Selenium toxicity induces pathological skeletal muscle contracture in many animal-models, and can result in respiratory failure. Previous research suggests the main cause of selenium-induced contracture is the oxidation of ryanodine receptors, causing uncontrolled Ca2+release. The results of this thesis show that selenium-induced contracture can occur by multiple independent mechanisms. These mechanisms involve changes to cellular redox state, which impair the function of the SE RCA pump and reduce the sensitivity of the contractile apparatus to Ca2+. This thesis also presents the possibility that selenium-induced contracture could be caused by mitochondrial-mediated cell death resulting in a rigor contracture.
|Award date||1 Jun 2018|
|Publication status||Unpublished - 2018|