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Tissue specificity of aryl hydrocarbon receptor (AhR) mediated responses and relative sensitivity of white sturgeon (Acipenser transmontanus) to an AhR agonist

Identifieur interne : 000050 ( PascalFrancis/Checkpoint ); précédent : 000049; suivant : 000051

Tissue specificity of aryl hydrocarbon receptor (AhR) mediated responses and relative sensitivity of white sturgeon (Acipenser transmontanus) to an AhR agonist

Auteurs : Jona. Doering [Canada] ; Steve Wiseman [Canada] ; Shawnc. Beitel [Canada] ; Brett J. Tendler [Canada] ; John P. Giesy [Canada, États-Unis, Hong Kong, République populaire de Chine] ; Markus Hecker [Canada]

Source :

RBID : Pascal:12-0200578

Descripteurs français

English descriptors

Abstract

Sturgeons are endangered in some parts of the world. Due to their benthic nature and longevity sturgeon are at greater risk of exposure to bioaccumulative contaminants such as dioxin-like compounds that are associated with sediments. Despite their endangered status, little research has been conducted to characterize the relative responsiveness of sturgeon to dioxin-like compounds. In an attempt to study the biological effects and possible associated risks of exposure to dioxin-like compounds in sturgeon, the molecular and biochemical responses of white sturgeon (Acipenser transmontanus) to a model aryl hydrocarbon receptor (AhR) agonist, β-naphthoflavone (βNF) were investigated. White sturgeon were injected intraperitoneally with one of three doses of βNF (0, 50, or 500 mg/kg, bw). Rainbow trout (Oncorhynchus mykiss) were used as a reference species since their responses have been well characterized in the past. Three days following injection with βNF, fish were euthanized and livers, gills, and intestines collected for biochemical and molecular analyses. White sturgeon exposed to βNF had significantly greater ethoxyresorufin O-deethylase (EROD) activity in liver (up to 37-fold), gill (up to 41-fold), and intestine (up to 36-fold) than did unexposed controls. Rainbow trout injected with βNF exhibited EROD activity that was significantly greater in liver (88-fold), than that of controls, but was undetectable in gills or intestine. Abundance of CYP1A transcript displayed a comparable pattern of tissue-specific induction with intestine (up to 189-fold), gills (up to 53-fold), and liver (up to 21-fold). Methoxyresorufin O-deethylase (MROD) and pentoxyresorufin O-deethylase (PROD) activities were undetectable in unexposed white sturgeon tissues while exposed tissues displayed MROD activity that was only moderately greater than the activity that could be detected. Differential inducibility among liver, gill, and intestine following exposure to an AhR agonist is likely associated with tissue-specific regulation of the AhR signalling pathway. Liver and gill of white sturgeon had significantly greater AhR transcript abundance than did the intestine, however following exposure to βNF, significantly greater induction in AhR transcript abundance was detected in intestine (up to 35-fold) compared to liver (up to 5-fold) or gills (up to 11-fold). It was shown that white sturgeon are responsive to AhR agonists in the liver, gill, and intestine and could be among the more sensitive fish species with regard to inducibility of CYP1A.


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Pascal:12-0200578

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<term>Cytochrome P450</term>
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<div type="abstract" xml:lang="en">Sturgeons are endangered in some parts of the world. Due to their benthic nature and longevity sturgeon are at greater risk of exposure to bioaccumulative contaminants such as dioxin-like compounds that are associated with sediments. Despite their endangered status, little research has been conducted to characterize the relative responsiveness of sturgeon to dioxin-like compounds. In an attempt to study the biological effects and possible associated risks of exposure to dioxin-like compounds in sturgeon, the molecular and biochemical responses of white sturgeon (Acipenser transmontanus) to a model aryl hydrocarbon receptor (AhR) agonist, β-naphthoflavone (βNF) were investigated. White sturgeon were injected intraperitoneally with one of three doses of βNF (0, 50, or 500 mg/kg, bw). Rainbow trout (Oncorhynchus mykiss) were used as a reference species since their responses have been well characterized in the past. Three days following injection with βNF, fish were euthanized and livers, gills, and intestines collected for biochemical and molecular analyses. White sturgeon exposed to βNF had significantly greater ethoxyresorufin O-deethylase (EROD) activity in liver (up to 37-fold), gill (up to 41-fold), and intestine (up to 36-fold) than did unexposed controls. Rainbow trout injected with βNF exhibited EROD activity that was significantly greater in liver (88-fold), than that of controls, but was undetectable in gills or intestine. Abundance of CYP1A transcript displayed a comparable pattern of tissue-specific induction with intestine (up to 189-fold), gills (up to 53-fold), and liver (up to 21-fold). Methoxyresorufin O-deethylase (MROD) and pentoxyresorufin O-deethylase (PROD) activities were undetectable in unexposed white sturgeon tissues while exposed tissues displayed MROD activity that was only moderately greater than the activity that could be detected. Differential inducibility among liver, gill, and intestine following exposure to an AhR agonist is likely associated with tissue-specific regulation of the AhR signalling pathway. Liver and gill of white sturgeon had significantly greater AhR transcript abundance than did the intestine, however following exposure to βNF, significantly greater induction in AhR transcript abundance was detected in intestine (up to 35-fold) compared to liver (up to 5-fold) or gills (up to 11-fold). It was shown that white sturgeon are responsive to AhR agonists in the liver, gill, and intestine and could be among the more sensitive fish species with regard to inducibility of CYP1A.</div>
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</fA14>
<fA14 i1="03">
<s1>Department of Zoology, Centre for Integrative Toxicology, Michigan State University</s1>
<s2>East Lansing, Mf 48824</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="04">
<s1>Department of Biology and Chemistry, City University of Hong Kong</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="05">
<s1>School of Biological Sciences, The University of Hong Kong</s1>
<s3>HKG</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06">
<s1>State Key Laboratory of Pollution Control and Resource Reuse and School of the Environment, Nanjing University</s1>
<s2>Nanjing</s2>
<s3>CHN</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="07">
<s1>School of the Environment and Sustainability, University of Saskatchewan</s1>
<s2>Saskatoon, SK</s2>
<s3>CAN</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20>
<s1>125-133</s1>
</fA20>
<fA21>
<s1>2012</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>18841</s2>
<s5>354000506905600150</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>3/4 p.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>12-0200578</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Aquatic toxicology</s0>
</fA64>
<fA66 i1="01">
<s0>NLD</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>Sturgeons are endangered in some parts of the world. Due to their benthic nature and longevity sturgeon are at greater risk of exposure to bioaccumulative contaminants such as dioxin-like compounds that are associated with sediments. Despite their endangered status, little research has been conducted to characterize the relative responsiveness of sturgeon to dioxin-like compounds. In an attempt to study the biological effects and possible associated risks of exposure to dioxin-like compounds in sturgeon, the molecular and biochemical responses of white sturgeon (Acipenser transmontanus) to a model aryl hydrocarbon receptor (AhR) agonist, β-naphthoflavone (βNF) were investigated. White sturgeon were injected intraperitoneally with one of three doses of βNF (0, 50, or 500 mg/kg, bw). Rainbow trout (Oncorhynchus mykiss) were used as a reference species since their responses have been well characterized in the past. Three days following injection with βNF, fish were euthanized and livers, gills, and intestines collected for biochemical and molecular analyses. White sturgeon exposed to βNF had significantly greater ethoxyresorufin O-deethylase (EROD) activity in liver (up to 37-fold), gill (up to 41-fold), and intestine (up to 36-fold) than did unexposed controls. Rainbow trout injected with βNF exhibited EROD activity that was significantly greater in liver (88-fold), than that of controls, but was undetectable in gills or intestine. Abundance of CYP1A transcript displayed a comparable pattern of tissue-specific induction with intestine (up to 189-fold), gills (up to 53-fold), and liver (up to 21-fold). Methoxyresorufin O-deethylase (MROD) and pentoxyresorufin O-deethylase (PROD) activities were undetectable in unexposed white sturgeon tissues while exposed tissues displayed MROD activity that was only moderately greater than the activity that could be detected. Differential inducibility among liver, gill, and intestine following exposure to an AhR agonist is likely associated with tissue-specific regulation of the AhR signalling pathway. Liver and gill of white sturgeon had significantly greater AhR transcript abundance than did the intestine, however following exposure to βNF, significantly greater induction in AhR transcript abundance was detected in intestine (up to 35-fold) compared to liver (up to 5-fold) or gills (up to 11-fold). It was shown that white sturgeon are responsive to AhR agonists in the liver, gill, and intestine and could be among the more sensitive fish species with regard to inducibility of CYP1A.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002A14D05A</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002A15B</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Spécificité tissu</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Tissue specificity</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Especificidad tejido</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Récepteur Ah</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Ah receptor</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Receptor Ah</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Agoniste</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Agonist</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Agonista</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Enzyme</s0>
<s2>FE</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Enzyme</s0>
<s2>FE</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Enzima</s0>
<s2>FE</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Milieu aquatique</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Aquatic environment</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Medio acuático</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Ecotoxicologie</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Ecotoxicology</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Ecotoxicología</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Toxicité</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Toxicity</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Toxicidad</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Marqueur biologique</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Biological marker</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Marcador biológico</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Cytochrome P450</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Cytochrome P450</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Citocromo P450</s0>
<s5>23</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Polluant organique persistant</s0>
<s5>24</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Persistent organic pollutant</s0>
<s5>24</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Contaminante organico persistente</s0>
<s5>24</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Dibenzo-p-dioxine(2,3,7,8-tétrachloro)</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>41</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE">
<s0>Dérivé de la dioxine</s0>
<s2>FR</s2>
<s5>42</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Dioxin derivatives</s0>
<s2>FR</s2>
<s5>42</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Acipenser transmontanus</s0>
<s2>NS</s2>
<s5>49</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Acipenser transmontanus</s0>
<s2>NS</s2>
<s5>49</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Acipenser transmontanus</s0>
<s2>NS</s2>
<s5>49</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE">
<s0>Oncorhynchus mykiss</s0>
<s2>NS</s2>
<s5>50</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Oncorhynchus mykiss</s0>
<s2>NS</s2>
<s5>50</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Oncorhynchus mykiss</s0>
<s2>NS</s2>
<s5>50</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE">
<s0>Cytochrome CYP1A</s0>
<s4>INC</s4>
<s5>87</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Composé organique</s0>
<s2>NA</s2>
<s5>17</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Organic compounds</s0>
<s2>NA</s2>
<s5>17</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Compuesto orgánico</s0>
<s2>NA</s2>
<s5>17</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Pisces</s0>
<s2>NS</s2>
<s5>29</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Pisces</s0>
<s2>NS</s2>
<s5>29</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Pisces</s0>
<s2>NS</s2>
<s5>29</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Acipenseridae</s0>
<s4>INC</s4>
<s5>70</s5>
</fC07>
<fN21>
<s1>156</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations>
<list>
<country>
<li>Canada</li>
<li>Hong Kong</li>
<li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
<region>
<li>Michigan</li>
</region>
<settlement>
<li>East Lansing</li>
</settlement>
<orgName>
<li>Université d'État du Michigan</li>
</orgName>
</list>
<tree>
<country name="Canada">
<noRegion>
<name sortKey="Doering, Jona" sort="Doering, Jona" uniqKey="Doering J" first="Jona." last="Doering">Jona. Doering</name>
</noRegion>
<name sortKey="Beitel, Shawnc" sort="Beitel, Shawnc" uniqKey="Beitel S" first="Shawnc." last="Beitel">Shawnc. Beitel</name>
<name sortKey="Giesy, John P" sort="Giesy, John P" uniqKey="Giesy J" first="John P." last="Giesy">John P. Giesy</name>
<name sortKey="Giesy, John P" sort="Giesy, John P" uniqKey="Giesy J" first="John P." last="Giesy">John P. Giesy</name>
<name sortKey="Hecker, Markus" sort="Hecker, Markus" uniqKey="Hecker M" first="Markus" last="Hecker">Markus Hecker</name>
<name sortKey="Hecker, Markus" sort="Hecker, Markus" uniqKey="Hecker M" first="Markus" last="Hecker">Markus Hecker</name>
<name sortKey="Tendler, Brett J" sort="Tendler, Brett J" uniqKey="Tendler B" first="Brett J." last="Tendler">Brett J. Tendler</name>
<name sortKey="Wiseman, Steve" sort="Wiseman, Steve" uniqKey="Wiseman S" first="Steve" last="Wiseman">Steve Wiseman</name>
</country>
<country name="États-Unis">
<region name="Michigan">
<name sortKey="Giesy, John P" sort="Giesy, John P" uniqKey="Giesy J" first="John P." last="Giesy">John P. Giesy</name>
</region>
</country>
<country name="Hong Kong">
<noRegion>
<name sortKey="Giesy, John P" sort="Giesy, John P" uniqKey="Giesy J" first="John P." last="Giesy">John P. Giesy</name>
</noRegion>
<name sortKey="Giesy, John P" sort="Giesy, John P" uniqKey="Giesy J" first="John P." last="Giesy">John P. Giesy</name>
</country>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Giesy, John P" sort="Giesy, John P" uniqKey="Giesy J" first="John P." last="Giesy">John P. Giesy</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

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