The mechanism of selenium-induced skeletal muscle dysfunction and weakness

Research output: ThesisMaster's Thesis

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Abstract

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.
Original languageEnglish
QualificationMasters
Awarding Institution
  • The University of Western Australia
Supervisors/Advisors
  • Bakker, Tony, Supervisor
  • Pinniger, Gavin, Supervisor
  • White, Robert, Supervisor
Thesis sponsors
Award date1 Jun 2018
DOIs
Publication statusUnpublished - 2018

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Muscle Weakness
Contracture
Selenium
Skeletal Muscle
Ryanodine Receptor Calcium Release Channel
Respiratory Insufficiency
Oxidation-Reduction
Cell Death
Animal Models
Research

Cite this

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title = "The mechanism of selenium-induced skeletal muscle dysfunction and weakness",
abstract = "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.",
keywords = "selenium, skeletal, toxicity, selenite, muscle, sodium selenite",
author = "Thomas Wilson",
year = "2018",
doi = "10.4225/23/5b2af9b60e3f8",
language = "English",
school = "The University of Western Australia",

}

TY - THES

T1 - The mechanism of selenium-induced skeletal muscle dysfunction and weakness

AU - Wilson, Thomas

PY - 2018

Y1 - 2018

N2 - 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.

AB - 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.

KW - selenium

KW - skeletal

KW - toxicity

KW - selenite

KW - muscle

KW - sodium selenite

U2 - 10.4225/23/5b2af9b60e3f8

DO - 10.4225/23/5b2af9b60e3f8

M3 - Master's Thesis

ER -