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Protective action of hydroxyethyl rutosides on singlet oxygen challenged cardiomyocytes
Author(s) -
Olbrich HansGeorg,
Grabisch Peter,
Großmann Alexander,
Rinne Thorsten,
Klepzig Harald,
Mutschler Ernst
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15725.x
Subject(s) - thiobarbituric acid , lipid peroxidation , singlet oxygen , reactive oxygen species , chemistry , myocyte , oxygen , tbars , viability assay , biochemistry , oxidative stress , pharmacology , biophysics , cell , medicine , biology , organic chemistry
1 The effect of a standardized mixture of β‐hydroxyethyl rutosides against oxidative damage in singlet oxygen‐challenged isolated cardiac myocytes from adult rats was investigated. The morphology of the myocytes was evaluated as an indicator for cell viability (elongated, rod shaped cells vs. hypercontracted, rounded cells). The determination of the production of thiobarbituric acid reactive substances served as an indicator for lipid peroxidation. 2 Exposure to singlet oxygen which was generated by photo‐excitation of rose bengal (10 −7 m ) reduced the number of rod shaped (vital) cardiomyocytes by 78.5 ± 2.5% and increased the production of thiobarbituric acid reactive substances by 1180 ± 150% in comparison to incubation with control buffer. 3 Coincubation of the cells with β‐hydroxyethyl rutosides (concentration range: 6.7 pg ml −1 to 670 μg ml −1 ) increased the number of rod shaped cardiomyocytes after exposure to singlet oxygen in a dose‐dependent bell‐shaped manner. A significant protective effect was observed at β‐hydroxyethyl rutosides concentrations ranging from 0.67 ng ml −1 to 67 ng ml −1 . 4 In spite of their protective action, β‐hydroxyethyl rutosides did not reduce the accumulation of thiobarbituric acid reactive substances, used as an indicator for lipid peroxidation. 5 The data suggest that β‐hydroxyethyl rutosides exert a protective action against oxygen radical‐induced damage of cardiac myocytes at very low concentrations without interfering with lipid peroxidation.