Sulfhydryl oxidation induces rapid calcium release from sarcoplasmic reticulum vesicles.

摘要: Micromolar concentrations of cupric ion (Cu2+) and mercaptans such as cysteine, cysteamine, homocysteine trigger large rapid Ca2+ release from skeletal muscle sarcoplasmic reticulum (SR) vesicles. At the used, Cu2+ alone does not induce nor cysteine alone; both are required to SR. is known catalyze autooxidation its disulfide form cystine; Cu2+/mercaptan-induced appears be caused by Cu2+-catalyzed formation a mixed between exogenous mercaptan critical sulfhydryl on transmembrane protein. In oxidized state SR highly permeable Ca2+. Supporting evidence for this interpretation follows. The order Ca2+-releasing reactivity same in which these compounds undergo oxidation forms presence Cu2+. efflux induced can reversed addition reducing agent dithiothreitol. Hypochlorous acid plumbagin, potential oxidants, vesicles; addition, Cu2+, catalyzes H2O2 enhances H2O2-induced release. Oxidation-induced partially or blocked ruthenium red local anesthetics procaine tetracaine. rates strongly Mg2+ dependent significantly higher heavy than light These data suggest that thus via "Ca2+ channel" group protein may principal means permeability regulated vivo.