TY - JOUR
T1 - Production of hydroxyl radicals and their disassociation from myocardial cell injury during calcium paradox
AU - Duncan, Eddy
AU - Onodera, Tomoya
AU - Ashraf, Muhammad
N1 - Funding Information:
This work was supported by NIH grant HL 41358. * Address correspondence to: Dr. M. Ashraf, Department of Pathology and Laboratory Medicine, University of Cincinnati Medical Center, 231 Bethesda Avenue, Cincinnati, OH 45267-0529.
PY - 1992
Y1 - 1992
N2 - The production of hydroxyl radicals during calcium paradox injury was investigated by measuring the production of 2,5-dihydroxybenzoic acid (2,5-DHBA) from salicylate. Four groups of rats were analyzed. In the first group, isolated hearts were perfused with calcium-free medium for 10 minutes followed by perfusion with medium containing Ca++ for 10 minutes. In the other groups, 0.25 μM N,N′-diphenyl-1,3-phenylenediamine (DPPD), 80 μM cytochrome c, or 450 U/ml catalase was added. Coronary effluent was analyzed for the presence of 2,5-DHBA, and tissue sections were examined using light microscopy. In the first group, 2,5-DHBA production began during the calcium-free period, peaked tenfold 60-90 sec. into the Ca repletion period, and declined thereafter. The increase in 2,5-DHBA was accompanied by severe cell damage. Cytochrome c reduced 2,5-DHBA production, and catalase almost completely inhibited 2,5-DHBA production, while DPPD had no effect on 2,5-DHBA production. None of the three additives provided any complete morphological protection. The data provide evidence for the production of hydroxyl radicals during calcium-paradox injury, that their production is dependent upon the presence of hydrogen peroxide, and that cell damage in the calcium paradox is not primarily mediated by the extracellular hydroxyl radicals.
AB - The production of hydroxyl radicals during calcium paradox injury was investigated by measuring the production of 2,5-dihydroxybenzoic acid (2,5-DHBA) from salicylate. Four groups of rats were analyzed. In the first group, isolated hearts were perfused with calcium-free medium for 10 minutes followed by perfusion with medium containing Ca++ for 10 minutes. In the other groups, 0.25 μM N,N′-diphenyl-1,3-phenylenediamine (DPPD), 80 μM cytochrome c, or 450 U/ml catalase was added. Coronary effluent was analyzed for the presence of 2,5-DHBA, and tissue sections were examined using light microscopy. In the first group, 2,5-DHBA production began during the calcium-free period, peaked tenfold 60-90 sec. into the Ca repletion period, and declined thereafter. The increase in 2,5-DHBA was accompanied by severe cell damage. Cytochrome c reduced 2,5-DHBA production, and catalase almost completely inhibited 2,5-DHBA production, while DPPD had no effect on 2,5-DHBA production. None of the three additives provided any complete morphological protection. The data provide evidence for the production of hydroxyl radicals during calcium-paradox injury, that their production is dependent upon the presence of hydrogen peroxide, and that cell damage in the calcium paradox is not primarily mediated by the extracellular hydroxyl radicals.
KW - Calcium paradox
KW - Catalase
KW - Free radicals
KW - HPLC
KW - Hydroxyl radical
KW - Oxygen-derived radicals
KW - Salicylate
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U2 - 10.1016/0891-5849(92)90053-J
DO - 10.1016/0891-5849(92)90053-J
M3 - Article
C2 - 1311280
AN - SCOPUS:0026552275
SN - 0891-5849
VL - 12
SP - 11
EP - 18
JO - Free Radical Biology and Medicine
JF - Free Radical Biology and Medicine
IS - 1
ER -