Hydrogen peroxide disrupts Ca2+ release from the sarcoplasmic reticulum of rat skeletal muscle fibers
Autor: | T. M. Nosek, Marco Brotto |
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Rok vydání: | 1996 |
Předmět: |
Male
medicine.medical_specialty Physiology Muscle Proteins Isometric exercise In Vitro Techniques Extensor digitorum longus muscle Superoxide dismutase chemistry.chemical_compound Isometric Contraction Physiology (medical) Internal medicine medicine Animals Muscle Skeletal chemistry.chemical_classification Reactive oxygen species NADPH oxidase biology Chemistry Superoxide Endoplasmic reticulum Hydrogen Peroxide Oxidants Rats Sarcoplasmic Reticulum Endocrinology Muscle Fibers Fast-Twitch biology.protein Calcium Reactive Oxygen Species Calcium-induced calcium release Muscle Contraction |
Zdroj: | Journal of Applied Physiology. 81:731-737 |
ISSN: | 1522-1601 8750-7587 |
Popis: | Reactive oxygen species such as superoxide (O2-) and H2O2 are produced at low levels in resting muscles and at substantially higher levels in exercising muscles. Increased respiratory activity with exercise leads to O2- production by the NADPH oxidase reaction and the subsequent generation of H2O2 from O2- by spontaneous dismutation or by the superoxide dismutase reaction. The long-lasting (24-h) depression of contractile function after exercise has been linked to damage of one or more proteins important in the excitation-contraction coupling process. We studied mechanically and chemically skinned fibers from the extensor digitorum longus muscle of the rat to evaluate the effects of a 5-min exposure to 1.0 mM H2O2 on muscle function. We found that H2O2 had no effect on the isometric force-producing properties of the contractile apparatus or on Ca2+ uptake by the sarcoplasmic reticulum. It did, however, significantly affect Ca2+ release from the sarcoplasmic reticulum. Maximum depolarization-induced Ca2+ release was inhibited, and the sensitivity to depolarization was decreased. Ca(2+)-induced release was completely blocked. We conclude that elevated levels of H2O2 with exercise are capable of damaging one or more proteins of the excitation-contraction coupling process to produce a disruption in function that can account, at least in part, for the long-lasting effects of fatiguing stimulation. |
Databáze: | OpenAIRE |
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