{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/129777"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/129777","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"The effects of iodoacetic acid on the mouse ovary","abstract":"Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","abstract_html":"Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","abstract_has_math":false,"creators":["Fields, Audrey"],"institution":"University of Illinois Urbana-Champaign","degree_name":"M.S.","degree_level":"Thesis","degree_discipline":"Nutritional Sciences","degree_department":null,"school":null,"contributors":["de Mejia, Elvira","Flaws, Jodi A","Ziv-Gal, Ayelet"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025-05-06","date_published":"2025-05-06","updated_at":"2026-07-22T22:25:05Z","subjects":["Iodoacetic Acid (IAA)","Oxidative stress","Water disinfection byproducts (DBP)"],"languages":["en","eng"],"rights":["Copyright 2025 Audrey Fields"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/2142/129777","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["de Mejia, Elvira","Flaws, Jodi A","Ziv-Gal, Ayelet"]},{"key":"dc:creator","label":"Author","values":["Fields, Audrey"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2025-05-06","2025-05"]},{"key":"dc:type","label":"Dc Type","values":["text","Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Nutritional Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M.S."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Iodoacetic Acid (IAA)","Oxidative stress","Water disinfection byproducts (DBP)"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en","eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 2025 Audrey Fields"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://hdl.handle.net/2142/129777"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","The student, Audrey Fields, accepted the attached license on 2025-05-05 at 14:47.","The student, Audrey Fields, submitted this Thesis for approval on 2025-05-05 at 15:05.","This Thesis was approved for publication on 2025-05-06 at 16:22.","DSpace SAF Submission Ingestion Package generated from Vireo submission #22212 on 2025-10-19 at 19:55:44","The incorporation of water disinfectants into the main water supply has significantly decreased the presence of waterborne diseases such as cholera. However, the interaction between disinfectants and organic material generates water disinfection byproducts (DBPs). Iodoacetic acid (IAA) is an unregulated DBP that has been reported as a reproductive toxicant. Our previous studies show that IAA inhibits follicle growth and alters the expression of steroidogenic factors in vitro, but its underlying mechanisms of action were unknown. Thus, both an in vivo experiments and in vitro experiments were conducted to test the hypothesis that IAA exposure causes ovarian toxicity by altering gene expression of oxidative stress markers in the mouse ovary. To test the hypothesis in vitro, ovarian antral follicles were collected from CD-1 mice between 40 and 42 days of age. The follicles were incubated in individual wells within a 96-well plate in media containing vehicle control (water) or IAA (2µM, 5µM, 10µM, 15µM) for 96 hours. At 0 hours, 24 hours, 48 hours, 72 hours, and 96 hours, follicle growth was measured over the 96-hour period. Following the 96-hour incubation, follicles were collected, RNA was extracted, reverse transcribed, and subjected to quantitative polymerase chain reaction (qPCR) to analyze the expression of glutathione markers (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1), superoxide dismutase markers (Sod1, Sod2), and apoptosis markers (Bax, Bcl2), and catalase. IAA exposure significantly increased expression of Gpx1 in the 5µM treatment group compared to control and increased Gsto1 in the 10µM and 15µM treatment groups when compared to control. IAA exposure did not alter Gpx2, Gsr, Gsta1, Gstm1, Gstp1, Gstt1, Sod1, Sod2, Cat, Bax, or Bcl2 expression compared to control. Following the results of the in vitro study, an additional hypothesis was tested regarding the potential rescuing of follicular growth and gene expression of oxidative stress and apoptosis markers in IAA-treated ovarian antral follicles due to the incorporation of an antioxidant in vitro. To test this hypothesis, ovarian antral follicles were collected from CD-1 mice between 40 and 42 days of age. The follicles were incubated in individual wells within a 96-well plate in media containing either a control (water), IAA (10µM), Trolox (5µM), or IAA (10µM) + Trolox (5µM) for 96 hours. At 0 hours, 24 hours, 48 hours, 72 hours, and 96 hours and follicle growth was measured over the 96-hour period. Following the 96-hour incubation, follicles were collected, RNA was extracted, reverse transcribed, and subjected to quantitative polymerase chain reaction (qPCR) to analyze the expression of glutathione markers (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1), superoxide dismutase markers (Sod1, Sod2), and apoptosis markers (Bax, Bcl2), and catalase. IAA exposure significantly increased expression of Gsto1 for the IAA (10µM) and the IAA (10µM) + Trolox (5µM) treatment groups when compared to control. IAA exposure did not alter Gpx1, Gpx2, Gsr, Gsta1, Gstm1, Gstp1, Gstt1, Sod1, Sod2, Cat, Bax, or Bcl2 expression compared to control. To test the hypothesis that IAA induces oxidative stress in the ovary in vivo, adult CD-1 mice were dosed with either water (control) or IAA (2.69, 53.78, 538.14, or 2,695.71µM) in their drinking water for 35 days. Following this, ovaries were collected when the mice were in diestrus, RNA was extracted, reverse transcribed, and subjected to quantitative polymerase chain reaction (qPCR) to analyze the expression of glutathione markers (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1), superoxide dismutase markers (Sod1, Sod2), and apoptosis markers (Bax, Bcl2), and catalase. IAA exposure decreased the expression of Bcl2 in the 2.69 µM, 53.78 µM, 538.14 µM, and 2,695.71µM treatment groups compared to control and it decreased the expression of Cat in the 2.69 µM, 53.78 µM, 538.14 µM and 2,695.71µM treatment groups compared to control. In addition, IAA significantly decreased the expression of Sod1 in the 2.69 µM, 53.78 µM and 538.14 µM IAA treatment groups compared to control, but it did not affect the expression of Sod2 compared to control. IAA exposure decreased expression of Gss in the 2.69 µM and 2,695.71µM treatment groups compared to control, Gsta1 in the 2.69 µM and 53.78 µM treatment groups compared to control, Gstp1 in the 53.78 µM treatment group compared to control, and Gstt1 in the 2.69 µM, 53.78 µM, and 2,695.71µM treatment groups compared to control. IAA exposure did not alter Gpx1, Gpx2, or Gsr compared to control. IAA exposure increased expression of Bax in the 53.78 µM, 538.14 µM, and 2,695.71µM treatment groups compared to control. IAA exposure increased expression of Gstm1 in the 53.78 µM, 538.14 µM, and 2,695.71µM treatment groups compared to control. Collectively, the data from this thesis project indicate that IAA exposure causes ovarian toxicity by altering oxidative stress pathways in the mouse ovary."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The effects of iodoacetic acid on the mouse ovary"]}]}],"canonical_facts":{"dc:contributor":["de Mejia, Elvira","Flaws, Jodi A","Ziv-Gal, Ayelet"],"dc:creator":["Fields, Audrey"],"dc:date":["2025-05-06","2025-05"],"dc:description":["Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2027-05-01","The student, Audrey Fields, accepted the attached license on 2025-05-05 at 14:47.","The student, Audrey Fields, submitted this Thesis for approval on 2025-05-05 at 15:05.","This Thesis was approved for publication on 2025-05-06 at 16:22.","DSpace SAF Submission Ingestion Package generated from Vireo submission #22212 on 2025-10-19 at 19:55:44","The incorporation of water disinfectants into the main water supply has significantly decreased the presence of waterborne diseases such as cholera. However, the interaction between disinfectants and organic material generates water disinfection byproducts (DBPs). Iodoacetic acid (IAA) is an unregulated DBP that has been reported as a reproductive toxicant. Our previous studies show that IAA inhibits follicle growth and alters the expression of steroidogenic factors in vitro, but its underlying mechanisms of action were unknown. Thus, both an in vivo experiments and in vitro experiments were conducted to test the hypothesis that IAA exposure causes ovarian toxicity by altering gene expression of oxidative stress markers in the mouse ovary. To test the hypothesis in vitro, ovarian antral follicles were collected from CD-1 mice between 40 and 42 days of age. The follicles were incubated in individual wells within a 96-well plate in media containing vehicle control (water) or IAA (2µM, 5µM, 10µM, 15µM) for 96 hours. At 0 hours, 24 hours, 48 hours, 72 hours, and 96 hours, follicle growth was measured over the 96-hour period. Following the 96-hour incubation, follicles were collected, RNA was extracted, reverse transcribed, and subjected to quantitative polymerase chain reaction (qPCR) to analyze the expression of glutathione markers (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1), superoxide dismutase markers (Sod1, Sod2), and apoptosis markers (Bax, Bcl2), and catalase. IAA exposure significantly increased expression of Gpx1 in the 5µM treatment group compared to control and increased Gsto1 in the 10µM and 15µM treatment groups when compared to control. IAA exposure did not alter Gpx2, Gsr, Gsta1, Gstm1, Gstp1, Gstt1, Sod1, Sod2, Cat, Bax, or Bcl2 expression compared to control. Following the results of the in vitro study, an additional hypothesis was tested regarding the potential rescuing of follicular growth and gene expression of oxidative stress and apoptosis markers in IAA-treated ovarian antral follicles due to the incorporation of an antioxidant in vitro. To test this hypothesis, ovarian antral follicles were collected from CD-1 mice between 40 and 42 days of age. The follicles were incubated in individual wells within a 96-well plate in media containing either a control (water), IAA (10µM), Trolox (5µM), or IAA (10µM) + Trolox (5µM) for 96 hours. At 0 hours, 24 hours, 48 hours, 72 hours, and 96 hours and follicle growth was measured over the 96-hour period. Following the 96-hour incubation, follicles were collected, RNA was extracted, reverse transcribed, and subjected to quantitative polymerase chain reaction (qPCR) to analyze the expression of glutathione markers (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1), superoxide dismutase markers (Sod1, Sod2), and apoptosis markers (Bax, Bcl2), and catalase. IAA exposure significantly increased expression of Gsto1 for the IAA (10µM) and the IAA (10µM) + Trolox (5µM) treatment groups when compared to control. IAA exposure did not alter Gpx1, Gpx2, Gsr, Gsta1, Gstm1, Gstp1, Gstt1, Sod1, Sod2, Cat, Bax, or Bcl2 expression compared to control. To test the hypothesis that IAA induces oxidative stress in the ovary in vivo, adult CD-1 mice were dosed with either water (control) or IAA (2.69, 53.78, 538.14, or 2,695.71µM) in their drinking water for 35 days. Following this, ovaries were collected when the mice were in diestrus, RNA was extracted, reverse transcribed, and subjected to quantitative polymerase chain reaction (qPCR) to analyze the expression of glutathione markers (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1), superoxide dismutase markers (Sod1, Sod2), and apoptosis markers (Bax, Bcl2), and catalase. IAA exposure decreased the expression of Bcl2 in the 2.69 µM, 53.78 µM, 538.14 µM, and 2,695.71µM treatment groups compared to control and it decreased the expression of Cat in the 2.69 µM, 53.78 µM, 538.14 µM and 2,695.71µM treatment groups compared to control. In addition, IAA significantly decreased the expression of Sod1 in the 2.69 µM, 53.78 µM and 538.14 µM IAA treatment groups compared to control, but it did not affect the expression of Sod2 compared to control. IAA exposure decreased expression of Gss in the 2.69 µM and 2,695.71µM treatment groups compared to control, Gsta1 in the 2.69 µM and 53.78 µM treatment groups compared to control, Gstp1 in the 53.78 µM treatment group compared to control, and Gstt1 in the 2.69 µM, 53.78 µM, and 2,695.71µM treatment groups compared to control. IAA exposure did not alter Gpx1, Gpx2, or Gsr compared to control. IAA exposure increased expression of Bax in the 53.78 µM, 538.14 µM, and 2,695.71µM treatment groups compared to control. IAA exposure increased expression of Gstm1 in the 53.78 µM, 538.14 µM, and 2,695.71µM treatment groups compared to control. Collectively, the data from this thesis project indicate that IAA exposure causes ovarian toxicity by altering oxidative stress pathways in the mouse ovary."],"dc:format":["application/pdf"],"dc:identifier":["https://hdl.handle.net/2142/129777"],"dc:language":["en","eng"],"dc:rights":["Copyright 2025 Audrey Fields"],"dc:subject":["Iodoacetic Acid (IAA)","Oxidative stress","Water disinfection byproducts (DBP)"],"dc:title":["The effects of iodoacetic acid on the mouse ovary"],"dc:type":["text","Thesis"],"thesis:degree_discipline":["Nutritional Sciences"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["M.S."],"thesis:institution_name":["University of Illinois Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:05Z"}