Hamadeh, Mazen J.2015-08-282015-08-282015-03-032015-08-28http://hdl.handle.net/10315/30029Vitamin 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.enAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.NutritionPhysiologyHealth sciencesElectronic Thesis or Dissertation2015-08-28Vitamin DHypovitaminosis DHypervitaminosis DAmyotrophic lateral sclerosisG93A mouseSpinal cordMotor neuronsNeuroprotectionOxidative stressInflammationAntioxidant capacityApoptosisNeurotrophic factorsNeuron countNeuron damage