Developmental toxicity of concanavalin a in rats: Association with restricted migration of neural crest cells
Concanavalin A (Con A), a plant lectin, was injected iv into pregnant rats as a single dose of 5, 10 or 20 mg/kg on gestational day (GD) 8, to investigate developmental toxicity in foetuses at term and to examine histologically embryos between GD 10 and 12. There were high incidences of various malf...
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| Veröffentlicht in: | Food and chemical toxicology 1996-08, Vol.34 (8), p.701-708 |
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| creator | Nishida, A. Kobayashi, T. Ariyuki, F. |
| description | Concanavalin A (Con A), a plant lectin, was injected iv into pregnant rats as a single dose of 5, 10 or 20 mg/kg on gestational day (GD) 8, to investigate developmental toxicity in foetuses at term and to examine histologically embryos between GD 10 and 12. There were high incidences of various malformations in the 10 and 20 mg/kg groups: externally, craniofacial dysplasia and closure defects of the ventral body wall; internally, anophthalmia and cardiovascular malformations; and in the skeleton, anomalies of the anterior region of the vertebrae and ribs. Histological examination revealed that neural crest cells (NCC) in the control embryos appeared to be streaming from the neural crest towards the ventral region on GD 10, 11 and 12, and reached the region of the branchial arches on GD 12. By contrast, those in the Con A-treated embryos were aggregated near the dorsal region on GD 10 and 11, and had not reached the destination even on GD 12. These findings suggest that pathogenesis of developmental toxicity of Con A in rats is associated with disturbance of NCC migration and inhibition of their pluripotentiality at the destination. |
| doi_str_mv | 10.1016/0278-6915(96)00037-3 |
| format | Article |
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There were high incidences of various malformations in the 10 and 20 mg/kg groups: externally, craniofacial dysplasia and closure defects of the ventral body wall; internally, anophthalmia and cardiovascular malformations; and in the skeleton, anomalies of the anterior region of the vertebrae and ribs. Histological examination revealed that neural crest cells (NCC) in the control embryos appeared to be streaming from the neural crest towards the ventral region on GD 10, 11 and 12, and reached the region of the branchial arches on GD 12. By contrast, those in the Con A-treated embryos were aggregated near the dorsal region on GD 10 and 11, and had not reached the destination even on GD 12. These findings suggest that pathogenesis of developmental toxicity of Con A in rats is associated with disturbance of NCC migration and inhibition of their pluripotentiality at the destination.</description><identifier>ISSN: 0278-6915</identifier><identifier>EISSN: 1873-6351</identifier><identifier>DOI: 10.1016/0278-6915(96)00037-3</identifier><identifier>PMID: 8883471</identifier><identifier>CODEN: FCTOD7</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Abnormalities, Drug-Induced ; Analysis of Variance ; Animals ; Biological and medical sciences ; Body Weight - drug effects ; Bone and Bones - abnormalities ; Bone and Bones - drug effects ; Brain - drug effects ; Brain - pathology ; Cell Movement - drug effects ; Concanavalin A - toxicity ; Craniofacial Abnormalities - chemically induced ; Embryology: invertebrates and vertebrates. Teratology ; Embryonic and Fetal Development - drug effects ; Female ; Fundamental and applied biological sciences. Psychology ; Gestational Age ; Heart Defects, Congenital - chemically induced ; Male ; Neural Crest - cytology ; Neural Crest - drug effects ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Teratology. Teratogens</subject><ispartof>Food and chemical toxicology, 1996-08, Vol.34 (8), p.701-708</ispartof><rights>1996</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-646fb69a8cc3717ce5e7d362db3f70b42477b8a71aafdafedf64663d4ccc83d93</citedby><cites>FETCH-LOGICAL-c417t-646fb69a8cc3717ce5e7d362db3f70b42477b8a71aafdafedf64663d4ccc83d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0278-6915(96)00037-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3251415$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8883471$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishida, A.</creatorcontrib><creatorcontrib>Kobayashi, T.</creatorcontrib><creatorcontrib>Ariyuki, F.</creatorcontrib><title>Developmental toxicity of concanavalin a in rats: Association with restricted migration of neural crest cells</title><title>Food and chemical toxicology</title><addtitle>Food Chem Toxicol</addtitle><description>Concanavalin A (Con A), a plant lectin, was injected iv into pregnant rats as a single dose of 5, 10 or 20 mg/kg on gestational day (GD) 8, to investigate developmental toxicity in foetuses at term and to examine histologically embryos between GD 10 and 12. There were high incidences of various malformations in the 10 and 20 mg/kg groups: externally, craniofacial dysplasia and closure defects of the ventral body wall; internally, anophthalmia and cardiovascular malformations; and in the skeleton, anomalies of the anterior region of the vertebrae and ribs. Histological examination revealed that neural crest cells (NCC) in the control embryos appeared to be streaming from the neural crest towards the ventral region on GD 10, 11 and 12, and reached the region of the branchial arches on GD 12. By contrast, those in the Con A-treated embryos were aggregated near the dorsal region on GD 10 and 11, and had not reached the destination even on GD 12. These findings suggest that pathogenesis of developmental toxicity of Con A in rats is associated with disturbance of NCC migration and inhibition of their pluripotentiality at the destination.</description><subject>Abnormalities, Drug-Induced</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Body Weight - drug effects</subject><subject>Bone and Bones - abnormalities</subject><subject>Bone and Bones - drug effects</subject><subject>Brain - drug effects</subject><subject>Brain - pathology</subject><subject>Cell Movement - drug effects</subject><subject>Concanavalin A - toxicity</subject><subject>Craniofacial Abnormalities - chemically induced</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Embryonic and Fetal Development - drug effects</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gestational Age</subject><subject>Heart Defects, Congenital - chemically induced</subject><subject>Male</subject><subject>Neural Crest - cytology</subject><subject>Neural Crest - drug effects</subject><subject>Pregnancy</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Teratology. 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Teratology</topic><topic>Embryonic and Fetal Development - drug effects</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gestational Age</topic><topic>Heart Defects, Congenital - chemically induced</topic><topic>Male</topic><topic>Neural Crest - cytology</topic><topic>Neural Crest - drug effects</topic><topic>Pregnancy</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Teratology. Teratogens</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishida, A.</creatorcontrib><creatorcontrib>Kobayashi, T.</creatorcontrib><creatorcontrib>Ariyuki, F.</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>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Food and chemical toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishida, A.</au><au>Kobayashi, T.</au><au>Ariyuki, F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Developmental toxicity of concanavalin a in rats: Association with restricted migration of neural crest cells</atitle><jtitle>Food and chemical toxicology</jtitle><addtitle>Food Chem Toxicol</addtitle><date>1996-08-01</date><risdate>1996</risdate><volume>34</volume><issue>8</issue><spage>701</spage><epage>708</epage><pages>701-708</pages><issn>0278-6915</issn><eissn>1873-6351</eissn><coden>FCTOD7</coden><abstract>Concanavalin A (Con A), a plant lectin, was injected iv into pregnant rats as a single dose of 5, 10 or 20 mg/kg on gestational day (GD) 8, to investigate developmental toxicity in foetuses at term and to examine histologically embryos between GD 10 and 12. There were high incidences of various malformations in the 10 and 20 mg/kg groups: externally, craniofacial dysplasia and closure defects of the ventral body wall; internally, anophthalmia and cardiovascular malformations; and in the skeleton, anomalies of the anterior region of the vertebrae and ribs. Histological examination revealed that neural crest cells (NCC) in the control embryos appeared to be streaming from the neural crest towards the ventral region on GD 10, 11 and 12, and reached the region of the branchial arches on GD 12. By contrast, those in the Con A-treated embryos were aggregated near the dorsal region on GD 10 and 11, and had not reached the destination even on GD 12. These findings suggest that pathogenesis of developmental toxicity of Con A in rats is associated with disturbance of NCC migration and inhibition of their pluripotentiality at the destination.</abstract><cop>Oxford</cop><cop>New York, NY</cop><pub>Elsevier Ltd</pub><pmid>8883471</pmid><doi>10.1016/0278-6915(96)00037-3</doi><tpages>8</tpages></addata></record> |
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| subjects | Abnormalities, Drug-Induced Analysis of Variance Animals Biological and medical sciences Body Weight - drug effects Bone and Bones - abnormalities Bone and Bones - drug effects Brain - drug effects Brain - pathology Cell Movement - drug effects Concanavalin A - toxicity Craniofacial Abnormalities - chemically induced Embryology: invertebrates and vertebrates. Teratology Embryonic and Fetal Development - drug effects Female Fundamental and applied biological sciences. Psychology Gestational Age Heart Defects, Congenital - chemically induced Male Neural Crest - cytology Neural Crest - drug effects Pregnancy Rats Rats, Sprague-Dawley Teratology. Teratogens |
| title | Developmental toxicity of concanavalin a in rats: Association with restricted migration of neural crest cells |
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