifier>EISSN: 1614-7499</identifier><identifier>DOI: 10.1007/s11356-019-06934-w</identifier><identifier>PMID: 31786756</identifier><language>eng</language><publisher>Germany: Springer Nature B.V</publisher><subject>Actin ; Alanine ; Alanine transaminase ; Alanine Transaminase - blood ; Ammonia ; Animals ; Apoptosis ; Aspartate Aminotransferases - blood ; Aspartate transaminase ; Brain ; Brain - drug effects ; Chemical compounds ; Disease Models, Animal ; Environmental science ; Evaluation ; Fibrosis ; Gamma irradiation ; Gamma Rays ; Glutathione ; Glutathione - metabolism ; Glutathione peroxidase ; Hepatic encephalopathy ; Hepatic Encephalopathy - chemically induced ; IL-1β ; Inflammation ; Interleukin-1beta ; Interleukins ; Irradiation ; Liver ; Liver - drug effects ; Liver Function Tests ; Male ; Malondialdehyde ; Malondialdehyde - metabolism ; Muscles ; Oxidation-Reduction ; Oxidative stress ; Oxidative Stress - drug effects ; Peroxidase ; Pharmacology ; Radiation dosage ; Rats ; Rats, Wistar ; Rodents ; Smooth muscle ; Thioacetamide ; Thioacetamide - toxicity ; Transaminase ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Environmental science and pollution research international, 2020-01, Vol.27 (1), p.334-343</ispartof><rights>Environmental Science and Pollution Research is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c325t-9c972b70b98cddb3469b2d42c1fcc145912ad7cae5ad8d4ec6c3f2c91240cbde3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31786756$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>El-Latif El-Ghazaly, Mona Abd</creatorcontrib><creatorcontrib>Rashed, Engy Refaat</creatorcontrib><creatorcontrib>Shafey, Ghada Mahmoud</creatorcontrib><creatorcontrib>Zaki, Hala Fahmy</creatorcontrib><creatorcontrib>Attia, Amina Salem</creatorcontrib><title>Amelioration of thioacetamide-induced hepatic encephalopathy in rats by low-dose gamma irradiation</title><title>Environmental science and pollution research international</title><addtitle>Environ Sci Pollut Res Int</addtitle><description>Brain affection is a common symptom of liver insufficiency. This study aimed to evaluate the role of low-dose γ irradiation (LDR) as a potential therapeutic agent in thioacetamide (TAA)-induced hepatic encephalopathy (HE) in rats. Effects of local and whole-body irradiation (0.5 Gy) on rat brain/liver were evaluated following the induction of HE by TAA (200 mg/kg/day/for 3 successive days). Serum activities of aspartate transaminase (AST) and alanine transaminase (ALT) and ammonia level were assessed. The effect of HE on brain was evaluated through the determination of brain contents of malondialdehyde (MDA), reduced glutathione (GSH), tumor necrosis factor-alpha (TNF-α), and interleukin-1beta (IL-1β) and glutathione peroxidase (GPx) activity. Moreover, apoptotic and inflammatory changes in brain and liver tissues were assessed together with alpha-smooth muscle actin (α-SMA); fibrosis marker. Results showed correction of the biochemical parameters which was supported by the results of the immunohistochemical examinations. LDR is a promising hepato- and neurotherapy against HE.</description><subject>Actin</subject><subject>Alanine</subject><subject>Alanine transaminase</subject><subject>Alanine Transaminase - blood</subject><subject>Ammonia</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Aspartate Aminotransferases - blood</subject><subject>Aspartate transaminase</subject><subject>Brain</subject><subject>Brain - drug effects</subject><subject>Chemical compounds</subject><subject>Disease Models, Animal</subject><subject>Environmental science</subject><subject>Evaluation</subject><subject>Fibrosis</subject><subject>Gamma irradiation</subject><subject>Gamma Rays</subject><subject>Glutathione</subject><subject>Glutathione - metabolism</subject><subject>Glutathione peroxidase</subject><subject>Hepatic encephalopathy</subject><subject>Hepatic Encephalopathy - chemically induced</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Interleukin-1beta</subject><subject>Interleukins</subject><subject>Irradiation</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver Function Tests</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - metabolism</subject><subject>Muscles</subject><subject>Oxidation-Reduction</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peroxidase</subject><subject>Pharmacology</subject><subject>Radiation dosage</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Thioacetamide</subject><subject>Thioacetamide - toxicity</subject><subject>Transaminase</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>0944-1344</issn><issn>1614-7499</issn><issn>1614-7499</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpd0EtLxDAQB_AgiruufgEPEvDiJZpXk-a4LL5gwYueS161WdqmNi3LfnuDrhdPwwy_-TMMANcE3xOM5UMihBUCYaIQFopxtD8BSyIIR5IrdQqWWHGOCON8AS5S2mFMsaLyHCwYkaWQhVgCs-58G-KopxB7GGs4NSFq6yfdBedR6N1svYONH7Kw0PfWD41uY26bAww9zJsJmgNs4x65mDz81F2nYRhH7cJP6iU4q3Wb_NWxrsDH0-P75gVt355fN-stsowWE1JWSWokNqq0zhnGhTLUcWpJbS3hhSJUO2m1L7QrHfdWWFZTm8ccW-M8W4G739xhjF-zT1PVhWR92-rexzlVlFEsWEkEzvT2H93FeezzdVlxRrnCBc_q5qhm03lXDWPo9Hio_r7HvgFjOXOJ</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>El-Latif El-Ghazaly, Mona Abd</creator><creator>Rashed, Engy Refaat</creator><creator>Shafey, Ghada Mahmoud</creator><creator>Zaki, Hala Fahmy</creator><creator>Attia, Amina Salem</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QL</scope><scope>7SN</scope><scope>7T7</scope><scope>7TV</scope><scope>7U7</scope><scope>7WY</scope><scope>7WZ</scope><scope>7X7</scope><scope>7XB</scope><scope>87Z</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8FL</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BEZIV</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FRNLG</scope><scope>FYUFA</scope><scope>F~G</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K60</scope><scope>K6~</scope><scope>K9.</scope><scope>L.-</scope><scope>M0C</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>P64</scope><scope>PATMY</scope><scope>PQBIZ</scope><scope>PQBZA</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>202001</creationdate><title>Amelioration of thioacetamide-induced hepatic encephalopathy in rats by low-dose gamma irradiation</title><author>El-Latif El-Ghazaly, Mona Abd ; Rashed, Engy Refaat ; Shafey, Ghada Mahmoud ; Zaki, Hala Fahmy ; Attia, Amina Salem</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c325t-9c972b70b98cddb3469b2d42c1fcc145912ad7cae5ad8d4ec6c3f2c91240cbde3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Actin</topic><topic>Alanine</topic><topic>Alanine transaminase</topic><topic>Alanine Transaminase - blood</topic><topic>Ammonia</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Aspartate Aminotransferases - blood</topic><topic>Aspartate transaminase</topic><topic>Brain</topic><topic>Brain - drug effects</topic><topic>Chemical compounds</topic><topic>Disease Models, Animal</topic><topic>Environmental science</topic><topic>Evaluation</topic><topic>Fibrosis</topic><topic>Gamma irradiation</topic><topic>Gamma Rays</topic><topic>Glutathione</topic><topic>Glutathione - metabolism</topic><topic>Glutathione peroxidase</topic><topic>Hepatic encephalopathy</topic><topic>Hepatic Encephalopathy - chemically induced</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Interleukin-1beta</topic><topic>Interleukins</topic><topic>Irradiation</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver Function Tests</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - metabolism</topic><topic>Muscles</topic><topic>Oxidation-Reduction</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - 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Academic</collection><jtitle>Environmental science and pollution research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>El-Latif El-Ghazaly, Mona Abd</au><au>Rashed, Engy Refaat</au><au>Shafey, Ghada Mahmoud</au><au>Zaki, Hala Fahmy</au><au>Attia, Amina Salem</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amelioration of thioacetamide-induced hepatic encephalopathy in rats by low-dose gamma irradiation</atitle><jtitle>Environmental science and pollution research international</jtitle><addtitle>Environ Sci Pollut Res Int</addtitle><date>2020-01</date><risdate>2020</risdate><volume>27</volume><issue>1</issue><spage>334</spage><epage>343</epage><pages>334-343</pages><issn>0944-1344</issn><issn>1614-7499</issn><eissn>1614-7499</eissn><abstract>Brain affection is a common symptom of liver insufficiency. This study aimed to evaluate the role of low-dose γ irradiation (LDR) as a potential therapeutic agent in thioacetamide (TAA)-induced hepatic encephalopathy (HE) in rats. Effects of local and whole-body irradiation (0.5 Gy) on rat brain/liver were evaluated following the induction of HE by TAA (200 mg/kg/day/for 3 successive days). Serum activities of aspartate transaminase (AST) and alanine transaminase (ALT) and ammonia level were assessed. The effect of HE on brain was evaluated through the determination of brain contents of malondialdehyde (MDA), reduced glutathione (GSH), tumor necrosis factor-alpha (TNF-α), and interleukin-1beta (IL-1β) and glutathione peroxidase (GPx) activity. Moreover, apoptotic and inflammatory changes in brain and liver tissues were assessed together with alpha-smooth muscle actin (α-SMA); fibrosis marker. Results showed correction of the biochemical parameters which was supported by the results of the immunohistochemical examinations. LDR is a promising hepato- and neurotherapy against HE.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>31786756</pmid><doi>10.1007/s11356-019-06934-w</doi><tpages>10</tpages></addata></record> |
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| subjects | Actin Alanine Alanine transaminase Alanine Transaminase - blood Ammonia Animals Apoptosis Aspartate Aminotransferases - blood Aspartate transaminase Brain Brain - drug effects Chemical compounds Disease Models, Animal Environmental science Evaluation Fibrosis Gamma irradiation Gamma Rays Glutathione Glutathione - metabolism Glutathione peroxidase Hepatic encephalopathy Hepatic Encephalopathy - chemically induced IL-1β Inflammation Interleukin-1beta Interleukins Irradiation Liver Liver - drug effects Liver Function Tests Male Malondialdehyde Malondialdehyde - metabolism Muscles Oxidation-Reduction Oxidative stress Oxidative Stress - drug effects Peroxidase Pharmacology Radiation dosage Rats Rats, Wistar Rodents Smooth muscle Thioacetamide Thioacetamide - toxicity Transaminase Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Amelioration of thioacetamide-induced hepatic encephalopathy in rats by low-dose gamma irradiation |
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