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Enhancement of BHA-induced proliferative rat forestomach lesion development by simultaneous treatment with other antioxidants
Synergistic effects of butylated hydroxyanisole (BHA) and other antioxidants on induction of rat forestomach lesions were investigated. Groups of F344 male rats were treated with 1% BHA phis 0.7% butylated hydroxytoluene (BHT), 1% BHA phis 1% propyl gallate (PG), 1% BHA plus 1% sodium L-ascorbate (S...
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Published in: | Carcinogenesis (New York) 1987-11, Vol.8 (11), p.1731-1735 |
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creator | Hirose, Masao Masuda, Atsuko Tsuda, Hiroyuki Uwagawa, Satoshi Ito, Nobuyuki |
description | Synergistic effects of butylated hydroxyanisole (BHA) and other antioxidants on induction of rat forestomach lesions were investigated. Groups of F344 male rats were treated with 1% BHA phis 0.7% butylated hydroxytoluene (BHT), 1% BHA phis 1% propyl gallate (PG), 1% BHA plus 1% sodium L-ascorbate (SA), 1% BHA phis 1% DL-α-tocopherol (α-TP), 0.4% BHT phis 0.4% BHA plus 0.4% PG plus 0.4% SA plus 0.4% α-TP, 1% BHA or 2% BHA. Further groups of 10 rats each received antioxidants without BHA as controls. Histo-togfcal examination revealed significantly increased incidences of hyperplasia in the groups given BHA together with SA or PG at the prefundic region or at the mid region respectively. The forestomach changes induced by BHA together with SA were equal to those induced by 2% BHA. On the other hand, simultaneous treatment with BHA and PG or α-TP reduced the incidence of hyperplasia at the prefundk region. It is concluded that mixed treatment with BHA and other antioxidants exerted enhancing or inhibitory effects on the induction of hyperplasia at different sites of the forestomach epithelium. |
doi_str_mv | 10.1093/carcin/8.11.1731 |
format | article |
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Groups of F344 male rats were treated with 1% BHA phis 0.7% butylated hydroxytoluene (BHT), 1% BHA phis 1% propyl gallate (PG), 1% BHA plus 1% sodium L-ascorbate (SA), 1% BHA phis 1% DL-α-tocopherol (α-TP), 0.4% BHT phis 0.4% BHA plus 0.4% PG plus 0.4% SA plus 0.4% α-TP, 1% BHA or 2% BHA. Further groups of 10 rats each received antioxidants without BHA as controls. Histo-togfcal examination revealed significantly increased incidences of hyperplasia in the groups given BHA together with SA or PG at the prefundic region or at the mid region respectively. The forestomach changes induced by BHA together with SA were equal to those induced by 2% BHA. On the other hand, simultaneous treatment with BHA and PG or α-TP reduced the incidence of hyperplasia at the prefundk region. It is concluded that mixed treatment with BHA and other antioxidants exerted enhancing or inhibitory effects on the induction of hyperplasia at different sites of the forestomach epithelium.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/8.11.1731</identifier><identifier>PMID: 3664967</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Antioxidants - toxicity ; Ascorbic Acid - toxicity ; Biological and medical sciences ; Butylated Hydroxyanisole - toxicity ; Carcinogenesis, carcinogens and anticarcinogens ; Cell Division - drug effects ; Chemical agents ; Drug Synergism ; Hyperplasia ; Male ; Medical sciences ; Propyl Gallate - toxicity ; Rats ; Rats, Inbred F344 ; Stomach - drug effects ; Stomach - pathology ; Tumors ; Vitamin E - toxicity</subject><ispartof>Carcinogenesis (New York), 1987-11, Vol.8 (11), p.1731-1735</ispartof><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-65366511b3270efdf98ca6dc9a2d8e00cd474bbfd2a765e5ba0f14db083ab2943</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7800014$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3664967$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirose, Masao</creatorcontrib><creatorcontrib>Masuda, Atsuko</creatorcontrib><creatorcontrib>Tsuda, Hiroyuki</creatorcontrib><creatorcontrib>Uwagawa, Satoshi</creatorcontrib><creatorcontrib>Ito, Nobuyuki</creatorcontrib><title>Enhancement of BHA-induced proliferative rat forestomach lesion development by simultaneous treatment with other antioxidants</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Synergistic effects of butylated hydroxyanisole (BHA) and other antioxidants on induction of rat forestomach lesions were investigated. Groups of F344 male rats were treated with 1% BHA phis 0.7% butylated hydroxytoluene (BHT), 1% BHA phis 1% propyl gallate (PG), 1% BHA plus 1% sodium L-ascorbate (SA), 1% BHA phis 1% DL-α-tocopherol (α-TP), 0.4% BHT phis 0.4% BHA plus 0.4% PG plus 0.4% SA plus 0.4% α-TP, 1% BHA or 2% BHA. Further groups of 10 rats each received antioxidants without BHA as controls. Histo-togfcal examination revealed significantly increased incidences of hyperplasia in the groups given BHA together with SA or PG at the prefundic region or at the mid region respectively. The forestomach changes induced by BHA together with SA were equal to those induced by 2% BHA. On the other hand, simultaneous treatment with BHA and PG or α-TP reduced the incidence of hyperplasia at the prefundk region. It is concluded that mixed treatment with BHA and other antioxidants exerted enhancing or inhibitory effects on the induction of hyperplasia at different sites of the forestomach epithelium.</description><subject>Animals</subject><subject>Antioxidants - toxicity</subject><subject>Ascorbic Acid - toxicity</subject><subject>Biological and medical sciences</subject><subject>Butylated Hydroxyanisole - toxicity</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Cell Division - drug effects</subject><subject>Chemical agents</subject><subject>Drug Synergism</subject><subject>Hyperplasia</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Propyl Gallate - toxicity</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Stomach - drug effects</subject><subject>Stomach - pathology</subject><subject>Tumors</subject><subject>Vitamin E - toxicity</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><recordid>eNo9UbuO1DAUtRBoGQZ6GiQXiC6zfsVJyp3VLoO0EgUgIRrLsa81hiQebGcfBf-OZzOa6hTnoXPPReg9JRtKOn5pdDR-umw3lG5ow-kLtKJCkorRlrxEK0IFrzjn4jV6k9JvQqjkdXeBLriUopPNCv27mfZ6MjDClHFweLu7qvxkZwMWH2IYvIOos78HXAC7ECHlMGqzxwMkHyZs4R6GcHj29084-XEesp4gzAnnCDo_Mw8-73HIe4hYT9mHR28LprfoldNDgncnXKMftzffr3fV3dfPX66v7iojuMiVrEvfmtKes4aAs65rjZbWdJrZFggxVjSi751lupE11L0mjgrbk5brnnWCr9GnJbec9HcuJ6jRJwPDsBRVtGYNqzkrQrIITQwpRXDqEP2o45OiRB0XV8viqlWUquPixfLhlD33I9iz4TRx4T-eeJ2MHlwsc_t0ljUtIcc3rVG1yHzK8HimdfyjSkhTq93PX4pt2-2tFN8U5_8BVzCdAA</recordid><startdate>19871101</startdate><enddate>19871101</enddate><creator>Hirose, Masao</creator><creator>Masuda, Atsuko</creator><creator>Tsuda, Hiroyuki</creator><creator>Uwagawa, Satoshi</creator><creator>Ito, Nobuyuki</creator><general>Oxford University Press</general><scope>BSCLL</scope><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>19871101</creationdate><title>Enhancement of BHA-induced proliferative rat forestomach lesion development by simultaneous treatment with other antioxidants</title><author>Hirose, Masao ; Masuda, Atsuko ; Tsuda, Hiroyuki ; Uwagawa, Satoshi ; Ito, Nobuyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-65366511b3270efdf98ca6dc9a2d8e00cd474bbfd2a765e5ba0f14db083ab2943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Animals</topic><topic>Antioxidants - toxicity</topic><topic>Ascorbic Acid - toxicity</topic><topic>Biological and medical sciences</topic><topic>Butylated Hydroxyanisole - toxicity</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Cell Division - drug effects</topic><topic>Chemical agents</topic><topic>Drug Synergism</topic><topic>Hyperplasia</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Propyl Gallate - toxicity</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Stomach - drug effects</topic><topic>Stomach - pathology</topic><topic>Tumors</topic><topic>Vitamin E - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hirose, Masao</creatorcontrib><creatorcontrib>Masuda, Atsuko</creatorcontrib><creatorcontrib>Tsuda, Hiroyuki</creatorcontrib><creatorcontrib>Uwagawa, Satoshi</creatorcontrib><creatorcontrib>Ito, Nobuyuki</creatorcontrib><collection>Istex</collection><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>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hirose, Masao</au><au>Masuda, Atsuko</au><au>Tsuda, Hiroyuki</au><au>Uwagawa, Satoshi</au><au>Ito, Nobuyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhancement of BHA-induced proliferative rat forestomach lesion development by simultaneous treatment with other antioxidants</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>1987-11-01</date><risdate>1987</risdate><volume>8</volume><issue>11</issue><spage>1731</spage><epage>1735</epage><pages>1731-1735</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Synergistic effects of butylated hydroxyanisole (BHA) and other antioxidants on induction of rat forestomach lesions were investigated. Groups of F344 male rats were treated with 1% BHA phis 0.7% butylated hydroxytoluene (BHT), 1% BHA phis 1% propyl gallate (PG), 1% BHA plus 1% sodium L-ascorbate (SA), 1% BHA phis 1% DL-α-tocopherol (α-TP), 0.4% BHT phis 0.4% BHA plus 0.4% PG plus 0.4% SA plus 0.4% α-TP, 1% BHA or 2% BHA. Further groups of 10 rats each received antioxidants without BHA as controls. Histo-togfcal examination revealed significantly increased incidences of hyperplasia in the groups given BHA together with SA or PG at the prefundic region or at the mid region respectively. The forestomach changes induced by BHA together with SA were equal to those induced by 2% BHA. On the other hand, simultaneous treatment with BHA and PG or α-TP reduced the incidence of hyperplasia at the prefundk region. It is concluded that mixed treatment with BHA and other antioxidants exerted enhancing or inhibitory effects on the induction of hyperplasia at different sites of the forestomach epithelium.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>3664967</pmid><doi>10.1093/carcin/8.11.1731</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antioxidants - toxicity Ascorbic Acid - toxicity Biological and medical sciences Butylated Hydroxyanisole - toxicity Carcinogenesis, carcinogens and anticarcinogens Cell Division - drug effects Chemical agents Drug Synergism Hyperplasia Male Medical sciences Propyl Gallate - toxicity Rats Rats, Inbred F344 Stomach - drug effects Stomach - pathology Tumors Vitamin E - toxicity |
title | Enhancement of BHA-induced proliferative rat forestomach lesion development by simultaneous treatment with other antioxidants |
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