Estrogen receptor agonists protect against acetaminophen-induced hepatorenal toxicity in rats
Acetaminophen-induced hepatorenal toxicity varies among sexes with controversial results among species. The aim was to compare the impact of sex and ovarian hormones on hepatorenal toxicity and to elucidate protective effects of estrogen and estrogen receptor (ER) agonists. Under anesthesia, female...
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| Veröffentlicht in: | Life sciences (1973) 2020-12, Vol.263, p.118561, Article 118561 |
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| creator | Koyuncuoğlu, Türkan Yıldırım, Alper Dertsiz, Ekin K. Yüksel, Meral Ercan, Feriha Yeğen, Berrak Ç. |
| description | Acetaminophen-induced hepatorenal toxicity varies among sexes with controversial results among species. The aim was to compare the impact of sex and ovarian hormones on hepatorenal toxicity and to elucidate protective effects of estrogen and estrogen receptor (ER) agonists.
Under anesthesia, female rats underwent ovariectomy (OVX) or sham-OVX. Starting at postsurgical 40th day, OVX-rats received subcutaneously (each, 1 mg/kg/day) 17β-estradiol (E2), ERβ-agonist (DPN) or ERα-agonist (PPT) for 10 days, while male and sham-OVX rats received vehicle for 10 days. Then, rats received either acetaminophen (3 g/kg) or saline by orogastric gavage and were decapitated at 24th h. Blood samples were obtained to measure serum ALT, AST, BUN, creatinine levels. Liver and kidney samples were obtained for histopathologic examination and for analyzing levels of luminol- and lucigenin-chemiluminescence, glutathione and myeloperoxidase activity.
Compared to their control groups, levels of AST, ALT, BUN, creatinine, hepatic and renal myeloperoxidase activity and chemiluminescence levels were increased, and hepatic glutathione level was decreased in acetaminophen-administered male groups, while ALT and hepatic chemiluminescence levels were not elevated in sham-OVX-rats. Both ER-agonists and E2 reduced BUN, creatinine and reversed all oxidative parameters in renal tissues of OVX-rats. Additionally, ERα-agonist reversed all hepatic injury parameters, while ERβ-agonist elevated hepatic glutathione level.
Acetaminophen toxicity in female rats presented with a more preserved hepatic function, while renal toxicity was not influenced by sex or by the lack of ovarian hormones. Pretreatment with estrogen or ER agonists, via their antioxidant actions, provided protective effects on acetaminophen-induced hepatorenal toxicity.
•Hepatic functions are more preserved in female rats with acetaminophen toxicity.•Acetaminophen renal toxicity is not related with sex/presence of ovarian hormones.•ERα and ERβ agonists are equally effective in reducing renal damage.•ERα agonist is more effective in improving hepatic damage.•Both ER agonists improve hepatorenal toxicity via their antioxidant actions. |
| doi_str_mv | 10.1016/j.lfs.2020.118561 |
| format | Article |
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Under anesthesia, female rats underwent ovariectomy (OVX) or sham-OVX. Starting at postsurgical 40th day, OVX-rats received subcutaneously (each, 1 mg/kg/day) 17β-estradiol (E2), ERβ-agonist (DPN) or ERα-agonist (PPT) for 10 days, while male and sham-OVX rats received vehicle for 10 days. Then, rats received either acetaminophen (3 g/kg) or saline by orogastric gavage and were decapitated at 24th h. Blood samples were obtained to measure serum ALT, AST, BUN, creatinine levels. Liver and kidney samples were obtained for histopathologic examination and for analyzing levels of luminol- and lucigenin-chemiluminescence, glutathione and myeloperoxidase activity.
Compared to their control groups, levels of AST, ALT, BUN, creatinine, hepatic and renal myeloperoxidase activity and chemiluminescence levels were increased, and hepatic glutathione level was decreased in acetaminophen-administered male groups, while ALT and hepatic chemiluminescence levels were not elevated in sham-OVX-rats. Both ER-agonists and E2 reduced BUN, creatinine and reversed all oxidative parameters in renal tissues of OVX-rats. Additionally, ERα-agonist reversed all hepatic injury parameters, while ERβ-agonist elevated hepatic glutathione level.
Acetaminophen toxicity in female rats presented with a more preserved hepatic function, while renal toxicity was not influenced by sex or by the lack of ovarian hormones. Pretreatment with estrogen or ER agonists, via their antioxidant actions, provided protective effects on acetaminophen-induced hepatorenal toxicity.
•Hepatic functions are more preserved in female rats with acetaminophen toxicity.•Acetaminophen renal toxicity is not related with sex/presence of ovarian hormones.•ERα and ERβ agonists are equally effective in reducing renal damage.•ERα agonist is more effective in improving hepatic damage.•Both ER agonists improve hepatorenal toxicity via their antioxidant actions.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2020.118561</identifier><identifier>PMID: 33045213</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>17β-Estradiol ; Acetaminophen ; Acetaminophen - toxicity ; Agonists ; Analgesics ; Analgesics, Non-Narcotic - toxicity ; Anesthesia ; Animals ; Antioxidants ; Chemical activity ; Chemical and Drug Induced Liver Injury - drug therapy ; Chemical and Drug Induced Liver Injury - etiology ; Chemical and Drug Induced Liver Injury - metabolism ; Chemical and Drug Induced Liver Injury - pathology ; Chemiluminescence ; Creatinine ; Estradiol - pharmacology ; Estrogen receptor agonists ; Estrogen receptors ; Estrogens ; Estrogens - pharmacology ; Female ; Glutathione ; Hepatorenal toxicity ; Hormones ; Kidney Diseases - drug therapy ; Kidney Diseases - etiology ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Kidneys ; Liver ; Male ; Males ; Nitriles - pharmacology ; Ovariectomy ; Ovaries ; Oxidative stress ; Oxidative Stress - drug effects ; Parameters ; Peroxidase ; Pretreatment ; Propionates - pharmacology ; Protective Agents - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors ; Receptors, Estrogen - chemistry ; Renal function ; Rodents ; Sex hormones ; Toxicity</subject><ispartof>Life sciences (1973), 2020-12, Vol.263, p.118561, Article 118561</ispartof><rights>2020</rights><rights>Copyright © 2020. Published by Elsevier Inc.</rights><rights>Copyright Elsevier BV Dec 15, 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-1e29994ff7801c8285f27f1d03bb5b6f56adef3415e49294d8adb9b1e76f749b3</citedby><cites>FETCH-LOGICAL-c381t-1e29994ff7801c8285f27f1d03bb5b6f56adef3415e49294d8adb9b1e76f749b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S002432052031314X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33045213$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koyuncuoğlu, Türkan</creatorcontrib><creatorcontrib>Yıldırım, Alper</creatorcontrib><creatorcontrib>Dertsiz, Ekin K.</creatorcontrib><creatorcontrib>Yüksel, Meral</creatorcontrib><creatorcontrib>Ercan, Feriha</creatorcontrib><creatorcontrib>Yeğen, Berrak Ç.</creatorcontrib><title>Estrogen receptor agonists protect against acetaminophen-induced hepatorenal toxicity in rats</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Acetaminophen-induced hepatorenal toxicity varies among sexes with controversial results among species. The aim was to compare the impact of sex and ovarian hormones on hepatorenal toxicity and to elucidate protective effects of estrogen and estrogen receptor (ER) agonists.
Under anesthesia, female rats underwent ovariectomy (OVX) or sham-OVX. Starting at postsurgical 40th day, OVX-rats received subcutaneously (each, 1 mg/kg/day) 17β-estradiol (E2), ERβ-agonist (DPN) or ERα-agonist (PPT) for 10 days, while male and sham-OVX rats received vehicle for 10 days. Then, rats received either acetaminophen (3 g/kg) or saline by orogastric gavage and were decapitated at 24th h. Blood samples were obtained to measure serum ALT, AST, BUN, creatinine levels. Liver and kidney samples were obtained for histopathologic examination and for analyzing levels of luminol- and lucigenin-chemiluminescence, glutathione and myeloperoxidase activity.
Compared to their control groups, levels of AST, ALT, BUN, creatinine, hepatic and renal myeloperoxidase activity and chemiluminescence levels were increased, and hepatic glutathione level was decreased in acetaminophen-administered male groups, while ALT and hepatic chemiluminescence levels were not elevated in sham-OVX-rats. Both ER-agonists and E2 reduced BUN, creatinine and reversed all oxidative parameters in renal tissues of OVX-rats. Additionally, ERα-agonist reversed all hepatic injury parameters, while ERβ-agonist elevated hepatic glutathione level.
Acetaminophen toxicity in female rats presented with a more preserved hepatic function, while renal toxicity was not influenced by sex or by the lack of ovarian hormones. Pretreatment with estrogen or ER agonists, via their antioxidant actions, provided protective effects on acetaminophen-induced hepatorenal toxicity.
•Hepatic functions are more preserved in female rats with acetaminophen toxicity.•Acetaminophen renal toxicity is not related with sex/presence of ovarian hormones.•ERα and ERβ agonists are equally effective in reducing renal damage.•ERα agonist is more effective in improving hepatic damage.•Both ER agonists improve hepatorenal toxicity via their antioxidant actions.</description><subject>17β-Estradiol</subject><subject>Acetaminophen</subject><subject>Acetaminophen - toxicity</subject><subject>Agonists</subject><subject>Analgesics</subject><subject>Analgesics, Non-Narcotic - toxicity</subject><subject>Anesthesia</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Chemical activity</subject><subject>Chemical and Drug Induced Liver Injury - drug therapy</subject><subject>Chemical and Drug Induced Liver Injury - etiology</subject><subject>Chemical and Drug Induced Liver Injury - metabolism</subject><subject>Chemical and Drug Induced Liver Injury - pathology</subject><subject>Chemiluminescence</subject><subject>Creatinine</subject><subject>Estradiol - pharmacology</subject><subject>Estrogen receptor agonists</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Estrogens - pharmacology</subject><subject>Female</subject><subject>Glutathione</subject><subject>Hepatorenal toxicity</subject><subject>Hormones</subject><subject>Kidney Diseases - drug therapy</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - pathology</subject><subject>Kidneys</subject><subject>Liver</subject><subject>Male</subject><subject>Males</subject><subject>Nitriles - pharmacology</subject><subject>Ovariectomy</subject><subject>Ovaries</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Parameters</subject><subject>Peroxidase</subject><subject>Pretreatment</subject><subject>Propionates - pharmacology</subject><subject>Protective Agents - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors</subject><subject>Receptors, Estrogen - chemistry</subject><subject>Renal function</subject><subject>Rodents</subject><subject>Sex hormones</subject><subject>Toxicity</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLAzEUhYMotlZ_gBsZcD01j8k8cCWlPqDgRpcSMpmbNkM7GZOM2H9vylSXri73cs7h3A-ha4LnBJP8rp1vtZ9TTONOSp6TEzQlZVGlOGfkFE0xplnKKOYTdOF9izHmvGDnaMIYzjglbIo-lj44u4YucaCgD9Ylcm0744NPemcDqBAP0nQ-TgVB7kxn-w10qemaQUGTbKCX0Qad3CbBfhtlwj4xMU8Gf4nOtNx6uDrOGXp_XL4tntPV69PL4mGVKlaSkBKgVVVlWhclJqqkJde00KTBrK55nWueywY0ywiHrKJV1pSyqauaQJHrIqtqNkO3Y26s_DmAD6K1g4uNvKCc0oxGK40qMqqUs9470KJ3ZifdXhAsDkBFKyJQcQAqRqDRc3NMHuodNH-OX4JRcD8KIP73ZcAJrwx0kYyJRINorPkn_gdmfYdM</recordid><startdate>20201215</startdate><enddate>20201215</enddate><creator>Koyuncuoğlu, Türkan</creator><creator>Yıldırım, Alper</creator><creator>Dertsiz, Ekin K.</creator><creator>Yüksel, Meral</creator><creator>Ercan, Feriha</creator><creator>Yeğen, Berrak Ç.</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20201215</creationdate><title>Estrogen receptor agonists protect against acetaminophen-induced hepatorenal toxicity in rats</title><author>Koyuncuoğlu, Türkan ; 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The aim was to compare the impact of sex and ovarian hormones on hepatorenal toxicity and to elucidate protective effects of estrogen and estrogen receptor (ER) agonists.
Under anesthesia, female rats underwent ovariectomy (OVX) or sham-OVX. Starting at postsurgical 40th day, OVX-rats received subcutaneously (each, 1 mg/kg/day) 17β-estradiol (E2), ERβ-agonist (DPN) or ERα-agonist (PPT) for 10 days, while male and sham-OVX rats received vehicle for 10 days. Then, rats received either acetaminophen (3 g/kg) or saline by orogastric gavage and were decapitated at 24th h. Blood samples were obtained to measure serum ALT, AST, BUN, creatinine levels. Liver and kidney samples were obtained for histopathologic examination and for analyzing levels of luminol- and lucigenin-chemiluminescence, glutathione and myeloperoxidase activity.
Compared to their control groups, levels of AST, ALT, BUN, creatinine, hepatic and renal myeloperoxidase activity and chemiluminescence levels were increased, and hepatic glutathione level was decreased in acetaminophen-administered male groups, while ALT and hepatic chemiluminescence levels were not elevated in sham-OVX-rats. Both ER-agonists and E2 reduced BUN, creatinine and reversed all oxidative parameters in renal tissues of OVX-rats. Additionally, ERα-agonist reversed all hepatic injury parameters, while ERβ-agonist elevated hepatic glutathione level.
Acetaminophen toxicity in female rats presented with a more preserved hepatic function, while renal toxicity was not influenced by sex or by the lack of ovarian hormones. Pretreatment with estrogen or ER agonists, via their antioxidant actions, provided protective effects on acetaminophen-induced hepatorenal toxicity.
•Hepatic functions are more preserved in female rats with acetaminophen toxicity.•Acetaminophen renal toxicity is not related with sex/presence of ovarian hormones.•ERα and ERβ agonists are equally effective in reducing renal damage.•ERα agonist is more effective in improving hepatic damage.•Both ER agonists improve hepatorenal toxicity via their antioxidant actions.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>33045213</pmid><doi>10.1016/j.lfs.2020.118561</doi></addata></record> |
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| subjects | 17β-Estradiol Acetaminophen Acetaminophen - toxicity Agonists Analgesics Analgesics, Non-Narcotic - toxicity Anesthesia Animals Antioxidants Chemical activity Chemical and Drug Induced Liver Injury - drug therapy Chemical and Drug Induced Liver Injury - etiology Chemical and Drug Induced Liver Injury - metabolism Chemical and Drug Induced Liver Injury - pathology Chemiluminescence Creatinine Estradiol - pharmacology Estrogen receptor agonists Estrogen receptors Estrogens Estrogens - pharmacology Female Glutathione Hepatorenal toxicity Hormones Kidney Diseases - drug therapy Kidney Diseases - etiology Kidney Diseases - metabolism Kidney Diseases - pathology Kidneys Liver Male Males Nitriles - pharmacology Ovariectomy Ovaries Oxidative stress Oxidative Stress - drug effects Parameters Peroxidase Pretreatment Propionates - pharmacology Protective Agents - pharmacology Rats Rats, Sprague-Dawley Receptors Receptors, Estrogen - chemistry Renal function Rodents Sex hormones Toxicity |
| title | Estrogen receptor agonists protect against acetaminophen-induced hepatorenal toxicity in rats |
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