{"id":{"repo_id":"york","oai_identifier":"oai:yorkspace.library.yorku.ca:10315/30029"},"canonical_url":"https://search.dev.ndltd.org/etd/york/oai:yorkspace.library.yorku.ca:10315/30029","repository":{"repo_id":"york","name":"York University","base_url":"https://yorkspace.library.yorku.ca/oai/request"},"display":{"title":"Analyzing Vitamin D3 Supplementation and Deficiency in the Spinal Cord of Transgenic G93A Mouse Model of Amyotrophic Lateral Sclerosis","abstract":"Vitamin D3 (D3) may impact ALS, a motoneurodegenerative disease. The study analyzed D3 supplementation at 50x the adequate intake (AI) and restriction at 2.5% the AI in the spinal cord of transgenic G93A, a mouse model of ALS. At 25 d, mice were provided food ad libitum with adequate (AI;1 IU D3/g feed), high (HiD; 50 IU D3/g feed) or deficient (DEF; 0.025 IU D3/g feed) D3. At 113 d, the spinal cords underwent protein analysis. HiD females exhibited D3 toxicity, evidenced by increased oxidative damage and apoptosis and lower antioxidant capacity vs. AI. HiD males exhibited lower oxidative damage, inflammation, apoptosis and neuron damage vs. AI. DEF females exhibited higher inflammation and a compensatory increase in GPx1 vs. AI. DEF males exhibited higher lipid peroxidation and lower antioxidant capacity vs. AI. In G93A mice, non-toxic doses of D3 attenuate disease pathophysiology, whereas deficiency worsens it in a sex-specific manner.","abstract_html":"Vitamin D3 (D3) may impact ALS, a motoneurodegenerative disease. The study analyzed D3 supplementation at 50x the adequate intake (AI) and restriction at 2.5% the AI in the spinal cord of transgenic G93A, a mouse model of ALS. At 25 d, mice were provided food ad libitum with adequate (AI;1 IU D3/g feed), high (HiD; 50 IU D3/g feed) or deficient (DEF; 0.025 IU D3/g feed) D3. At 113 d, the spinal cords underwent protein analysis. HiD females exhibited D3 toxicity, evidenced by increased oxidative damage and apoptosis and lower antioxidant capacity vs. AI. HiD males exhibited lower oxidative damage, inflammation, apoptosis and neuron damage vs. AI. DEF females exhibited higher inflammation and a compensatory increase in GPx1 vs. AI. DEF males exhibited higher lipid peroxidation and lower antioxidant capacity vs. AI. In G93A mice, non-toxic doses of D3 attenuate disease pathophysiology, whereas deficiency worsens it in a sex-specific manner.","abstract_has_math":false,"creators":["Moghimi, Elnaz"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Hamadeh, Mazen J."],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-08-28","date_published":"2015-08-28","updated_at":"2026-07-24T06:33:43Z","subjects":["Nutrition","Physiology","Health sciences"],"languages":["en"],"rights":["Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10315/30029","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Hamadeh, Mazen J."]},{"key":"dc:creator","label":"Author","values":["Moghimi, Elnaz"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2015-08-28T15:27:27Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2015-08-28T15:27:27Z"]},{"key":"dc:date.issued","label":"Date","values":["2015-08-28"]},{"key":"dc:type","label":"Dc Type","values":["Electronic Thesis or Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Nutrition","Physiology","Health sciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10315/30029"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Vitamin D3 (D3) may impact ALS, a motoneurodegenerative disease. The study analyzed D3 supplementation at 50x the adequate intake (AI) and restriction at 2.5% the AI in the spinal cord of transgenic G93A, a mouse model of ALS. At 25 d, mice were provided food ad libitum with adequate (AI;1 IU D3/g feed), high (HiD; 50 IU D3/g feed) or deficient (DEF; 0.025 IU D3/g feed) D3. At 113 d, the spinal cords underwent protein analysis. HiD females exhibited D3 toxicity, evidenced by increased oxidative damage and apoptosis and lower antioxidant capacity vs. AI. HiD males exhibited lower oxidative damage, inflammation, apoptosis and neuron damage vs. AI. DEF females exhibited higher inflammation and a compensatory increase in GPx1 vs. AI. DEF males exhibited higher lipid peroxidation and lower antioxidant capacity vs. AI. In G93A mice, non-toxic doses of D3 attenuate disease pathophysiology, whereas deficiency worsens it in a sex-specific manner."]},{"key":"dc:title","label":"Title","values":["Analyzing Vitamin D3 Supplementation and Deficiency in the Spinal Cord of Transgenic G93A Mouse Model of Amyotrophic Lateral Sclerosis"]}]}],"canonical_facts":{"dc:contributor.advisor":["Hamadeh, Mazen J."],"dc:creator":["Moghimi, Elnaz"],"dc:date.accessioned":["2015-08-28T15:27:27Z"],"dc:date.available":["2015-08-28T15:27:27Z"],"dc:date.issued":["2015-08-28"],"dc:description.abstract":["Vitamin D3 (D3) may impact ALS, a motoneurodegenerative disease. The study analyzed D3 supplementation at 50x the adequate intake (AI) and restriction at 2.5% the AI in the spinal cord of transgenic G93A, a mouse model of ALS. At 25 d, mice were provided food ad libitum with adequate (AI;1 IU D3/g feed), high (HiD; 50 IU D3/g feed) or deficient (DEF; 0.025 IU D3/g feed) D3. At 113 d, the spinal cords underwent protein analysis. HiD females exhibited D3 toxicity, evidenced by increased oxidative damage and apoptosis and lower antioxidant capacity vs. AI. HiD males exhibited lower oxidative damage, inflammation, apoptosis and neuron damage vs. AI. DEF females exhibited higher inflammation and a compensatory increase in GPx1 vs. AI. DEF males exhibited higher lipid peroxidation and lower antioxidant capacity vs. AI. In G93A mice, non-toxic doses of D3 attenuate disease pathophysiology, whereas deficiency worsens it in a sex-specific manner."],"dc:identifier.uri":["http://hdl.handle.net/10315/30029"],"dc:language.iso":["en"],"dc:rights":["Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests."],"dc:subject":["Nutrition","Physiology","Health sciences"],"dc:title":["Analyzing Vitamin D3 Supplementation and Deficiency in the Spinal Cord of Transgenic G93A Mouse Model of Amyotrophic Lateral Sclerosis"],"dc:type":["Electronic Thesis or Dissertation"]},"updated_at":"2026-07-24T06:33:43Z"}