Effects of thermotherapy and dimethyl sulfoxide treatments on healthy and type 2 diabetes human skeletal muscle myoblast cell lines
| dc.contributor.advisor | Sparks, Jean | |
| dc.contributor.author | Lindstrom, Janette | |
| dc.contributor.committeeMember | Omoruyi, Felix | |
| dc.contributor.committeeMember | Mozzachiodi, Riccardo | |
| dc.contributor.committeeMember | Newmire, Daniel | |
| dc.date.accessioned | 2021-06-25T16:36:49Z | |
| dc.date.available | 2021-06-25T16:36:49Z | |
| dc.date.issued | 2020-12 | |
| dc.description.abstract | Diabetes mellitus (diabetes) is a chronic metabolic disease characterized by elevated blood glucose levels with associated disordered carbohydrate and lipid metabolism. Type 2 diabetes (T2D) specifically has been shown to cause a decrease in skeletal muscle mass due to oxidative stress. Thermotherapy has been determined to help reduce oxidative stress through increasing heat shock protein activation resulting in restored human skeletal muscle mass. Dimethyl sulfoxide (DMSO) is a common reagent used to help cells cryofreeze safely or act as a solvent for water–insoluble substances to apply directly to the cells. This study investigated a treatment option for T2D through thermotherapy and the effect of high concentrations of DMSO on healthy (HSMM) and T2D (D–HSMM) human skeletal muscle cells. The goals were to determine the effect of thermotherapy long–term (chronic) and short–term (acute) on HSMM and D–HSMM cell viabilities and oxidative stress, and DMSO on cell viabilities. Results for thermotherapy indicated no beneficial impact on the cell viability (> 40% live cells in both treatments) of HSMM and D–HSMM cells. Thermotherapy allowed reactive oxidative species (ROS) to increase due to the presence of malondialdehyde (MDA) and little to no activity of the biological defense markers reduced glutathione (GSH), sodium dismutase (SOD), and catalase for both treatment options. The acute treatment had a significant increase (P ≤ 0.05) of MDA and GSH molecules compared to the chronic treatment. The chronic treatment had a significant increase (P ≤ 0.05) of catalase activity compared to the acute treatment. The SOD activity had no significant change (P > 0.05) between the chronic and acute treatments. The DMSO treatment resulted in a significant decrease in cell viability (< 30% live cells) in both HSMM and D–HSMM cells. Thermotherapy caused an increase of ROS indicating increased oxidative stress suggesting further research is needed to determine the benefits and harms of heat stressing muscles. High concentrations of DMSO application on the cells were toxic as they resulted in increased cell death levels. | en_US |
| dc.description.college | College of Science and Engineering | en_US |
| dc.description.department | Life Sciences | en_US |
| dc.format.extent | 57 pages | en_US |
| dc.identifier.uri | https://hdl.handle.net/1969.6/89697 | |
| dc.language.iso | en_US | en_US |
| dc.rights | Attribution-NoDerivatives 4.0 International | * |
| dc.rights | This material is made available for use in research, teaching, and private study, pursuant to U.S. Copyright law. The user assumes full responsibility for any use of the materials, including but not limited to, infringement of copyright and publication rights of reproduced materials. Any materials used should be fully credited with its source. All rights are reserved and retained regardless of current or future development or laws that may apply to fair use standards. Permission for publication of this material, in part or in full, must be secured with the author and/or publisher. | en_US |
| dc.rights.uri | http://creativecommons.org/licenses/by-nd/4.0/ | * |
| dc.title | Effects of thermotherapy and dimethyl sulfoxide treatments on healthy and type 2 diabetes human skeletal muscle myoblast cell lines | en_US |
| dc.type | Text | en_US |
| dc.type.genre | Thesis | en_US |
| thesis.degree.discipline | Biology | en_US |
| thesis.degree.grantor | Texas A & M University--Corpus Christi | en_US |
| thesis.degree.level | Masters | en_US |
| thesis.degree.name | Master of Science | en_US |