Iodoacetic acid affects estrous cyclicity, ovarian gene expression, and hormone levels in mice
Iodoacetic acid (IAA) is a water disinfection byproduct that is an ovarian toxicant in vitro. However, information on the effects of IAA on ovarian function in vivo was limited. Thus, we determined whether IAA exposure affects estrous cyclicity, steroidogenesis, and ovarian gene expression in mice....
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| Veröffentlicht in: | Biology of reproduction 2021-10, Vol.105 (4), p.1030-1042 |
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| creator | Gonsioroski, Andressa Meling, Daryl D Gao, Liying Plewa, Michael J Flaws, Jodi A |
| description | Iodoacetic acid (IAA) is a water disinfection byproduct that is an ovarian toxicant in vitro. However, information on the effects of IAA on ovarian function in vivo was limited. Thus, we determined whether IAA exposure affects estrous cyclicity, steroidogenesis, and ovarian gene expression in mice. Adult CD-1 mice were dosed with water or IAA (0.5–500 mg/L) in the drinking water for 35–40 days during which estrous cyclicity was monitored for 14 days. Ovaries were analyzed for expression of apoptotic factors, cell cycle regulators, steroidogenic factors, estrogen receptors, oxidative stress markers, and a proliferation marker. Sera were collected to measure pregnenolone, androstenedione, testosterone, estradiol, inhibin B, and follicle-stimulating hormone (FSH) levels. IAA exposure decreased the time that the mice spent in proestrus compared to control. IAA exposure decreased expression of the proapoptotic factor Bok and the cell cycle regulator Ccnd2 compared to control. IAA exposure increased expression of the proapoptotic factors Bax and Aimf1, the antiapoptotic factor Bcl2l10, the cell cycle regulators Ccna2, Ccnb1, Ccne1, and Cdk4, and estrogen receptor Esr1 compared to control. IAA exposure decreased expression of Sod1 and increased expression of Cat, Gpx and Nrf2. IAA exposure did not affect expression of Star, Cyp11a1, Cyp17a1, Hsd17b1, Hsd3b1, Esr2, or Ki67 compared to control. IAA exposure decreased estradiol levels, but did not alter other hormone levels compared to control. In conclusion, IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Summary sentence IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Graphical Abstract |
| doi_str_mv | 10.1093/biolre/ioab108 |
| format | Article |
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However, information on the effects of IAA on ovarian function in vivo was limited. Thus, we determined whether IAA exposure affects estrous cyclicity, steroidogenesis, and ovarian gene expression in mice. Adult CD-1 mice were dosed with water or IAA (0.5–500 mg/L) in the drinking water for 35–40 days during which estrous cyclicity was monitored for 14 days. Ovaries were analyzed for expression of apoptotic factors, cell cycle regulators, steroidogenic factors, estrogen receptors, oxidative stress markers, and a proliferation marker. Sera were collected to measure pregnenolone, androstenedione, testosterone, estradiol, inhibin B, and follicle-stimulating hormone (FSH) levels. IAA exposure decreased the time that the mice spent in proestrus compared to control. IAA exposure decreased expression of the proapoptotic factor Bok and the cell cycle regulator Ccnd2 compared to control. IAA exposure increased expression of the proapoptotic factors Bax and Aimf1, the antiapoptotic factor Bcl2l10, the cell cycle regulators Ccna2, Ccnb1, Ccne1, and Cdk4, and estrogen receptor Esr1 compared to control. IAA exposure decreased expression of Sod1 and increased expression of Cat, Gpx and Nrf2. IAA exposure did not affect expression of Star, Cyp11a1, Cyp17a1, Hsd17b1, Hsd3b1, Esr2, or Ki67 compared to control. IAA exposure decreased estradiol levels, but did not alter other hormone levels compared to control. In conclusion, IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Summary sentence IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Graphical Abstract</description><identifier>ISSN: 0006-3363</identifier><identifier>EISSN: 1529-7268</identifier><identifier>DOI: 10.1093/biolre/ioab108</identifier><identifier>PMID: 34086879</identifier><language>eng</language><publisher>United States: Society for the Study of Reproduction</publisher><subject>17β-Estradiol ; Analysis ; Androstenedione ; Animals ; Apoptosis ; Cell cycle ; Cytochrome P-450 ; Disinfection ; disinfection byproducts ; Drinking water ; Enzyme Inhibitors - pharmacology ; Estradiol ; Estrogen receptors ; Estrogens ; estrous cycle ; Estrous Cycle - drug effects ; Estrous Cycle - physiology ; Estrus cycle ; Female ; Follicle-stimulating hormone ; Gene expression ; Gene Expression - drug effects ; Genes ; Hormones - metabolism ; Infection control ; Inhibin ; Instrument industry ; Iodoacetic acid ; Iodoacetic Acid - pharmacology ; Mice ; Ovaries ; ovary ; Ovary - drug effects ; Ovary - physiology ; Oxidative stress ; Pregnenolone ; Progesterone ; Reproductive status ; RESEARCH ARTICLE ; Steroidogenesis ; Superoxide dismutase ; Testosterone ; Toxicants</subject><ispartof>Biology of reproduction, 2021-10, Vol.105 (4), p.1030-1042</ispartof><rights>The Author(s) 2021. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com journals.permissions@oup.com</rights><rights>The Author(s) 2021. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com 2021</rights><rights>The Author(s) 2021. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</rights><rights>COPYRIGHT 2021 Oxford University Press</rights><rights>The Author(s) 2021. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b556t-79a6a2ef5102b8ef0db85f8abeb51907f021f6f36af603e6e95db01c8d85d2613</citedby><cites>FETCH-LOGICAL-b556t-79a6a2ef5102b8ef0db85f8abeb51907f021f6f36af603e6e95db01c8d85d2613</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,1585,27925,27926</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34086879$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gonsioroski, Andressa</creatorcontrib><creatorcontrib>Meling, Daryl D</creatorcontrib><creatorcontrib>Gao, Liying</creatorcontrib><creatorcontrib>Plewa, Michael J</creatorcontrib><creatorcontrib>Flaws, Jodi A</creatorcontrib><title>Iodoacetic acid affects estrous cyclicity, ovarian gene expression, and hormone levels in mice</title><title>Biology of reproduction</title><addtitle>Biol Reprod</addtitle><description>Iodoacetic acid (IAA) is a water disinfection byproduct that is an ovarian toxicant in vitro. However, information on the effects of IAA on ovarian function in vivo was limited. Thus, we determined whether IAA exposure affects estrous cyclicity, steroidogenesis, and ovarian gene expression in mice. Adult CD-1 mice were dosed with water or IAA (0.5–500 mg/L) in the drinking water for 35–40 days during which estrous cyclicity was monitored for 14 days. Ovaries were analyzed for expression of apoptotic factors, cell cycle regulators, steroidogenic factors, estrogen receptors, oxidative stress markers, and a proliferation marker. Sera were collected to measure pregnenolone, androstenedione, testosterone, estradiol, inhibin B, and follicle-stimulating hormone (FSH) levels. IAA exposure decreased the time that the mice spent in proestrus compared to control. IAA exposure decreased expression of the proapoptotic factor Bok and the cell cycle regulator Ccnd2 compared to control. IAA exposure increased expression of the proapoptotic factors Bax and Aimf1, the antiapoptotic factor Bcl2l10, the cell cycle regulators Ccna2, Ccnb1, Ccne1, and Cdk4, and estrogen receptor Esr1 compared to control. IAA exposure decreased expression of Sod1 and increased expression of Cat, Gpx and Nrf2. IAA exposure did not affect expression of Star, Cyp11a1, Cyp17a1, Hsd17b1, Hsd3b1, Esr2, or Ki67 compared to control. IAA exposure decreased estradiol levels, but did not alter other hormone levels compared to control. In conclusion, IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Summary sentence IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Graphical Abstract</description><subject>17β-Estradiol</subject><subject>Analysis</subject><subject>Androstenedione</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell cycle</subject><subject>Cytochrome P-450</subject><subject>Disinfection</subject><subject>disinfection byproducts</subject><subject>Drinking water</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Estradiol</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>estrous cycle</subject><subject>Estrous Cycle - drug effects</subject><subject>Estrous Cycle - physiology</subject><subject>Estrus cycle</subject><subject>Female</subject><subject>Follicle-stimulating hormone</subject><subject>Gene expression</subject><subject>Gene Expression - drug effects</subject><subject>Genes</subject><subject>Hormones - metabolism</subject><subject>Infection control</subject><subject>Inhibin</subject><subject>Instrument industry</subject><subject>Iodoacetic acid</subject><subject>Iodoacetic Acid - pharmacology</subject><subject>Mice</subject><subject>Ovaries</subject><subject>ovary</subject><subject>Ovary - drug effects</subject><subject>Ovary - physiology</subject><subject>Oxidative stress</subject><subject>Pregnenolone</subject><subject>Progesterone</subject><subject>Reproductive status</subject><subject>RESEARCH ARTICLE</subject><subject>Steroidogenesis</subject><subject>Superoxide dismutase</subject><subject>Testosterone</subject><subject>Toxicants</subject><issn>0006-3363</issn><issn>1529-7268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFks1rGzEQxUVpaBy31x6LoJcGvIk-LK32EgghbQOBXNprhVY7chR2JVfaNfV_Hxm76QeBoINg9JunmcdD6D0lZ5Q0_Lz1sU9w7qNpKVGv0IwK1lQ1k-o1mhFCZMW55MfoJOcHQuiSM_4GHfMlUVLVzQz9uIldNBZGb7GxvsPGObBjxpDHFKeM7db23vpxu8BxY5I3Aa8gAIZf6wQ5-xgW2IQO38c0xFLvYQN9xj7gwVt4i46c6TO8O9xz9P3z9berr9Xt3Zebq8vbqhVCjlXdGGkYOEEJaxU40rVKOGVaaAVtSO0Io046Lo2ThIOERnQtoVZ1SnRMUj5HF3vd9dQO0FkIYzK9Xic_mLTV0Xj970vw93oVN1oJSqXkReDTQSDFn1NZXg8-W-h7E6DYoJngtSzmFXaOPv6HPsQphbJeoZqaca7I8g-1Mj1oH1ws_9qdqL6sCVViKdlu7rNnqHI6KPYVP50v9ecabIo5J3BPO1Kid4nQ-0ToQyJKw4e_nXnCf0egAKd7IE7rl8UWe7bUy3Av4Y9sgNGL</recordid><startdate>20211001</startdate><enddate>20211001</enddate><creator>Gonsioroski, Andressa</creator><creator>Meling, Daryl D</creator><creator>Gao, Liying</creator><creator>Plewa, Michael J</creator><creator>Flaws, Jodi A</creator><general>Society for the Study of Reproduction</general><general>Oxford University Press</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20211001</creationdate><title>Iodoacetic acid affects estrous cyclicity, ovarian gene expression, and hormone levels in mice</title><author>Gonsioroski, Andressa ; Meling, Daryl D ; Gao, Liying ; Plewa, Michael J ; Flaws, Jodi A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b556t-79a6a2ef5102b8ef0db85f8abeb51907f021f6f36af603e6e95db01c8d85d2613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>17β-Estradiol</topic><topic>Analysis</topic><topic>Androstenedione</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell cycle</topic><topic>Cytochrome P-450</topic><topic>Disinfection</topic><topic>disinfection byproducts</topic><topic>Drinking water</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Estradiol</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>estrous cycle</topic><topic>Estrous Cycle - drug effects</topic><topic>Estrous Cycle - physiology</topic><topic>Estrus cycle</topic><topic>Female</topic><topic>Follicle-stimulating hormone</topic><topic>Gene expression</topic><topic>Gene Expression - drug effects</topic><topic>Genes</topic><topic>Hormones - metabolism</topic><topic>Infection control</topic><topic>Inhibin</topic><topic>Instrument industry</topic><topic>Iodoacetic acid</topic><topic>Iodoacetic Acid - pharmacology</topic><topic>Mice</topic><topic>Ovaries</topic><topic>ovary</topic><topic>Ovary - drug effects</topic><topic>Ovary - physiology</topic><topic>Oxidative stress</topic><topic>Pregnenolone</topic><topic>Progesterone</topic><topic>Reproductive status</topic><topic>RESEARCH ARTICLE</topic><topic>Steroidogenesis</topic><topic>Superoxide dismutase</topic><topic>Testosterone</topic><topic>Toxicants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gonsioroski, Andressa</creatorcontrib><creatorcontrib>Meling, Daryl D</creatorcontrib><creatorcontrib>Gao, Liying</creatorcontrib><creatorcontrib>Plewa, Michael J</creatorcontrib><creatorcontrib>Flaws, Jodi A</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biology of reproduction</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gonsioroski, Andressa</au><au>Meling, Daryl D</au><au>Gao, Liying</au><au>Plewa, Michael J</au><au>Flaws, Jodi A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iodoacetic acid affects estrous cyclicity, ovarian gene expression, and hormone levels in mice</atitle><jtitle>Biology of reproduction</jtitle><addtitle>Biol Reprod</addtitle><date>2021-10-01</date><risdate>2021</risdate><volume>105</volume><issue>4</issue><spage>1030</spage><epage>1042</epage><pages>1030-1042</pages><issn>0006-3363</issn><eissn>1529-7268</eissn><abstract>Iodoacetic acid (IAA) is a water disinfection byproduct that is an ovarian toxicant in vitro. However, information on the effects of IAA on ovarian function in vivo was limited. Thus, we determined whether IAA exposure affects estrous cyclicity, steroidogenesis, and ovarian gene expression in mice. Adult CD-1 mice were dosed with water or IAA (0.5–500 mg/L) in the drinking water for 35–40 days during which estrous cyclicity was monitored for 14 days. Ovaries were analyzed for expression of apoptotic factors, cell cycle regulators, steroidogenic factors, estrogen receptors, oxidative stress markers, and a proliferation marker. Sera were collected to measure pregnenolone, androstenedione, testosterone, estradiol, inhibin B, and follicle-stimulating hormone (FSH) levels. IAA exposure decreased the time that the mice spent in proestrus compared to control. IAA exposure decreased expression of the proapoptotic factor Bok and the cell cycle regulator Ccnd2 compared to control. IAA exposure increased expression of the proapoptotic factors Bax and Aimf1, the antiapoptotic factor Bcl2l10, the cell cycle regulators Ccna2, Ccnb1, Ccne1, and Cdk4, and estrogen receptor Esr1 compared to control. IAA exposure decreased expression of Sod1 and increased expression of Cat, Gpx and Nrf2. IAA exposure did not affect expression of Star, Cyp11a1, Cyp17a1, Hsd17b1, Hsd3b1, Esr2, or Ki67 compared to control. IAA exposure decreased estradiol levels, but did not alter other hormone levels compared to control. In conclusion, IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Summary sentence IAA exposure alters estrous cyclicity, ovarian gene expression, and estradiol levels in mice. Graphical Abstract</abstract><cop>United States</cop><pub>Society for the Study of Reproduction</pub><pmid>34086879</pmid><doi>10.1093/biolre/ioab108</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 17β-Estradiol Analysis Androstenedione Animals Apoptosis Cell cycle Cytochrome P-450 Disinfection disinfection byproducts Drinking water Enzyme Inhibitors - pharmacology Estradiol Estrogen receptors Estrogens estrous cycle Estrous Cycle - drug effects Estrous Cycle - physiology Estrus cycle Female Follicle-stimulating hormone Gene expression Gene Expression - drug effects Genes Hormones - metabolism Infection control Inhibin Instrument industry Iodoacetic acid Iodoacetic Acid - pharmacology Mice Ovaries ovary Ovary - drug effects Ovary - physiology Oxidative stress Pregnenolone Progesterone Reproductive status RESEARCH ARTICLE Steroidogenesis Superoxide dismutase Testosterone Toxicants |
| title | Iodoacetic acid affects estrous cyclicity, ovarian gene expression, and hormone levels in mice |
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