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Ameliorative Effects of Selenium on Cadmium-Induced Injury in the Chicken Ovary: Mechanisms of Oxidative Stress and Endoplasmic Reticulum Stress in Cadmium-Induced Apoptosis
Despite the well-established toxicity of cadmium (Cd) to animals and the ameliorative effects of selenium (Se), some specific mechanisms in the chicken ovary are not yet clarified. To explore the mechanism by which the toxicity effect of Cd is induced and explore the effect of supranutritional Se on...
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Published in: | Biological trace element research 2018-08, Vol.184 (2), p.463-473 |
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description | Despite the well-established toxicity of cadmium (Cd) to animals and the ameliorative effects of selenium (Se), some specific mechanisms in the chicken ovary are not yet clarified. To explore the mechanism by which the toxicity effect of Cd is induced and explore the effect of supranutritional Se on Cd toxicity in female bird reproduction, forty-eight 50-day-old Isa Brown female chickens were divided randomly into four groups. Group I (control group) was fed the basic diet containing 0.2 mg/kg Se. Group II (Se-treated group) was fed the basic diet supplemented with sodium selenite (Na
2
SeO
3
), and the total Se content was 2 mg/kg. Group III (Se + Cd-treated group) was fed the basic diet supplemented with Na
2
SeO
3
; the total Se content was 2 mg/kg, and it was supplemented with 150 mg/kg cadmium chloride (CdCl
2
). Group IV (Cd-treated group) was with the basic diet supplemented with 150 mg/kg CdCl
2
. The Cd, estradiol (E2), and progestogen (P4) contents changed after subchronic Cd exposure in chicken ovarian tissue; subsequently, oxidative stress occurred and activated the endoplasmic reticulum (ER) pathway to induce apoptosis. Further, Se decreased the accumulation of Cd in ovarian tissue, increased the E2 and P4 contents, alleviated oxidative stress, and reduced apoptosis via the ER stress pathway. The present results demonstrated that Cd could induce apoptosis via the ER stress pathway in chicken ovarian tissue and that Se had a significant antagonistic effect. These results are potentially valuable for finding a strategy to prevent Cd poisoning. |
doi_str_mv | 10.1007/s12011-017-1193-x |
format | article |
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2
SeO
3
), and the total Se content was 2 mg/kg. Group III (Se + Cd-treated group) was fed the basic diet supplemented with Na
2
SeO
3
; the total Se content was 2 mg/kg, and it was supplemented with 150 mg/kg cadmium chloride (CdCl
2
). Group IV (Cd-treated group) was with the basic diet supplemented with 150 mg/kg CdCl
2
. The Cd, estradiol (E2), and progestogen (P4) contents changed after subchronic Cd exposure in chicken ovarian tissue; subsequently, oxidative stress occurred and activated the endoplasmic reticulum (ER) pathway to induce apoptosis. Further, Se decreased the accumulation of Cd in ovarian tissue, increased the E2 and P4 contents, alleviated oxidative stress, and reduced apoptosis via the ER stress pathway. The present results demonstrated that Cd could induce apoptosis via the ER stress pathway in chicken ovarian tissue and that Se had a significant antagonistic effect. These results are potentially valuable for finding a strategy to prevent Cd poisoning.</description><identifier>ISSN: 0163-4984</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-017-1193-x</identifier><identifier>PMID: 29090375</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>17β-Estradiol ; Activating Transcription Factor 4 - genetics ; Activating Transcription Factor 4 - metabolism ; Animal tissues ; Animals ; Apoptosis ; Apoptosis - drug effects ; Basic diets ; Biochemistry ; Biomedical and Life Sciences ; Biotechnology ; Cadmium ; Cadmium - administration & dosage ; Cadmium - toxicity ; Cadmium chloride ; Chickens ; Diet ; Dietary Supplements ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - drug effects ; Estrogen receptors ; Female ; Females ; Gene Expression - drug effects ; Life Sciences ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Nutrition ; Oncology ; Organ Size - drug effects ; Ovaries ; Ovary - drug effects ; Ovary - metabolism ; Ovary - pathology ; Oxidative stress ; Oxidative Stress - drug effects ; Poultry ; Random Allocation ; Selenium ; Selenium - administration & dosage ; Selenium - pharmacology ; Sex hormones ; Sodium ; Sodium selenite ; Tissue ; Toxicity</subject><ispartof>Biological trace element research, 2018-08, Vol.184 (2), p.463-473</ispartof><rights>Springer Science+Business Media, LLC 2017</rights><rights>Biological Trace Element Research is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-aa0c3853763545d69b54f96abec75a9c0126a0af519f0631f3c68b445ec3303a3</citedby><cites>FETCH-LOGICAL-c438t-aa0c3853763545d69b54f96abec75a9c0126a0af519f0631f3c68b445ec3303a3</cites><orcidid>0000-0003-0183-5459</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29090375$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wan, Na</creatorcontrib><creatorcontrib>Xu, Zhe</creatorcontrib><creatorcontrib>Liu, Tianqi</creatorcontrib><creatorcontrib>Min, Yahong</creatorcontrib><creatorcontrib>Li, Shu</creatorcontrib><title>Ameliorative Effects of Selenium on Cadmium-Induced Injury in the Chicken Ovary: Mechanisms of Oxidative Stress and Endoplasmic Reticulum Stress in Cadmium-Induced Apoptosis</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>Despite the well-established toxicity of cadmium (Cd) to animals and the ameliorative effects of selenium (Se), some specific mechanisms in the chicken ovary are not yet clarified. To explore the mechanism by which the toxicity effect of Cd is induced and explore the effect of supranutritional Se on Cd toxicity in female bird reproduction, forty-eight 50-day-old Isa Brown female chickens were divided randomly into four groups. Group I (control group) was fed the basic diet containing 0.2 mg/kg Se. Group II (Se-treated group) was fed the basic diet supplemented with sodium selenite (Na
2
SeO
3
), and the total Se content was 2 mg/kg. Group III (Se + Cd-treated group) was fed the basic diet supplemented with Na
2
SeO
3
; the total Se content was 2 mg/kg, and it was supplemented with 150 mg/kg cadmium chloride (CdCl
2
). Group IV (Cd-treated group) was with the basic diet supplemented with 150 mg/kg CdCl
2
. The Cd, estradiol (E2), and progestogen (P4) contents changed after subchronic Cd exposure in chicken ovarian tissue; subsequently, oxidative stress occurred and activated the endoplasmic reticulum (ER) pathway to induce apoptosis. Further, Se decreased the accumulation of Cd in ovarian tissue, increased the E2 and P4 contents, alleviated oxidative stress, and reduced apoptosis via the ER stress pathway. The present results demonstrated that Cd could induce apoptosis via the ER stress pathway in chicken ovarian tissue and that Se had a significant antagonistic effect. These results are potentially valuable for finding a strategy to prevent Cd poisoning.</description><subject>17β-Estradiol</subject><subject>Activating Transcription Factor 4 - genetics</subject><subject>Activating Transcription Factor 4 - metabolism</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Basic diets</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>Cadmium</subject><subject>Cadmium - administration & dosage</subject><subject>Cadmium - toxicity</subject><subject>Cadmium chloride</subject><subject>Chickens</subject><subject>Diet</subject><subject>Dietary Supplements</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Estrogen receptors</subject><subject>Female</subject><subject>Females</subject><subject>Gene Expression - drug effects</subject><subject>Life Sciences</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nutrition</subject><subject>Oncology</subject><subject>Organ Size - drug effects</subject><subject>Ovaries</subject><subject>Ovary - drug effects</subject><subject>Ovary - metabolism</subject><subject>Ovary - pathology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Poultry</subject><subject>Random Allocation</subject><subject>Selenium</subject><subject>Selenium - administration & dosage</subject><subject>Selenium - pharmacology</subject><subject>Sex hormones</subject><subject>Sodium</subject><subject>Sodium selenite</subject><subject>Tissue</subject><subject>Toxicity</subject><issn>0163-4984</issn><issn>1559-0720</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kdGOEyEUhonRuHX1AbwxJF7jHoaBKd41TVebrGni6jWhDFjqDIwws-k-lO8ou1P1wnjFSfjO9yfnR-g1hXcUoLnKtAJKCdCGUCoZOT1BC8q5JNBU8BQtgApGarmsL9CLnI9QwEqy5-iikiCBNXyBfq562_mY9OjvLN44Z82YcXT41nY2-KnHMeC1bvsykm1oJ2NbvA3HKd1jH_B4sHh98Oa7DXh3p9P9e_zJmoMOPvePmt3Jt7P7dkw2Z6xDizehjUOnc-8N_mxHb6auBJ0B_2_eaojDGLPPL9Ezp7tsX53fS_T1evNl_ZHc7D5s16sbYmq2HInWYNiSs0YwXvNWyD2vnRR6b03DtTRAK6FBO06lA8GoY0Ys93XNrWEMmGaX6O3sHVL8Mdk8qmOcUiiRqgLBK8F5zQpFZ8qkmHOyTg3J9-UIioJ6KEjNBalyd_VQkDqVnTdn87Tvbftn43cjBahmIJev8M2mv9H_t_4CYIaeHw</recordid><startdate>20180801</startdate><enddate>20180801</enddate><creator>Wan, Na</creator><creator>Xu, Zhe</creator><creator>Liu, Tianqi</creator><creator>Min, Yahong</creator><creator>Li, Shu</creator><general>Springer US</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7QH</scope><scope>7QP</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>F1W</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H97</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>L.G</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0003-0183-5459</orcidid></search><sort><creationdate>20180801</creationdate><title>Ameliorative Effects of Selenium on Cadmium-Induced Injury in the Chicken Ovary: Mechanisms of Oxidative Stress and Endoplasmic Reticulum Stress in Cadmium-Induced Apoptosis</title><author>Wan, Na ; Xu, Zhe ; Liu, Tianqi ; Min, Yahong ; Li, Shu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-aa0c3853763545d69b54f96abec75a9c0126a0af519f0631f3c68b445ec3303a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>17β-Estradiol</topic><topic>Activating Transcription Factor 4 - genetics</topic><topic>Activating Transcription Factor 4 - metabolism</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Basic diets</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biotechnology</topic><topic>Cadmium</topic><topic>Cadmium - administration & dosage</topic><topic>Cadmium - toxicity</topic><topic>Cadmium chloride</topic><topic>Chickens</topic><topic>Diet</topic><topic>Dietary Supplements</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Estrogen receptors</topic><topic>Female</topic><topic>Females</topic><topic>Gene Expression - drug effects</topic><topic>Life Sciences</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nutrition</topic><topic>Oncology</topic><topic>Organ Size - drug effects</topic><topic>Ovaries</topic><topic>Ovary - drug effects</topic><topic>Ovary - metabolism</topic><topic>Ovary - pathology</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Poultry</topic><topic>Random Allocation</topic><topic>Selenium</topic><topic>Selenium - administration & dosage</topic><topic>Selenium - pharmacology</topic><topic>Sex hormones</topic><topic>Sodium</topic><topic>Sodium selenite</topic><topic>Tissue</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wan, Na</creatorcontrib><creatorcontrib>Xu, Zhe</creatorcontrib><creatorcontrib>Liu, Tianqi</creatorcontrib><creatorcontrib>Min, Yahong</creatorcontrib><creatorcontrib>Li, Shu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Aqualine</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest Biological Science Journals</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><jtitle>Biological trace element research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wan, Na</au><au>Xu, Zhe</au><au>Liu, Tianqi</au><au>Min, Yahong</au><au>Li, Shu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ameliorative Effects of Selenium on Cadmium-Induced Injury in the Chicken Ovary: Mechanisms of Oxidative Stress and Endoplasmic Reticulum Stress in Cadmium-Induced Apoptosis</atitle><jtitle>Biological trace element research</jtitle><stitle>Biol Trace Elem Res</stitle><addtitle>Biol Trace Elem Res</addtitle><date>2018-08-01</date><risdate>2018</risdate><volume>184</volume><issue>2</issue><spage>463</spage><epage>473</epage><pages>463-473</pages><issn>0163-4984</issn><eissn>1559-0720</eissn><abstract>Despite the well-established toxicity of cadmium (Cd) to animals and the ameliorative effects of selenium (Se), some specific mechanisms in the chicken ovary are not yet clarified. To explore the mechanism by which the toxicity effect of Cd is induced and explore the effect of supranutritional Se on Cd toxicity in female bird reproduction, forty-eight 50-day-old Isa Brown female chickens were divided randomly into four groups. Group I (control group) was fed the basic diet containing 0.2 mg/kg Se. Group II (Se-treated group) was fed the basic diet supplemented with sodium selenite (Na
2
SeO
3
), and the total Se content was 2 mg/kg. Group III (Se + Cd-treated group) was fed the basic diet supplemented with Na
2
SeO
3
; the total Se content was 2 mg/kg, and it was supplemented with 150 mg/kg cadmium chloride (CdCl
2
). Group IV (Cd-treated group) was with the basic diet supplemented with 150 mg/kg CdCl
2
. The Cd, estradiol (E2), and progestogen (P4) contents changed after subchronic Cd exposure in chicken ovarian tissue; subsequently, oxidative stress occurred and activated the endoplasmic reticulum (ER) pathway to induce apoptosis. Further, Se decreased the accumulation of Cd in ovarian tissue, increased the E2 and P4 contents, alleviated oxidative stress, and reduced apoptosis via the ER stress pathway. The present results demonstrated that Cd could induce apoptosis via the ER stress pathway in chicken ovarian tissue and that Se had a significant antagonistic effect. These results are potentially valuable for finding a strategy to prevent Cd poisoning.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29090375</pmid><doi>10.1007/s12011-017-1193-x</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-0183-5459</orcidid></addata></record> |
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subjects | 17β-Estradiol Activating Transcription Factor 4 - genetics Activating Transcription Factor 4 - metabolism Animal tissues Animals Apoptosis Apoptosis - drug effects Basic diets Biochemistry Biomedical and Life Sciences Biotechnology Cadmium Cadmium - administration & dosage Cadmium - toxicity Cadmium chloride Chickens Diet Dietary Supplements Endoplasmic reticulum Endoplasmic Reticulum Stress - drug effects Estrogen receptors Female Females Gene Expression - drug effects Life Sciences Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Nutrition Oncology Organ Size - drug effects Ovaries Ovary - drug effects Ovary - metabolism Ovary - pathology Oxidative stress Oxidative Stress - drug effects Poultry Random Allocation Selenium Selenium - administration & dosage Selenium - pharmacology Sex hormones Sodium Sodium selenite Tissue Toxicity |
title | Ameliorative Effects of Selenium on Cadmium-Induced Injury in the Chicken Ovary: Mechanisms of Oxidative Stress and Endoplasmic Reticulum Stress in Cadmium-Induced Apoptosis |
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