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Oxidative damage to Ca 2+ ‐ATPase sarcoplasmic reticulum by HOCl and protective effect of some antioxidants
Author(s) -
Štrosová Miriam,
Škuciová Mária,
Horáková L'Ubica
Publication year - 2005
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520240113
Subject(s) - trolox , chemistry , hypochlorous acid , antioxidant , atpase , enzyme , biochemistry , endoplasmic reticulum , antioxidant capacity
Abstract Injury of rabbit skeletal sarcoplasmic reticulum (SR) induced by hypochlorous acid (HOCl) was studied. HOCl inhibited Ca 2+ ‐ATPase activity in a concentration‐dependent manner (IC 50 =100 μmol/l). The concentration of 13.5 μmol/l HOCl reduced the level of sulfhydryl (SH) groups by 50%, yet it did not influence the enzyme activity. In comparison with SH group oxidation and enzyme activity inhibition, a significantly longer time was necessary for the generation of protein carbonyls in SR injured by HOCl. Protective effects of some antioxidants (stobadine, trolox, EGb 761, Pycnogenol®) were studied in SR oxidatively injured by HOCl. Trolox and EGb 761 exerted a protective effect on ATPase activity and on SH groups of SR oxidatively modified by HOCl. Stobadine and Pycnogenol® inhibited markedly protein carbonyl formation. Stobadine was the only antioxidant able to scavenge HOCl. In conclusion, the protective effects of antioxidants against decrease of Ca 2+ ‐ATPase activity induced by HOCl might be caused by protection of SH groups. The compounds with both antioxidant and Ca 2+ ‐ATPase protecting effect offer dual defense against tissue damage occurring, e.g. in aging process.