Administration of anabolic steroid during adolescence induces long-term cardiac hypertrophy and increases susceptibility to ischemia/reperfusion injury in adult Wistar rats
•Chronic administration of AAS during adolescence promoted persistent cardiac hypertrophy in adulthood.•Cardiac hypertrophy was characterized by up-regulation in the βMHC expression, compatible with pathologic hypertrophy.•Susceptibility to myocardial IR injury in adult life was significantly increa...
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| creator | Seara, Fernando de Azevedo Cruz Barbosa, Raiana Andrade Quintanilha de Oliveira, Dahienne Ferreira Gran da Silva, Diorney Luiz Souza Carvalho, Adriana Bastos Freitas Ferreira, Andrea Claudia Matheus Nascimento, José Hamilton Olivares, Emerson Lopes |
| description | •Chronic administration of AAS during adolescence promoted persistent cardiac hypertrophy in adulthood.•Cardiac hypertrophy was characterized by up-regulation in the βMHC expression, compatible with pathologic hypertrophy.•Susceptibility to myocardial IR injury in adult life was significantly increased by AAS administration in adolescence.•Molecular evidences support that down-regulation of catalase might have a pathophysiological role.
Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia. We tested the hypothesis that chronic AAS exposure in the pre/pubertal phase increases the susceptibility to myocardial ischemia/reperfusion (IR) injury in adult rats. Male Wistar rats (26day old) were treated with vehicle (Control, n=12) or testosterone propionate (TP) (AAS, 5mgkg−1 n=12) 5 times/week during 5 weeks. At the end of AAS exposure, rats underwent 23days of washout period and were submitted to euthanasia. Langendorff-perfused hearts were submitted to IR injury and evaluated for mechanical dysfunctions and infarct size. Molecular analysis was performed by mRNA levels of α-myosin heavy chain (MHC), βMHC and brain-derived natriuretic peptide (BNP), ryanodine receptor (RyR2) and sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) by quantitative RT-PCR (qRT-PCR). The expression of AT1 receptor and KATP channel subunits (Kir6.1 and SURa) was analyzed by qRT-PCR and Western Blot. NADPH oxidase (Nox)-related reactive oxygen species generation was assessed by spectrofluorimetry. The expression of antioxidant enzymes was measured by qRT-PCR in order to address a potential role of redox unbalance. AAS exposure promoted long-term cardiac hypertrophy characterized by increased expression of βMHC and βMHC/αMHC ratio. Baseline derivative of pressure (dP/dt) was impaired by AAS exposure. Postischemic recovery of mechanical properties was impaired (decreased left ventricle [LV] developed pressure and maximal dP/dt; increased LV end-diastolic pressure and minimal dP/dt) a |
| doi_str_mv | 10.1016/j.jsbmb.2017.01.012 |
| format | Article |
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Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia. We tested the hypothesis that chronic AAS exposure in the pre/pubertal phase increases the susceptibility to myocardial ischemia/reperfusion (IR) injury in adult rats. Male Wistar rats (26day old) were treated with vehicle (Control, n=12) or testosterone propionate (TP) (AAS, 5mgkg−1 n=12) 5 times/week during 5 weeks. At the end of AAS exposure, rats underwent 23days of washout period and were submitted to euthanasia. Langendorff-perfused hearts were submitted to IR injury and evaluated for mechanical dysfunctions and infarct size. Molecular analysis was performed by mRNA levels of α-myosin heavy chain (MHC), βMHC and brain-derived natriuretic peptide (BNP), ryanodine receptor (RyR2) and sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) by quantitative RT-PCR (qRT-PCR). The expression of AT1 receptor and KATP channel subunits (Kir6.1 and SURa) was analyzed by qRT-PCR and Western Blot. NADPH oxidase (Nox)-related reactive oxygen species generation was assessed by spectrofluorimetry. The expression of antioxidant enzymes was measured by qRT-PCR in order to address a potential role of redox unbalance. AAS exposure promoted long-term cardiac hypertrophy characterized by increased expression of βMHC and βMHC/αMHC ratio. Baseline derivative of pressure (dP/dt) was impaired by AAS exposure. Postischemic recovery of mechanical properties was impaired (decreased left ventricle [LV] developed pressure and maximal dP/dt; increased LV end-diastolic pressure and minimal dP/dt) and infarct size was larger in the AAS group. Catalase mRNA expression was significantly decreased in the AAS group. In conclusion, chronic administration of AAS during adolescence promoted long-term pathological cardiac hypertrophy and persistent increase in the susceptibility to myocardial IR injury possible due to disturbances on catalase expression.</description><identifier>ISSN: 0960-0760</identifier><identifier>EISSN: 1879-1220</identifier><identifier>DOI: 10.1016/j.jsbmb.2017.01.012</identifier><identifier>PMID: 28179209</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adolescence ; Adolescents ; Aging ; Anabolic Agents - administration & dosage ; Anabolic Agents - toxicity ; Anabolic steroids ; Androgens ; Androgens - administration & dosage ; Androgens - toxicity ; Angiotensin AT1 receptors ; Angiotensin II ; Animals ; Antioxidants ; Blood pressure ; Brain natriuretic peptide ; Ca2+-transporting ATPase ; Calcium (reticular) ; Cardiac muscle ; Cardiomegaly - chemically induced ; Cardiomegaly - physiopathology ; Catalase ; Catalase - antagonists & inhibitors ; Catalase - genetics ; Catalase - metabolism ; Coronary Vessels - drug effects ; Coronary Vessels - physiopathology ; Down-regulation ; Dysautonomia ; Enzymes ; Gene expression ; Gene Expression Regulation, Developmental - drug effects ; Heart ; Heart - drug effects ; Heart - physiopathology ; Heart attacks ; Heart diseases ; Hypertrophy ; Injections, Intramuscular ; IR injury ; Ischemia ; Male ; Mechanical properties ; Myocardial infarction ; Myocardial Ischemia - chemically induced ; Myocardial Ischemia - pathology ; Myocardial Ischemia - physiopathology ; Myocardial Reperfusion Injury - chemically induced ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - physiopathology ; Myocardium - enzymology ; Myocardium - metabolism ; Myocardium - pathology ; Myosin Heavy Chains - chemistry ; Myosin Heavy Chains - genetics ; Myosin Heavy Chains - metabolism ; NAD(P)H oxidase ; Polymerase chain reaction ; Potassium channels (inwardly-rectifying) ; Random Allocation ; Rats, Wistar ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reperfusion ; Ryanodine receptors ; Steroids ; Testosterone ; Testosterone Propionate - administration & dosage ; Testosterone Propionate - toxicity ; Time Factors</subject><ispartof>The Journal of steroid biochemistry and molecular biology, 2017-07, Vol.171, p.34-42</ispartof><rights>2017</rights><rights>Copyright © 2017. Published by Elsevier Ltd.</rights><rights>Copyright Elsevier BV Jul 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-6395dae5cd8e0d300e494e6f3a0763d6c73d313acd00d4d7056f42eb6159211b3</citedby><cites>FETCH-LOGICAL-c387t-6395dae5cd8e0d300e494e6f3a0763d6c73d313acd00d4d7056f42eb6159211b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0960076017300122$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28179209$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seara, Fernando de Azevedo Cruz</creatorcontrib><creatorcontrib>Barbosa, Raiana Andrade Quintanilha</creatorcontrib><creatorcontrib>de Oliveira, Dahienne Ferreira</creatorcontrib><creatorcontrib>Gran da Silva, Diorney Luiz Souza</creatorcontrib><creatorcontrib>Carvalho, Adriana Bastos</creatorcontrib><creatorcontrib>Freitas Ferreira, Andrea Claudia</creatorcontrib><creatorcontrib>Matheus Nascimento, José Hamilton</creatorcontrib><creatorcontrib>Olivares, Emerson Lopes</creatorcontrib><title>Administration of anabolic steroid during adolescence induces long-term cardiac hypertrophy and increases susceptibility to ischemia/reperfusion injury in adult Wistar rats</title><title>The Journal of steroid biochemistry and molecular biology</title><addtitle>J Steroid Biochem Mol Biol</addtitle><description>•Chronic administration of AAS during adolescence promoted persistent cardiac hypertrophy in adulthood.•Cardiac hypertrophy was characterized by up-regulation in the βMHC expression, compatible with pathologic hypertrophy.•Susceptibility to myocardial IR injury in adult life was significantly increased by AAS administration in adolescence.•Molecular evidences support that down-regulation of catalase might have a pathophysiological role.
Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia. We tested the hypothesis that chronic AAS exposure in the pre/pubertal phase increases the susceptibility to myocardial ischemia/reperfusion (IR) injury in adult rats. Male Wistar rats (26day old) were treated with vehicle (Control, n=12) or testosterone propionate (TP) (AAS, 5mgkg−1 n=12) 5 times/week during 5 weeks. At the end of AAS exposure, rats underwent 23days of washout period and were submitted to euthanasia. Langendorff-perfused hearts were submitted to IR injury and evaluated for mechanical dysfunctions and infarct size. Molecular analysis was performed by mRNA levels of α-myosin heavy chain (MHC), βMHC and brain-derived natriuretic peptide (BNP), ryanodine receptor (RyR2) and sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) by quantitative RT-PCR (qRT-PCR). The expression of AT1 receptor and KATP channel subunits (Kir6.1 and SURa) was analyzed by qRT-PCR and Western Blot. NADPH oxidase (Nox)-related reactive oxygen species generation was assessed by spectrofluorimetry. The expression of antioxidant enzymes was measured by qRT-PCR in order to address a potential role of redox unbalance. AAS exposure promoted long-term cardiac hypertrophy characterized by increased expression of βMHC and βMHC/αMHC ratio. Baseline derivative of pressure (dP/dt) was impaired by AAS exposure. Postischemic recovery of mechanical properties was impaired (decreased left ventricle [LV] developed pressure and maximal dP/dt; increased LV end-diastolic pressure and minimal dP/dt) and infarct size was larger in the AAS group. Catalase mRNA expression was significantly decreased in the AAS group. In conclusion, chronic administration of AAS during adolescence promoted long-term pathological cardiac hypertrophy and persistent increase in the susceptibility to myocardial IR injury possible due to disturbances on catalase expression.</description><subject>Adolescence</subject><subject>Adolescents</subject><subject>Aging</subject><subject>Anabolic Agents - administration & dosage</subject><subject>Anabolic Agents - toxicity</subject><subject>Anabolic steroids</subject><subject>Androgens</subject><subject>Androgens - administration & dosage</subject><subject>Androgens - toxicity</subject><subject>Angiotensin AT1 receptors</subject><subject>Angiotensin II</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Blood pressure</subject><subject>Brain natriuretic peptide</subject><subject>Ca2+-transporting ATPase</subject><subject>Calcium (reticular)</subject><subject>Cardiac muscle</subject><subject>Cardiomegaly - chemically induced</subject><subject>Cardiomegaly - physiopathology</subject><subject>Catalase</subject><subject>Catalase - antagonists & inhibitors</subject><subject>Catalase - genetics</subject><subject>Catalase - metabolism</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - physiopathology</subject><subject>Down-regulation</subject><subject>Dysautonomia</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Developmental - drug effects</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Hypertrophy</subject><subject>Injections, Intramuscular</subject><subject>IR injury</subject><subject>Ischemia</subject><subject>Male</subject><subject>Mechanical properties</subject><subject>Myocardial infarction</subject><subject>Myocardial Ischemia - chemically induced</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardial Reperfusion Injury - chemically induced</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myosin Heavy Chains - chemistry</subject><subject>Myosin Heavy Chains - genetics</subject><subject>Myosin Heavy Chains - metabolism</subject><subject>NAD(P)H oxidase</subject><subject>Polymerase chain reaction</subject><subject>Potassium channels (inwardly-rectifying)</subject><subject>Random Allocation</subject><subject>Rats, Wistar</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reperfusion</subject><subject>Ryanodine receptors</subject><subject>Steroids</subject><subject>Testosterone</subject><subject>Testosterone Propionate - administration & dosage</subject><subject>Testosterone Propionate - toxicity</subject><subject>Time Factors</subject><issn>0960-0760</issn><issn>1879-1220</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUGL1TAUhYsoznP0FwgScOOmb26SNmkXLoZBR2HAjeIypMntvJQ2eSap0P_kjzRv3ujChXDhbr5z7uGeqnpNYU-BiqtpP6VhGfYMqNwDLcOeVDvayb6mjMHTage9gBqkgIvqRUoTAHBO5fPqgnVU9gz6XfXr2i7Ou5Sjzi54EkaivR7C7AxJGWNwltg1On9PtA0zJoPeIHHergYTmYO_rwu2EKOjddqQw3bEmGM4HrbiZAtpIupU2LQW8TG7wc0ubyQH4pI54OL0VcQiGtd0SuD8tMatrHJwnTP5XsLpSEq-9LJ6Nuo54avHfVl9-_jh682n-u7L7eeb67va8E7mWvC-tRpbYzsEywGw6RsUI9flF9wKI7nllGtjAWxjJbRibBgOgrY9o3Tgl9W7s-8xhh8rpqyWEhXnWXsMa1K0E0L0nEFT0Lf_oFNYoy_pFO1lT1vOpSwUP1MmhpQijuoY3aLjpiioU5lqUg9lqlOZCmgZVlRvHr3XYUH7V_OnvQK8PwNYnvHTYVTJuFM_1kU0Wdng_nvgN6K3tak</recordid><startdate>201707</startdate><enddate>201707</enddate><creator>Seara, Fernando de Azevedo Cruz</creator><creator>Barbosa, Raiana Andrade Quintanilha</creator><creator>de Oliveira, Dahienne Ferreira</creator><creator>Gran da Silva, Diorney Luiz Souza</creator><creator>Carvalho, Adriana Bastos</creator><creator>Freitas Ferreira, Andrea Claudia</creator><creator>Matheus Nascimento, José Hamilton</creator><creator>Olivares, Emerson Lopes</creator><general>Elsevier Ltd</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>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201707</creationdate><title>Administration of anabolic steroid during adolescence induces long-term cardiac hypertrophy and increases susceptibility to ischemia/reperfusion injury in adult Wistar rats</title><author>Seara, Fernando de Azevedo Cruz ; Barbosa, Raiana Andrade Quintanilha ; de Oliveira, Dahienne Ferreira ; Gran da Silva, Diorney Luiz Souza ; Carvalho, Adriana Bastos ; Freitas Ferreira, Andrea Claudia ; Matheus Nascimento, José Hamilton ; Olivares, Emerson Lopes</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-6395dae5cd8e0d300e494e6f3a0763d6c73d313acd00d4d7056f42eb6159211b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adolescence</topic><topic>Adolescents</topic><topic>Aging</topic><topic>Anabolic Agents - administration & dosage</topic><topic>Anabolic Agents - toxicity</topic><topic>Anabolic steroids</topic><topic>Androgens</topic><topic>Androgens - administration & dosage</topic><topic>Androgens - toxicity</topic><topic>Angiotensin AT1 receptors</topic><topic>Angiotensin II</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Blood pressure</topic><topic>Brain natriuretic peptide</topic><topic>Ca2+-transporting ATPase</topic><topic>Calcium (reticular)</topic><topic>Cardiac muscle</topic><topic>Cardiomegaly - chemically induced</topic><topic>Cardiomegaly - physiopathology</topic><topic>Catalase</topic><topic>Catalase - antagonists & inhibitors</topic><topic>Catalase - genetics</topic><topic>Catalase - metabolism</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - physiopathology</topic><topic>Down-regulation</topic><topic>Dysautonomia</topic><topic>Enzymes</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Developmental - drug effects</topic><topic>Heart</topic><topic>Heart - 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metabolism</topic><topic>Reperfusion</topic><topic>Ryanodine receptors</topic><topic>Steroids</topic><topic>Testosterone</topic><topic>Testosterone Propionate - administration & dosage</topic><topic>Testosterone Propionate - toxicity</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seara, Fernando de Azevedo Cruz</creatorcontrib><creatorcontrib>Barbosa, Raiana Andrade Quintanilha</creatorcontrib><creatorcontrib>de Oliveira, Dahienne Ferreira</creatorcontrib><creatorcontrib>Gran da Silva, Diorney Luiz Souza</creatorcontrib><creatorcontrib>Carvalho, Adriana Bastos</creatorcontrib><creatorcontrib>Freitas Ferreira, Andrea Claudia</creatorcontrib><creatorcontrib>Matheus Nascimento, José Hamilton</creatorcontrib><creatorcontrib>Olivares, Emerson Lopes</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seara, Fernando de Azevedo Cruz</au><au>Barbosa, Raiana Andrade Quintanilha</au><au>de Oliveira, Dahienne Ferreira</au><au>Gran da Silva, Diorney Luiz Souza</au><au>Carvalho, Adriana Bastos</au><au>Freitas Ferreira, Andrea Claudia</au><au>Matheus Nascimento, José Hamilton</au><au>Olivares, Emerson Lopes</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Administration of anabolic steroid during adolescence induces long-term cardiac hypertrophy and increases susceptibility to ischemia/reperfusion injury in adult Wistar rats</atitle><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle><addtitle>J Steroid Biochem Mol Biol</addtitle><date>2017-07</date><risdate>2017</risdate><volume>171</volume><spage>34</spage><epage>42</epage><pages>34-42</pages><issn>0960-0760</issn><eissn>1879-1220</eissn><abstract>•Chronic administration of AAS during adolescence promoted persistent cardiac hypertrophy in adulthood.•Cardiac hypertrophy was characterized by up-regulation in the βMHC expression, compatible with pathologic hypertrophy.•Susceptibility to myocardial IR injury in adult life was significantly increased by AAS administration in adolescence.•Molecular evidences support that down-regulation of catalase might have a pathophysiological role.
Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia. We tested the hypothesis that chronic AAS exposure in the pre/pubertal phase increases the susceptibility to myocardial ischemia/reperfusion (IR) injury in adult rats. Male Wistar rats (26day old) were treated with vehicle (Control, n=12) or testosterone propionate (TP) (AAS, 5mgkg−1 n=12) 5 times/week during 5 weeks. At the end of AAS exposure, rats underwent 23days of washout period and were submitted to euthanasia. Langendorff-perfused hearts were submitted to IR injury and evaluated for mechanical dysfunctions and infarct size. Molecular analysis was performed by mRNA levels of α-myosin heavy chain (MHC), βMHC and brain-derived natriuretic peptide (BNP), ryanodine receptor (RyR2) and sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) by quantitative RT-PCR (qRT-PCR). The expression of AT1 receptor and KATP channel subunits (Kir6.1 and SURa) was analyzed by qRT-PCR and Western Blot. NADPH oxidase (Nox)-related reactive oxygen species generation was assessed by spectrofluorimetry. The expression of antioxidant enzymes was measured by qRT-PCR in order to address a potential role of redox unbalance. AAS exposure promoted long-term cardiac hypertrophy characterized by increased expression of βMHC and βMHC/αMHC ratio. Baseline derivative of pressure (dP/dt) was impaired by AAS exposure. Postischemic recovery of mechanical properties was impaired (decreased left ventricle [LV] developed pressure and maximal dP/dt; increased LV end-diastolic pressure and minimal dP/dt) and infarct size was larger in the AAS group. Catalase mRNA expression was significantly decreased in the AAS group. In conclusion, chronic administration of AAS during adolescence promoted long-term pathological cardiac hypertrophy and persistent increase in the susceptibility to myocardial IR injury possible due to disturbances on catalase expression.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>28179209</pmid><doi>10.1016/j.jsbmb.2017.01.012</doi><tpages>9</tpages></addata></record> |
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| ispartof | The Journal of steroid biochemistry and molecular biology, 2017-07, Vol.171, p.34-42 |
| issn | 0960-0760 1879-1220 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1866693204 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adolescence Adolescents Aging Anabolic Agents - administration & dosage Anabolic Agents - toxicity Anabolic steroids Androgens Androgens - administration & dosage Androgens - toxicity Angiotensin AT1 receptors Angiotensin II Animals Antioxidants Blood pressure Brain natriuretic peptide Ca2+-transporting ATPase Calcium (reticular) Cardiac muscle Cardiomegaly - chemically induced Cardiomegaly - physiopathology Catalase Catalase - antagonists & inhibitors Catalase - genetics Catalase - metabolism Coronary Vessels - drug effects Coronary Vessels - physiopathology Down-regulation Dysautonomia Enzymes Gene expression Gene Expression Regulation, Developmental - drug effects Heart Heart - drug effects Heart - physiopathology Heart attacks Heart diseases Hypertrophy Injections, Intramuscular IR injury Ischemia Male Mechanical properties Myocardial infarction Myocardial Ischemia - chemically induced Myocardial Ischemia - pathology Myocardial Ischemia - physiopathology Myocardial Reperfusion Injury - chemically induced Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - physiopathology Myocardium - enzymology Myocardium - metabolism Myocardium - pathology Myosin Heavy Chains - chemistry Myosin Heavy Chains - genetics Myosin Heavy Chains - metabolism NAD(P)H oxidase Polymerase chain reaction Potassium channels (inwardly-rectifying) Random Allocation Rats, Wistar Reactive oxygen species Reactive Oxygen Species - metabolism Reperfusion Ryanodine receptors Steroids Testosterone Testosterone Propionate - administration & dosage Testosterone Propionate - toxicity Time Factors |
| title | Administration of anabolic steroid during adolescence induces long-term cardiac hypertrophy and increases susceptibility to ischemia/reperfusion injury in adult Wistar rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T02%3A25%3A42IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Administration%20of%20anabolic%20steroid%20during%20adolescence%20induces%20long-term%20cardiac%20hypertrophy%20and%20increases%20susceptibility%20to%20ischemia/reperfusion%20injury%20in%20adult%20Wistar%20rats&rft.jtitle=The%20Journal%20of%20steroid%20biochemistry%20and%20molecular%20biology&rft.au=Seara,%20Fernando%20de%20Azevedo%20Cruz&rft.date=2017-07&rft.volume=171&rft.spage=34&rft.epage=42&rft.pages=34-42&rft.issn=0960-0760&rft.eissn=1879-1220&rft_id=info:doi/10.1016/j.jsbmb.2017.01.012&rft_dat=%3Cproquest_cross%3E1866693204%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1979153377&rft_id=info:pmid/28179209&rft_els_id=S0960076017300122&rfr_iscdi=true |