The rodent nongenotoxic hepatocarcinogen and peroxisome proliferator nafenopin inhibits intercellular communication in rat but not guinea-pig hepatocytes, perturbing S-phase but ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-06

AUTHORS

Fiona J. Elcock, J. Kevin Chipman, Ruth A. Roberts

ABSTRACT

Previously, we have shown that the peroxisome proliferator (PP), nafenopin, induces S-phase in␣rat hepatocytes and suppresses apoptosis in hepatocytes from both rat and guinea-pig. Here, we confirm and extend these findings by defining the time course of␣growth perturbation and by correlating this with species differences in loss of gap junctional intercellular communication (GJIC). GJIC is associated with nongenotoxic carcinogenesis, possibly reflecting a tumour suppresser role of the connexins. Fluorescence microscopy of Hoechst 33258-stained rat or guinea-pig hepatocyte monolayers showed 1% apoptosis during the first 8 h of culture, peaking to 2–2.5% at 20–24 h. Nafenopin suppressed apoptosis compared with controls in both rat and guinea-pig, measured at 20 h and 24 h onwards, respectively. The induction of S-phase in rat hepatocytes by nafenopin could be detected as early as 4 h after compound addition whereas S-phase was not altered by nafenopin in guinea-pig hepatocytes. Intercellular communication as measured by intercellular transfer of microinjected Lucifer Yellow CH was observed during the first 14 h of primary rat hepatocyte culture peaking at a maximum value of 88 ± 3.0% after 7 h. In hepatocyte cultures from guinea-pig, dye-coupling levels were maintained between 88 ± 3.0 and 93 ± 3.0% within 2–10 h of culture and by 12 h showed only a slight decrease to 72 ± 3.0%. In the rat, significant inhibition was observed at 4 h after administration of nafenopin since GJIC was reduced by 20 ± 5% compared with vehicle control. By contrast, in the presence of nafenopin, the level of dye-coupling between guinea-pig hepatocytes did not decrease but remained between 85 ± 5 and 93 ± 3.0%, similar to that observed in control guinea-pig cultures. The data obtained contribute to our understanding of the role of GJIC inhibition in the perturbation of cell survival and proliferation caused by nongenotoxic hepatocarcinogens. More... »

PAGES

439-444

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s002040050524

DOI

http://dx.doi.org/10.1007/s002040050524

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043565911

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9708883


Indexing Status Check whether this publication has been indexed by Scopus and Web Of Science using the SN Indexing Status Tool
Incoming Citations Browse incoming citations for this publication using opencitations.net

JSON-LD is the canonical representation for SciGraph data.

TIP: You can open this SciGraph record using an external JSON-LD service: JSON-LD Playground Google SDTT

[
  {
    "@context": "https://springernature.github.io/scigraph/jsonld/sgcontext.json", 
    "about": [
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/11", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Medical and Health Sciences", 
        "type": "DefinedTerm"
      }, 
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/1103", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Clinical Sciences", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Animals", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Apoptosis", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Carcinogens", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Cell Communication", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Gap Junctions", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Guinea Pigs", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Liver", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Male", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Nafenopin", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Rats", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Rats, Wistar", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "S Phase", 
        "type": "DefinedTerm"
      }
    ], 
    "author": [
      {
        "affiliation": {
          "alternateName": "School of Biochemistry, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK, GB", 
          "id": "http://www.grid.ac/institutes/grid.6572.6", 
          "name": [
            "School of Biochemistry, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK, GB"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Elcock", 
        "givenName": "Fiona J.", 
        "id": "sg:person.0673213377.87", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.0673213377.87"
        ], 
        "type": "Person"
      }, 
      {
        "affiliation": {
          "alternateName": "School of Biochemistry, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK, GB", 
          "id": "http://www.grid.ac/institutes/grid.6572.6", 
          "name": [
            "School of Biochemistry, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK, GB"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Chipman", 
        "givenName": "J. Kevin", 
        "id": "sg:person.01072542354.75", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01072542354.75"
        ], 
        "type": "Person"
      }, 
      {
        "affiliation": {
          "alternateName": "Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, SK10 4TJ, UK, GB", 
          "id": "http://www.grid.ac/institutes/grid.417815.e", 
          "name": [
            "Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, SK10 4TJ, UK, GB"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Roberts", 
        "givenName": "Ruth A.", 
        "id": "sg:person.01031115541.10", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01031115541.10"
        ], 
        "type": "Person"
      }
    ], 
    "datePublished": "1998-06", 
    "datePublishedReg": "1998-06-01", 
    "description": "Abstract Previously, we have shown that the peroxisome proliferator (PP), nafenopin, induces S-phase in\u2423rat hepatocytes and suppresses apoptosis in hepatocytes from both rat and guinea-pig. Here, we confirm and extend these findings by defining the time course of\u2423growth perturbation and by correlating this with species differences in loss of gap junctional intercellular communication (GJIC). GJIC is associated with nongenotoxic carcinogenesis, possibly reflecting a tumour suppresser role of the connexins. Fluorescence microscopy of Hoechst 33258-stained rat or guinea-pig hepatocyte monolayers showed 1% apoptosis during the first 8 h of culture, peaking to 2\u20132.5% at 20\u201324 h. Nafenopin suppressed apoptosis compared with controls in both rat and guinea-pig, measured at 20 h and 24 h onwards, respectively. The induction of S-phase in rat hepatocytes by nafenopin could be detected as early as 4 h after compound addition whereas S-phase was not altered by nafenopin in guinea-pig hepatocytes. Intercellular communication as measured by intercellular transfer of microinjected Lucifer Yellow CH was observed during the first 14 h of primary rat hepatocyte culture peaking at a maximum value of 88 \u00b1 3.0% after 7 h. In hepatocyte cultures from guinea-pig, dye-coupling levels were maintained between 88 \u00b1 3.0 and 93 \u00b1 3.0% within 2\u201310 h of culture and by 12 h showed only a slight decrease to 72 \u00b1 3.0%. In the rat, significant inhibition was observed at 4 h after administration of nafenopin since GJIC was reduced by 20 \u00b1 5% compared with vehicle control. By contrast, in the presence of nafenopin, the level of dye-coupling between guinea-pig hepatocytes did not decrease but remained between 85 \u00b1 5 and 93 \u00b1 3.0%, similar to that observed in control guinea-pig cultures. The data obtained contribute to our understanding of the role of GJIC inhibition in the perturbation of cell survival and proliferation caused by nongenotoxic hepatocarcinogens.", 
    "genre": "article", 
    "id": "sg:pub.10.1007/s002040050524", 
    "inLanguage": "en", 
    "isAccessibleForFree": false, 
    "isPartOf": [
      {
        "id": "sg:journal.1019669", 
        "issn": [
          "0340-5761", 
          "1432-0738"
        ], 
        "name": "Archives of Toxicology", 
        "publisher": "Springer Nature", 
        "type": "Periodical"
      }, 
      {
        "issueNumber": "7", 
        "type": "PublicationIssue"
      }, 
      {
        "type": "PublicationVolume", 
        "volumeNumber": "72"
      }
    ], 
    "keywords": [
      "gap junctional intercellular communication", 
      "guinea-pig hepatocytes", 
      "nongenotoxic hepatocarcinogens", 
      "peroxisome proliferator", 
      "administration of nafenopin", 
      "intercellular communication", 
      "guinea-pig", 
      "rodent nongenotoxic hepatocarcinogens", 
      "microinjected Lucifer Yellow CH", 
      "junctional intercellular communication", 
      "peroxisome proliferator nafenopin", 
      "hepatocyte cultures", 
      "GJIC inhibition", 
      "rat hepatocytes", 
      "rats", 
      "nongenotoxic carcinogenesis", 
      "significant inhibition", 
      "Lucifer Yellow CH", 
      "primary rat hepatocyte cultures", 
      "presence of nafenopin", 
      "rat hepatocyte cultures", 
      "nafenopin", 
      "vehicle control", 
      "time course", 
      "hepatocytes", 
      "apoptosis", 
      "cell survival", 
      "intercellular transfer", 
      "Yellow CH", 
      "hepatocarcinogens", 
      "species differences", 
      "inhibition", 
      "hepatocyte monolayers", 
      "slight decrease", 
      "administration", 
      "proliferator", 
      "carcinogenesis", 
      "survival", 
      "culture", 
      "levels", 
      "control", 
      "proliferation", 
      "role", 
      "induction", 
      "fluorescence microscopy", 
      "connexins", 
      "findings", 
      "growth perturbations", 
      "course", 
      "contributes", 
      "decrease", 
      "differences", 
      "contrast", 
      "loss", 
      "presence", 
      "compound addition", 
      "addition", 
      "data", 
      "phase", 
      "understanding", 
      "communication", 
      "Abstract", 
      "values", 
      "microscopy", 
      "monolayers", 
      "perturbations", 
      "transfer", 
      "CH", 
      "maximum value", 
      "tumour suppresser role", 
      "suppresser role", 
      "Hoechst 33258-stained rat", 
      "guinea-pig hepatocyte monolayers", 
      "dye-coupling levels", 
      "control guinea-pig cultures", 
      "guinea-pig cultures", 
      "proliferator nafenopin"
    ], 
    "name": "The rodent nongenotoxic hepatocarcinogen and peroxisome proliferator nafenopin inhibits intercellular communication in rat but not guinea-pig hepatocytes, perturbing S-phase but not apoptosis", 
    "pagination": "439-444", 
    "productId": [
      {
        "name": "dimensions_id", 
        "type": "PropertyValue", 
        "value": [
          "pub.1043565911"
        ]
      }, 
      {
        "name": "doi", 
        "type": "PropertyValue", 
        "value": [
          "10.1007/s002040050524"
        ]
      }, 
      {
        "name": "pubmed_id", 
        "type": "PropertyValue", 
        "value": [
          "9708883"
        ]
      }
    ], 
    "sameAs": [
      "https://doi.org/10.1007/s002040050524", 
      "https://app.dimensions.ai/details/publication/pub.1043565911"
    ], 
    "sdDataset": "articles", 
    "sdDatePublished": "2022-01-01T18:08", 
    "sdLicense": "https://scigraph.springernature.com/explorer/license/", 
    "sdPublisher": {
      "name": "Springer Nature - SN SciGraph project", 
      "type": "Organization"
    }, 
    "sdSource": "s3://com-springernature-scigraph/baseset/20220101/entities/gbq_results/article/article_284.jsonl", 
    "type": "ScholarlyArticle", 
    "url": "https://doi.org/10.1007/s002040050524"
  }
]
 

Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/pub.10.1007/s002040050524'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1007/s002040050524'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1007/s002040050524'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1007/s002040050524'


 

This table displays all metadata directly associated to this object as RDF triples.

204 TRIPLES      21 PREDICATES      116 URIs      108 LITERALS      19 BLANK NODES

Subject Predicate Object
1 sg:pub.10.1007/s002040050524 schema:about N0d005427b2624cd0aca4688ce63aaa9f
2 N15db452d15974fa083b839b36a62d5d3
3 N30cbe242363e4534bf9439dc2e3f332d
4 N5e8de114d4164f5f96c8bc0feadc3f45
5 N71694588133b4fee98abbd0925f05cc5
6 N86f29d3d709a4ec091bac12c8a3663a4
7 N8ad5ea019a7b48acbf987e5ba788de92
8 N98dcd042abda4b92be25f2619debd0fd
9 N9fec45a8af8541a1b99e78434fce3eab
10 Nd6a392427cd74fe69dec3f51c045a2df
11 Ndf21392a2cf94a6d8e1aca82d6e1ad90
12 Nf1f4921281884cd588d6def19eb98242
13 anzsrc-for:11
14 anzsrc-for:1103
15 schema:author Nb1efbe8338764158ae48dd57fd898e09
16 schema:datePublished 1998-06
17 schema:datePublishedReg 1998-06-01
18 schema:description Abstract Previously, we have shown that the peroxisome proliferator (PP), nafenopin, induces S-phase in␣rat hepatocytes and suppresses apoptosis in hepatocytes from both rat and guinea-pig. Here, we confirm and extend these findings by defining the time course of␣growth perturbation and by correlating this with species differences in loss of gap junctional intercellular communication (GJIC). GJIC is associated with nongenotoxic carcinogenesis, possibly reflecting a tumour suppresser role of the connexins. Fluorescence microscopy of Hoechst 33258-stained rat or guinea-pig hepatocyte monolayers showed 1% apoptosis during the first 8 h of culture, peaking to 2–2.5% at 20–24 h. Nafenopin suppressed apoptosis compared with controls in both rat and guinea-pig, measured at 20 h and 24 h onwards, respectively. The induction of S-phase in rat hepatocytes by nafenopin could be detected as early as 4 h after compound addition whereas S-phase was not altered by nafenopin in guinea-pig hepatocytes. Intercellular communication as measured by intercellular transfer of microinjected Lucifer Yellow CH was observed during the first 14 h of primary rat hepatocyte culture peaking at a maximum value of 88 ± 3.0% after 7 h. In hepatocyte cultures from guinea-pig, dye-coupling levels were maintained between 88 ± 3.0 and 93 ± 3.0% within 2–10 h of culture and by 12 h showed only a slight decrease to 72 ± 3.0%. In the rat, significant inhibition was observed at 4 h after administration of nafenopin since GJIC was reduced by 20 ± 5% compared with vehicle control. By contrast, in the presence of nafenopin, the level of dye-coupling between guinea-pig hepatocytes did not decrease but remained between 85 ± 5 and 93 ± 3.0%, similar to that observed in control guinea-pig cultures. The data obtained contribute to our understanding of the role of GJIC inhibition in the perturbation of cell survival and proliferation caused by nongenotoxic hepatocarcinogens.
19 schema:genre article
20 schema:inLanguage en
21 schema:isAccessibleForFree false
22 schema:isPartOf N8a3bba240a9a465bb02860eba589a7ba
23 Nc96dc72817664e1f9755c8d0bc56d374
24 sg:journal.1019669
25 schema:keywords Abstract
26 CH
27 GJIC inhibition
28 Hoechst 33258-stained rat
29 Lucifer Yellow CH
30 Yellow CH
31 addition
32 administration
33 administration of nafenopin
34 apoptosis
35 carcinogenesis
36 cell survival
37 communication
38 compound addition
39 connexins
40 contrast
41 contributes
42 control
43 control guinea-pig cultures
44 course
45 culture
46 data
47 decrease
48 differences
49 dye-coupling levels
50 findings
51 fluorescence microscopy
52 gap junctional intercellular communication
53 growth perturbations
54 guinea-pig
55 guinea-pig cultures
56 guinea-pig hepatocyte monolayers
57 guinea-pig hepatocytes
58 hepatocarcinogens
59 hepatocyte cultures
60 hepatocyte monolayers
61 hepatocytes
62 induction
63 inhibition
64 intercellular communication
65 intercellular transfer
66 junctional intercellular communication
67 levels
68 loss
69 maximum value
70 microinjected Lucifer Yellow CH
71 microscopy
72 monolayers
73 nafenopin
74 nongenotoxic carcinogenesis
75 nongenotoxic hepatocarcinogens
76 peroxisome proliferator
77 peroxisome proliferator nafenopin
78 perturbations
79 phase
80 presence
81 presence of nafenopin
82 primary rat hepatocyte cultures
83 proliferation
84 proliferator
85 proliferator nafenopin
86 rat hepatocyte cultures
87 rat hepatocytes
88 rats
89 rodent nongenotoxic hepatocarcinogens
90 role
91 significant inhibition
92 slight decrease
93 species differences
94 suppresser role
95 survival
96 time course
97 transfer
98 tumour suppresser role
99 understanding
100 values
101 vehicle control
102 schema:name The rodent nongenotoxic hepatocarcinogen and peroxisome proliferator nafenopin inhibits intercellular communication in rat but not guinea-pig hepatocytes, perturbing S-phase but not apoptosis
103 schema:pagination 439-444
104 schema:productId Nb5ad02a36dce490cbbfbf516bec92cf9
105 Nc6a5bd638ab8427f80f2486e3079cde9
106 Nfb33368431f7417d9fd7184c78892584
107 schema:sameAs https://app.dimensions.ai/details/publication/pub.1043565911
108 https://doi.org/10.1007/s002040050524
109 schema:sdDatePublished 2022-01-01T18:08
110 schema:sdLicense https://scigraph.springernature.com/explorer/license/
111 schema:sdPublisher Nb63ac2584c9b4736835bc0251b2a208a
112 schema:url https://doi.org/10.1007/s002040050524
113 sgo:license sg:explorer/license/
114 sgo:sdDataset articles
115 rdf:type schema:ScholarlyArticle
116 N01c5fd0ccd6641d6af4f9f8234acf16f rdf:first sg:person.01072542354.75
117 rdf:rest Nda3baac3abce46dbbf02958c7ef85dd4
118 N0d005427b2624cd0aca4688ce63aaa9f schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
119 schema:name Rats
120 rdf:type schema:DefinedTerm
121 N15db452d15974fa083b839b36a62d5d3 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
122 schema:name Rats, Wistar
123 rdf:type schema:DefinedTerm
124 N30cbe242363e4534bf9439dc2e3f332d schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
125 schema:name Male
126 rdf:type schema:DefinedTerm
127 N5e8de114d4164f5f96c8bc0feadc3f45 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
128 schema:name Guinea Pigs
129 rdf:type schema:DefinedTerm
130 N71694588133b4fee98abbd0925f05cc5 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
131 schema:name S Phase
132 rdf:type schema:DefinedTerm
133 N86f29d3d709a4ec091bac12c8a3663a4 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
134 schema:name Cell Communication
135 rdf:type schema:DefinedTerm
136 N8a3bba240a9a465bb02860eba589a7ba schema:issueNumber 7
137 rdf:type schema:PublicationIssue
138 N8ad5ea019a7b48acbf987e5ba788de92 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
139 schema:name Nafenopin
140 rdf:type schema:DefinedTerm
141 N98dcd042abda4b92be25f2619debd0fd schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
142 schema:name Gap Junctions
143 rdf:type schema:DefinedTerm
144 N9fec45a8af8541a1b99e78434fce3eab schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
145 schema:name Apoptosis
146 rdf:type schema:DefinedTerm
147 Nb1efbe8338764158ae48dd57fd898e09 rdf:first sg:person.0673213377.87
148 rdf:rest N01c5fd0ccd6641d6af4f9f8234acf16f
149 Nb5ad02a36dce490cbbfbf516bec92cf9 schema:name pubmed_id
150 schema:value 9708883
151 rdf:type schema:PropertyValue
152 Nb63ac2584c9b4736835bc0251b2a208a schema:name Springer Nature - SN SciGraph project
153 rdf:type schema:Organization
154 Nc6a5bd638ab8427f80f2486e3079cde9 schema:name dimensions_id
155 schema:value pub.1043565911
156 rdf:type schema:PropertyValue
157 Nc96dc72817664e1f9755c8d0bc56d374 schema:volumeNumber 72
158 rdf:type schema:PublicationVolume
159 Nd6a392427cd74fe69dec3f51c045a2df schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
160 schema:name Carcinogens
161 rdf:type schema:DefinedTerm
162 Nda3baac3abce46dbbf02958c7ef85dd4 rdf:first sg:person.01031115541.10
163 rdf:rest rdf:nil
164 Ndf21392a2cf94a6d8e1aca82d6e1ad90 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
165 schema:name Liver
166 rdf:type schema:DefinedTerm
167 Nf1f4921281884cd588d6def19eb98242 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
168 schema:name Animals
169 rdf:type schema:DefinedTerm
170 Nfb33368431f7417d9fd7184c78892584 schema:name doi
171 schema:value 10.1007/s002040050524
172 rdf:type schema:PropertyValue
173 anzsrc-for:11 schema:inDefinedTermSet anzsrc-for:
174 schema:name Medical and Health Sciences
175 rdf:type schema:DefinedTerm
176 anzsrc-for:1103 schema:inDefinedTermSet anzsrc-for:
177 schema:name Clinical Sciences
178 rdf:type schema:DefinedTerm
179 sg:journal.1019669 schema:issn 0340-5761
180 1432-0738
181 schema:name Archives of Toxicology
182 schema:publisher Springer Nature
183 rdf:type schema:Periodical
184 sg:person.01031115541.10 schema:affiliation grid-institutes:grid.417815.e
185 schema:familyName Roberts
186 schema:givenName Ruth A.
187 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01031115541.10
188 rdf:type schema:Person
189 sg:person.01072542354.75 schema:affiliation grid-institutes:grid.6572.6
190 schema:familyName Chipman
191 schema:givenName J. Kevin
192 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01072542354.75
193 rdf:type schema:Person
194 sg:person.0673213377.87 schema:affiliation grid-institutes:grid.6572.6
195 schema:familyName Elcock
196 schema:givenName Fiona J.
197 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.0673213377.87
198 rdf:type schema:Person
199 grid-institutes:grid.417815.e schema:alternateName Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, SK10 4TJ, UK, GB
200 schema:name Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, SK10 4TJ, UK, GB
201 rdf:type schema:Organization
202 grid-institutes:grid.6572.6 schema:alternateName School of Biochemistry, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK, GB
203 schema:name School of Biochemistry, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK, GB
204 rdf:type schema:Organization
 




Preview window. Press ESC to close (or click here)


...