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Amelioration of ethanol-induced growth retardation by all- trans-retinoic acid and α-tocopherol in shell-less culture of the chick embryo
The mechanisms of teratogenic action of ethanol (EtOH) were investigated by testing the hypothesis that all- trans-retinoic acid and/or α-tocopherol ameliorates ethanol-induced embryonic growth retardation. Chicken embryos were explanted in shell-less cultures and a single dose of EtOH (15, 30, or 5...
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Published in: | Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2004-05, Vol.18 (3), p.407-412 |
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creator | Satiroglu-Tufan, N.Lale Tufan, A.Cevik |
description | The mechanisms of teratogenic action of ethanol (EtOH) were investigated by testing the hypothesis that all-
trans-retinoic acid and/or α-tocopherol ameliorates ethanol-induced embryonic growth retardation. Chicken embryos were explanted in shell-less cultures and a single dose of EtOH (15, 30, or 50%) or 50% EtOH with either all-
trans-retinoic acid (10
−8
M) or α-tocopherol (0.05
M) or a mix of all-
trans-retinoic acid (10
−8
M) and α-tocopherol (0.05
M) was applied to the center of the blastodisc. EtOH significantly increased the mortality rate and induced growth retardation in a dose-dependent manner. In addition, EtOH increased malondialdehyde (MDA) levels, an indicator of oxidative stress and cell damage, in a dose dependent manner. All-
trans-retinoic acid, the active form of Vitamin A, and/or α-tocopherol, an antioxidant, co-treatment with EtOH significantly diminished both the EtOH-induced mortality and growth retardation. However, only α-tocopherol co-treatment reduced the MDA levels. Thus, the mechanisms of teratogenic action of EtOH appear to involve initiation of oxidative stress as well as perturbation of retinoic acid (RA) signaling. It also appears likely that these mechanisms work independently of each other. |
doi_str_mv | 10.1016/j.reprotox.2004.01.005 |
format | article |
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trans-retinoic acid and/or α-tocopherol ameliorates ethanol-induced embryonic growth retardation. Chicken embryos were explanted in shell-less cultures and a single dose of EtOH (15, 30, or 50%) or 50% EtOH with either all-
trans-retinoic acid (10
−8
M) or α-tocopherol (0.05
M) or a mix of all-
trans-retinoic acid (10
−8
M) and α-tocopherol (0.05
M) was applied to the center of the blastodisc. EtOH significantly increased the mortality rate and induced growth retardation in a dose-dependent manner. In addition, EtOH increased malondialdehyde (MDA) levels, an indicator of oxidative stress and cell damage, in a dose dependent manner. All-
trans-retinoic acid, the active form of Vitamin A, and/or α-tocopherol, an antioxidant, co-treatment with EtOH significantly diminished both the EtOH-induced mortality and growth retardation. However, only α-tocopherol co-treatment reduced the MDA levels. Thus, the mechanisms of teratogenic action of EtOH appear to involve initiation of oxidative stress as well as perturbation of retinoic acid (RA) signaling. It also appears likely that these mechanisms work independently of each other.</description><identifier>ISSN: 0890-6238</identifier><identifier>EISSN: 1873-1708</identifier><identifier>DOI: 10.1016/j.reprotox.2004.01.005</identifier><identifier>PMID: 15082076</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Alcoholism and acute alcohol poisoning ; All- trans-retinoic acid ; Animals ; Antioxidants - pharmacology ; Biological and medical sciences ; Body Weight - drug effects ; Chick Embryo ; Dose-Response Relationship, Drug ; Embryo Culture Techniques ; Embryology: invertebrates and vertebrates. Teratology ; Ethanol ; Ethanol - antagonists & inhibitors ; Ethanol - toxicity ; FAS ; Fetal Growth Retardation - chemically induced ; Fetal Growth Retardation - pathology ; Fundamental and applied biological sciences. Psychology ; Growth retardation ; Malondialdehyde - metabolism ; Medical sciences ; Teratogens ; Teratology. Teratogens ; Toxicology ; Tretinoin - pharmacology ; Vitamin E - pharmacology ; α-Tocopherol</subject><ispartof>Reproductive toxicology (Elmsford, N.Y.), 2004-05, Vol.18 (3), p.407-412</ispartof><rights>2004 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-f37897bdb04bafe385ba9fef5bcca6ee82e69daa436dc005b8d3ab6da863f1093</citedby><cites>FETCH-LOGICAL-c456t-f37897bdb04bafe385ba9fef5bcca6ee82e69daa436dc005b8d3ab6da863f1093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15678166$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15082076$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Satiroglu-Tufan, N.Lale</creatorcontrib><creatorcontrib>Tufan, A.Cevik</creatorcontrib><title>Amelioration of ethanol-induced growth retardation by all- trans-retinoic acid and α-tocopherol in shell-less culture of the chick embryo</title><title>Reproductive toxicology (Elmsford, N.Y.)</title><addtitle>Reprod Toxicol</addtitle><description>The mechanisms of teratogenic action of ethanol (EtOH) were investigated by testing the hypothesis that all-
trans-retinoic acid and/or α-tocopherol ameliorates ethanol-induced embryonic growth retardation. Chicken embryos were explanted in shell-less cultures and a single dose of EtOH (15, 30, or 50%) or 50% EtOH with either all-
trans-retinoic acid (10
−8
M) or α-tocopherol (0.05
M) or a mix of all-
trans-retinoic acid (10
−8
M) and α-tocopherol (0.05
M) was applied to the center of the blastodisc. EtOH significantly increased the mortality rate and induced growth retardation in a dose-dependent manner. In addition, EtOH increased malondialdehyde (MDA) levels, an indicator of oxidative stress and cell damage, in a dose dependent manner. All-
trans-retinoic acid, the active form of Vitamin A, and/or α-tocopherol, an antioxidant, co-treatment with EtOH significantly diminished both the EtOH-induced mortality and growth retardation. However, only α-tocopherol co-treatment reduced the MDA levels. Thus, the mechanisms of teratogenic action of EtOH appear to involve initiation of oxidative stress as well as perturbation of retinoic acid (RA) signaling. It also appears likely that these mechanisms work independently of each other.</description><subject>Alcoholism and acute alcohol poisoning</subject><subject>All- trans-retinoic acid</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Body Weight - drug effects</subject><subject>Chick Embryo</subject><subject>Dose-Response Relationship, Drug</subject><subject>Embryo Culture Techniques</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Ethanol</subject><subject>Ethanol - antagonists & inhibitors</subject><subject>Ethanol - toxicity</subject><subject>FAS</subject><subject>Fetal Growth Retardation - chemically induced</subject><subject>Fetal Growth Retardation - pathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Growth retardation</subject><subject>Malondialdehyde - metabolism</subject><subject>Medical sciences</subject><subject>Teratogens</subject><subject>Teratology. Teratogens</subject><subject>Toxicology</subject><subject>Tretinoin - pharmacology</subject><subject>Vitamin E - pharmacology</subject><subject>α-Tocopherol</subject><issn>0890-6238</issn><issn>1873-1708</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqFkU1uFDEQRi0EIkPgCpE3sOvG7h_bvSOKgCBFYgNrq2xX0x562oPtBuYK3IaLcKZ4NINgl5UXflX16XuEXHFWc8bF620dcR9DDj_rhrGuZrxmrH9ENlzJtuKSqcdkw9TAKtG06oI8S2nLCigH-ZRc8J6phkmxIb-udzj7ECH7sNAwUswTLGGu_OJWi45-ieFHnmjEDNGdKHOgMM8VzRGWVJUfvwRvKVjvKCyO_vld5WDDfsIYZuoXmiYs_IwpUbvOeY14vJQnpHby9ivFnYmH8Jw8GWFO-OL8XpLP795-urmt7j6-_3BzfVfZrhe5GlupBmmcYZ2BEVvVGxhGHHtjLQhE1aAYHEDXCmdLJ0a5FoxwoEQ7cja0l-TVaW_p79uKKeudT7YkhAXDmjQfZCM63j0MyqYTTc8LKE6gjSGliKPeR7-DeNCc6aMuvdV_demjLs24LtHK4NX5wmp26P6Nnf0U4OUZgGRhHkvj1qf_OCEVF0fuzYnDUtx3j1En63EpAn1Em7UL_qEs9_3qu8A</recordid><startdate>20040501</startdate><enddate>20040501</enddate><creator>Satiroglu-Tufan, N.Lale</creator><creator>Tufan, A.Cevik</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20040501</creationdate><title>Amelioration of ethanol-induced growth retardation by all- trans-retinoic acid and α-tocopherol in shell-less culture of the chick embryo</title><author>Satiroglu-Tufan, N.Lale ; Tufan, A.Cevik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-f37897bdb04bafe385ba9fef5bcca6ee82e69daa436dc005b8d3ab6da863f1093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alcoholism and acute alcohol poisoning</topic><topic>All- trans-retinoic acid</topic><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Body Weight - drug effects</topic><topic>Chick Embryo</topic><topic>Dose-Response Relationship, Drug</topic><topic>Embryo Culture Techniques</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>Ethanol</topic><topic>Ethanol - antagonists & inhibitors</topic><topic>Ethanol - toxicity</topic><topic>FAS</topic><topic>Fetal Growth Retardation - chemically induced</topic><topic>Fetal Growth Retardation - pathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Growth retardation</topic><topic>Malondialdehyde - metabolism</topic><topic>Medical sciences</topic><topic>Teratogens</topic><topic>Teratology. Teratogens</topic><topic>Toxicology</topic><topic>Tretinoin - pharmacology</topic><topic>Vitamin E - pharmacology</topic><topic>α-Tocopherol</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Satiroglu-Tufan, N.Lale</creatorcontrib><creatorcontrib>Tufan, A.Cevik</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Reproductive toxicology (Elmsford, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Satiroglu-Tufan, N.Lale</au><au>Tufan, A.Cevik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amelioration of ethanol-induced growth retardation by all- trans-retinoic acid and α-tocopherol in shell-less culture of the chick embryo</atitle><jtitle>Reproductive toxicology (Elmsford, N.Y.)</jtitle><addtitle>Reprod Toxicol</addtitle><date>2004-05-01</date><risdate>2004</risdate><volume>18</volume><issue>3</issue><spage>407</spage><epage>412</epage><pages>407-412</pages><issn>0890-6238</issn><eissn>1873-1708</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The mechanisms of teratogenic action of ethanol (EtOH) were investigated by testing the hypothesis that all-
trans-retinoic acid and/or α-tocopherol ameliorates ethanol-induced embryonic growth retardation. Chicken embryos were explanted in shell-less cultures and a single dose of EtOH (15, 30, or 50%) or 50% EtOH with either all-
trans-retinoic acid (10
−8
M) or α-tocopherol (0.05
M) or a mix of all-
trans-retinoic acid (10
−8
M) and α-tocopherol (0.05
M) was applied to the center of the blastodisc. EtOH significantly increased the mortality rate and induced growth retardation in a dose-dependent manner. In addition, EtOH increased malondialdehyde (MDA) levels, an indicator of oxidative stress and cell damage, in a dose dependent manner. All-
trans-retinoic acid, the active form of Vitamin A, and/or α-tocopherol, an antioxidant, co-treatment with EtOH significantly diminished both the EtOH-induced mortality and growth retardation. However, only α-tocopherol co-treatment reduced the MDA levels. Thus, the mechanisms of teratogenic action of EtOH appear to involve initiation of oxidative stress as well as perturbation of retinoic acid (RA) signaling. It also appears likely that these mechanisms work independently of each other.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15082076</pmid><doi>10.1016/j.reprotox.2004.01.005</doi><tpages>6</tpages></addata></record> |
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subjects | Alcoholism and acute alcohol poisoning All- trans-retinoic acid Animals Antioxidants - pharmacology Biological and medical sciences Body Weight - drug effects Chick Embryo Dose-Response Relationship, Drug Embryo Culture Techniques Embryology: invertebrates and vertebrates. Teratology Ethanol Ethanol - antagonists & inhibitors Ethanol - toxicity FAS Fetal Growth Retardation - chemically induced Fetal Growth Retardation - pathology Fundamental and applied biological sciences. Psychology Growth retardation Malondialdehyde - metabolism Medical sciences Teratogens Teratology. Teratogens Toxicology Tretinoin - pharmacology Vitamin E - pharmacology α-Tocopherol |
title | Amelioration of ethanol-induced growth retardation by all- trans-retinoic acid and α-tocopherol in shell-less culture of the chick embryo |
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