Date of Last Revision
2023-05-03 12:51:15
Major
Chemistry - Biochemistry
Degree Name
Bachelor of Science
Date of Expected Graduation
Spring 2019
Abstract
Cuprizone is a copper chelator that induces demyelination in the central nervous system when fed to mice. This compound is thought to target Complex IV and disrupt mitochondrial metabolism leading to loss of myelin-producing oligodendrocytes. In this proposal, we further examine the chemical and toxicological properties of cuprizone. Immunofluorescence imaging and microarray data on MO3.13 cells treated with cuprizone revealed the possibility of alterations in lysosomal function, as well as mitochondrial disruption via mTOR and Electron Transport Chain (ETC) related pathways. Cell viability assays conducted suggest that addition of Branched-Chain Amino Acids, most commonly used from literature, leucine, can increase cell vitality after being treated with cuprizone. Additional studies examined the solubility of cuprizone and interaction with zinc. Taken altogether, this experiment reveals that cuprizone affects lysosomal and mitochondrial function, and provides insight into leucine supplementation at an attempt to rescue cells from neurotoxicity.
Research Sponsor
Dr. Leah Shriver
First Reader
Dr. Sailaja Paruchuri
Second Reader
Dr. Michael Konopka
Recommended Citation
Ley, Michael, "Leucine Supplementation in Cuprizone-Induced Oligodendrocyte Toxicity" (2019). Williams Honors College, Honors Research Projects. 890.
https://ideaexchange.uakron.edu/honors_research_projects/890
Included in
Amino Acids, Peptides, and Proteins Commons, Biochemical Phenomena, Metabolism, and Nutrition Commons, Biological Factors Commons, Chemical and Pharmacologic Phenomena Commons, Medical Biochemistry Commons