{"id":{"repo_id":"sask","oai_identifier":"oai:harvest.usask.ca:10388/17549"},"canonical_url":"https://search.dev.ndltd.org/etd/sask/oai:harvest.usask.ca:10388/17549","repository":{"repo_id":"sask","name":"University of Saskatchewan","base_url":"https://harvest.usask.ca/server/oai/request"},"display":{"title":"Exploring combined effects of arsenic and selenium exposure on larval zebrafish (Danio rerio)","abstract":"Arsenic contamination in aquatic ecosystems is a major environmental concern, with arsenite (As³⁺) being highly toxic. Selenium (Se) helps mitigate oxidative stress and hence could reduce the toxic effects of arsenic. However, Se can also be toxic at high concentrations. Given that these metalloids commonly co-occur in the environment, there is a pressing need for further research into their combined effects on aquatic life. To investigate this interplay, zebrafish embryos were exposed to As alone (as arsenite) or in combination with two different chemical forms of Se including As 120 μg/L alone (as arsenite), As 120 μg/L + Se 25 μg/L (as selenite), As 120 μg/L + Se 120 μg/L (as selenite), and As 120 μg/L + Se 2.5 μg/L (as selenomethionine, SeMet) until 4 days post-fertilization. There was no significant difference in the survival, hatching and deformity rate when fish were exposed to both As and Se. Co-exposure to As and Se significantly affected thigmotactic behaviour and reflexive movement (for all p < 0.001), with 2.5 µg/L Se mitigating As-induced impairments. While reactive oxygen species (ROS) levels were elevated in larvae exposed to As alone and As + Se 25 µg/L, there was a markedly reduced ROS level in the As + Se 120 µg/L and As + SeMet 2.5 µg/L treatments, highlighting selenium’s antioxidant efficacy. A marked suppression of genes related to antioxidant (Mn-SOD, gpx), neurogenesis (ngn1, hucs, bdnf, sf1), dopaminergic (Sncgb, otpa, robo2, th1), serotonergic (pet1, tph2), and motor neuron (pax2a) was observed following arsenic exposure. At the same time, co-treatment with As + Se 25 µg/L partially restored nrf2a expression (p < 0.05). These findings highlight the potential for naturally co-occurring Se to modulate As toxicity in aquatic environments, underscoring the importance of considering chemical interactions when assessing ecological risks.","abstract_html":"Arsenic contamination in aquatic ecosystems is a major environmental concern, with arsenite (As³⁺) being highly toxic. Selenium (Se) helps mitigate oxidative stress and hence could reduce the toxic effects of arsenic. However, Se can also be toxic at high concentrations. Given that these metalloids commonly co-occur in the environment, there is a pressing need for further research into their combined effects on aquatic life. To investigate this interplay, zebrafish embryos were exposed to As alone (as arsenite) or in combination with two different chemical forms of Se including As 120 μg/L alone (as arsenite), As 120 μg/L + Se 25 μg/L (as selenite), As 120 μg/L + Se 120 μg/L (as selenite), and As 120 μg/L + Se 2.5 μg/L (as selenomethionine, SeMet) until 4 days post-fertilization. There was no significant difference in the survival, hatching and deformity rate when fish were exposed to both As and Se. Co-exposure to As and Se significantly affected thigmotactic behaviour and reflexive movement (for all p < 0.001), with 2.5 µg/L Se mitigating As-induced impairments. While reactive oxygen species (ROS) levels were elevated in larvae exposed to As alone and As + Se 25 µg/L, there was a markedly reduced ROS level in the As + Se 120 µg/L and As + SeMet 2.5 µg/L treatments, highlighting selenium’s antioxidant efficacy. A marked suppression of genes related to antioxidant (Mn-SOD, gpx), neurogenesis (ngn1, hucs, bdnf, sf1), dopaminergic (Sncgb, otpa, robo2, th1), serotonergic (pet1, tph2), and motor neuron (pax2a) was observed following arsenic exposure. At the same time, co-treatment with As + Se 25 µg/L partially restored nrf2a expression (p < 0.05). These findings highlight the potential for naturally co-occurring Se to modulate As toxicity in aquatic environments, underscoring the importance of considering chemical interactions when assessing ecological risks.","abstract_has_math":false,"creators":["Luo, Owen H"],"institution":"University of Saskatchewan","degree_name":"Master of Science (M.Sc.)","degree_level":"Masters","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":[],"advisors":["Chivers, Douglas","Niyogi, Soumya"],"committee_chairs":[],"committee_members":["Ferrari, Maud","Weber, Lynn"],"year":2025,"date_issued":"2025-11-18","date_published":"2025-11-18","updated_at":"2026-07-24T04:27:16Z","subjects":["Arsenic","Selenium","Zebrafish","Toxicity"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/10388/17549","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Chivers, Douglas","Niyogi, Soumya"]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Ferrari, Maud","Weber, Lynn"]},{"key":"dc:creator","label":"Author","values":["Luo, Owen H"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2025-11-18T16:19:29Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2025-11-18T16:19:29Z"]},{"key":"dc:date.issued","label":"Date","values":["2025-11-18"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (M.Sc.)"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Saskatchewan"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Arsenic","Selenium","Zebrafish","Toxicity"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/10388/17549"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Arsenic contamination in aquatic ecosystems is a major environmental concern, with arsenite (As³⁺) being highly toxic. Selenium (Se) helps mitigate oxidative stress and hence could reduce the toxic effects of arsenic. However, Se can also be toxic at high concentrations. Given that these metalloids commonly co-occur in the environment, there is a pressing need for further research into their combined effects on aquatic life. To investigate this interplay, zebrafish embryos were exposed to As alone (as arsenite) or in combination with two different chemical forms of Se including As 120 μg/L alone (as arsenite), As 120 μg/L + Se 25 μg/L (as selenite), As 120 μg/L + Se 120 μg/L (as selenite), and As 120 μg/L + Se 2.5 μg/L (as selenomethionine, SeMet) until 4 days post-fertilization. There was no significant difference in the survival, hatching and deformity rate when fish were exposed to both As and Se. Co-exposure to As and Se significantly affected thigmotactic behaviour and reflexive movement (for all p < 0.001), with 2.5 µg/L Se mitigating As-induced impairments. While reactive oxygen species (ROS) levels were elevated in larvae exposed to As alone and As + Se 25 µg/L, there was a markedly reduced ROS level in the As + Se 120 µg/L and As + SeMet 2.5 µg/L treatments, highlighting selenium’s antioxidant efficacy. A marked suppression of genes related to antioxidant (Mn-SOD, gpx), neurogenesis (ngn1, hucs, bdnf, sf1), dopaminergic (Sncgb, otpa, robo2, th1), serotonergic (pet1, tph2), and motor neuron (pax2a) was observed following arsenic exposure. At the same time, co-treatment with As + Se 25 µg/L partially restored nrf2a expression (p < 0.05). These findings highlight the potential for naturally co-occurring Se to modulate As toxicity in aquatic environments, underscoring the importance of considering chemical interactions when assessing ecological risks."]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Exploring combined effects of arsenic and selenium exposure on larval zebrafish (Danio rerio)"]}]}],"canonical_facts":{"dc:contributor.advisor":["Chivers, Douglas","Niyogi, Soumya"],"dc:contributor.committeemember":["Ferrari, Maud","Weber, Lynn"],"dc:creator":["Luo, Owen H"],"dc:date.accessioned":["2025-11-18T16:19:29Z"],"dc:date.available":["2025-11-18T16:19:29Z"],"dc:date.issued":["2025-11-18"],"dc:description.abstract":["Arsenic contamination in aquatic ecosystems is a major environmental concern, with arsenite (As³⁺) being highly toxic. Selenium (Se) helps mitigate oxidative stress and hence could reduce the toxic effects of arsenic. However, Se can also be toxic at high concentrations. Given that these metalloids commonly co-occur in the environment, there is a pressing need for further research into their combined effects on aquatic life. To investigate this interplay, zebrafish embryos were exposed to As alone (as arsenite) or in combination with two different chemical forms of Se including As 120 μg/L alone (as arsenite), As 120 μg/L + Se 25 μg/L (as selenite), As 120 μg/L + Se 120 μg/L (as selenite), and As 120 μg/L + Se 2.5 μg/L (as selenomethionine, SeMet) until 4 days post-fertilization. There was no significant difference in the survival, hatching and deformity rate when fish were exposed to both As and Se. Co-exposure to As and Se significantly affected thigmotactic behaviour and reflexive movement (for all p < 0.001), with 2.5 µg/L Se mitigating As-induced impairments. While reactive oxygen species (ROS) levels were elevated in larvae exposed to As alone and As + Se 25 µg/L, there was a markedly reduced ROS level in the As + Se 120 µg/L and As + SeMet 2.5 µg/L treatments, highlighting selenium’s antioxidant efficacy. A marked suppression of genes related to antioxidant (Mn-SOD, gpx), neurogenesis (ngn1, hucs, bdnf, sf1), dopaminergic (Sncgb, otpa, robo2, th1), serotonergic (pet1, tph2), and motor neuron (pax2a) was observed following arsenic exposure. At the same time, co-treatment with As + Se 25 µg/L partially restored nrf2a expression (p < 0.05). These findings highlight the potential for naturally co-occurring Se to modulate As toxicity in aquatic environments, underscoring the importance of considering chemical interactions when assessing ecological risks."],"dc:format.mimetype":["application/pdf"],"dc:identifier.uri":["https://hdl.handle.net/10388/17549"],"dc:language.iso":["en"],"dc:subject":["Arsenic","Selenium","Zebrafish","Toxicity"],"dc:title":["Exploring combined effects of arsenic and selenium exposure on larval zebrafish (Danio rerio)"],"dc:type":["Thesis"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Masters"],"thesis:degree_name":["Master of Science (M.Sc.)"],"thesis:institution_name":["University of Saskatchewan"]},"updated_at":"2026-07-24T04:27:16Z"}