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Effects of long-term nonylphenol exposure on myocardial fibrosis and cardiac function in rats

Background Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The...

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Published in:Environmental sciences Europe 2021-12, Vol.33 (1), Article 96
Main Authors: Liu, Chao, Ni, Chengyu, Liu, Weichu, Yang, Xiaolian, Zhang, Renyi, Zhang, Jianling, Luo, Man, Xu, Jie, Yu, Jie
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Ni, Chengyu
Liu, Weichu
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Xu, Jie
Yu, Jie
description Background Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague–Dawley rats were randomly divided into four groups ( n  = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results The NP level in the heart of the NP groups was significantly higher than those in the control group ( F  = 43.658, P  
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Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague–Dawley rats were randomly divided into four groups ( n  = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results The NP level in the heart of the NP groups was significantly higher than those in the control group ( F  = 43.658, P  &lt; 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group ( P  &lt; 0.05). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP-treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group ( P  &lt; 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups ( P  &lt; 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity. Highlights Chronic NP exposure induced myocardial fibrosis and cardiac functional damage. NP increased the expression of myocardial collagen I and III and cardiac enzymes. NP caused cardiac structure changes with thinner ventricular wall and enlarged ventricular cavity.</description><identifier>ISSN: 2190-4707</identifier><identifier>EISSN: 2190-4715</identifier><identifier>DOI: 10.1186/s12302-021-00539-2</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Aspartate aminotransferase ; Biopsy ; Cardiovascular diseases ; Chronic exposure ; Collagen ; Collagen (type I) ; Collagen (type III) ; Connective tissues ; Creatine ; Creatine kinase ; Dehydrogenase ; Dehydrogenases ; Dosage ; Earth and Environmental Science ; Ecotoxicology ; Environment ; Enzymes ; Estrogens ; Exposure ; Fibrosis ; Fractures ; Heart ; Inflammation ; Kinases ; L-Lactate dehydrogenase ; Lactate dehydrogenase ; Lactic acid ; Muscles ; Myocardium ; Natural Toxins - Environmental Fate and Safe Water Supply ; Nonylphenol ; Pollution ; Structure-function relationships ; Thickness ; Ventricle</subject><ispartof>Environmental sciences Europe, 2021-12, Vol.33 (1), Article 96</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c363t-5726baf671044bfa67725c433472ff1bf378aee9e795989980f2bda640d809e3</citedby><cites>FETCH-LOGICAL-c363t-5726baf671044bfa67725c433472ff1bf378aee9e795989980f2bda640d809e3</cites><orcidid>0000-0002-4796-7177</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Liu, Chao</creatorcontrib><creatorcontrib>Ni, Chengyu</creatorcontrib><creatorcontrib>Liu, Weichu</creatorcontrib><creatorcontrib>Yang, Xiaolian</creatorcontrib><creatorcontrib>Zhang, Renyi</creatorcontrib><creatorcontrib>Zhang, Jianling</creatorcontrib><creatorcontrib>Luo, Man</creatorcontrib><creatorcontrib>Xu, Jie</creatorcontrib><creatorcontrib>Yu, Jie</creatorcontrib><title>Effects of long-term nonylphenol exposure on myocardial fibrosis and cardiac function in rats</title><title>Environmental sciences Europe</title><addtitle>Environ Sci Eur</addtitle><description>Background Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague–Dawley rats were randomly divided into four groups ( n  = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results The NP level in the heart of the NP groups was significantly higher than those in the control group ( F  = 43.658, P  &lt; 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group ( P  &lt; 0.05). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP-treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group ( P  &lt; 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups ( P  &lt; 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity. Highlights Chronic NP exposure induced myocardial fibrosis and cardiac functional damage. NP increased the expression of myocardial collagen I and III and cardiac enzymes. NP caused cardiac structure changes with thinner ventricular wall and enlarged ventricular cavity.</description><subject>Aspartate aminotransferase</subject><subject>Biopsy</subject><subject>Cardiovascular diseases</subject><subject>Chronic exposure</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen (type III)</subject><subject>Connective tissues</subject><subject>Creatine</subject><subject>Creatine kinase</subject><subject>Dehydrogenase</subject><subject>Dehydrogenases</subject><subject>Dosage</subject><subject>Earth and Environmental Science</subject><subject>Ecotoxicology</subject><subject>Environment</subject><subject>Enzymes</subject><subject>Estrogens</subject><subject>Exposure</subject><subject>Fibrosis</subject><subject>Fractures</subject><subject>Heart</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>Muscles</subject><subject>Myocardium</subject><subject>Natural Toxins - Environmental Fate and Safe Water Supply</subject><subject>Nonylphenol</subject><subject>Pollution</subject><subject>Structure-function relationships</subject><subject>Thickness</subject><subject>Ventricle</subject><issn>2190-4707</issn><issn>2190-4715</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kE1LAzEQhoMoWGr_gKeA52g-NsnmKKV-QMFLrxKy2aRu2SZrsgv23xtd0ZtzmWF43nmHF4Brgm8JqcVdJpRhijAlCGPOFKJnYEGJwqiShJ__zlheglXOB1yK01pWfAFeN947O2YYPexj2KPRpSMMMZz64c2F2EP3McQ8JQdjgMdTtCa1nemh75oUc5ehCS2clxb6KdixK2AXYDJjvgIX3vTZrX76EuweNrv1E9q-PD6v77fIMsFGxCUVjfFCElxVjTdCSsptxVglqfek8UzWxjnlpOKqVqrGnjatERVua6wcW4Kb-eyQ4vvk8qgPcUqhOGrKBS0eTPBC0Zmy5fGcnNdD6o4mnTTB-itIPQepS5D6O0hNi4jNolzgsHfp7_Q_qk-2PXYN</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Liu, Chao</creator><creator>Ni, Chengyu</creator><creator>Liu, Weichu</creator><creator>Yang, Xiaolian</creator><creator>Zhang, Renyi</creator><creator>Zhang, Jianling</creator><creator>Luo, Man</creator><creator>Xu, Jie</creator><creator>Yu, Jie</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8C1</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PYCSY</scope><orcidid>https://orcid.org/0000-0002-4796-7177</orcidid></search><sort><creationdate>20211201</creationdate><title>Effects of long-term nonylphenol exposure on myocardial fibrosis and cardiac function in rats</title><author>Liu, Chao ; 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Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague–Dawley rats were randomly divided into four groups ( n  = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results The NP level in the heart of the NP groups was significantly higher than those in the control group ( F  = 43.658, P  &lt; 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group ( P  &lt; 0.05). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP-treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group ( P  &lt; 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups ( P  &lt; 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity. Highlights Chronic NP exposure induced myocardial fibrosis and cardiac functional damage. NP increased the expression of myocardial collagen I and III and cardiac enzymes. NP caused cardiac structure changes with thinner ventricular wall and enlarged ventricular cavity.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><doi>10.1186/s12302-021-00539-2</doi><orcidid>https://orcid.org/0000-0002-4796-7177</orcidid><oa>free_for_read</oa></addata></record>
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subjects Aspartate aminotransferase
Biopsy
Cardiovascular diseases
Chronic exposure
Collagen
Collagen (type I)
Collagen (type III)
Connective tissues
Creatine
Creatine kinase
Dehydrogenase
Dehydrogenases
Dosage
Earth and Environmental Science
Ecotoxicology
Environment
Enzymes
Estrogens
Exposure
Fibrosis
Fractures
Heart
Inflammation
Kinases
L-Lactate dehydrogenase
Lactate dehydrogenase
Lactic acid
Muscles
Myocardium
Natural Toxins - Environmental Fate and Safe Water Supply
Nonylphenol
Pollution
Structure-function relationships
Thickness
Ventricle
title Effects of long-term nonylphenol exposure on myocardial fibrosis and cardiac function in rats
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