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Antioxidants prevented oxidative injury of SR induced by Fe 2+ /H 2 O 2 /ascorbate system but failed to prevent Ca 2+ ‐ATPase activity decrease
Author(s) -
Horáková Lubica,
Štrosová Miriam,
Škuciová Mária
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.5520240112
Subject(s) - trolox , chemistry , antioxidant , oxidative stress , biochemistry , lipid peroxidation , atpase , endoplasmic reticulum , protein carbonylation , enzyme , dpph
Dysfunction of sarcoplasmic reticulum (SR) Ca 2+ ‐ATPase induced by oxidative stress may be a contributing factor to the development of serious age related diseases. Incubation of sarcoplasmic reticulum (SR) vesicles of rabbit skeletal muscles with Fe 2+ /H 2 O 2 /ascorbate decreased the SH group content of SR approximately to 35% and Ca 2+ ‐ATPase activity to 50% of control not oxidized sample. Protein carbonyls increased twofold, lipid peroxidation was also significantly elevated. The antioxidant effects of trolox, the pyridoindole derivative stobadine and of the standardized extracts from bark of Pinus Pinaster Pycnogenol® (Pyc) and from leaves of Ginkgo biloba (EGb 761) were studied on oxidatively injured SR. All antioxidants exerted preventive effects against the oxidized lipids and protein SH groups of SR vesicles. Trolox and stobadine did not influence protein carbonyl formation, while flavonoid extracts prevented carbonyl generation, probably by binding to protein. The preventive effects of the antioxidants studied on lipids and protein SH groups were however not associated with protection of Ca 2+ ‐ATPase activity. Stobadine and trolox exerted no effect on enzyme activity, Pyc and EGb 761 enhanced the inhibitory effect of Ca 2+ ‐ATPase activity in oxidatively injured SR. Concluding, under the conditions of oxidative stress induced by Fe 2+ /H 2 O 2 /ascorbate against SR of rabbit skeletal muscle, the agents studied demonstrated antioxidant effects yet failed to protect Ca 2+ ‐ATPase activity.