Oxidation of methionine in proteins of isolated rat heart myocytes and tissue slices by neutrophil-generated oxygen free radicals

1986 ◽  
Vol 18 ◽  
pp. 28-28
Author(s):  
H FLISS ◽  
G DOCHERTY
1991 ◽  
Vol 69 (10) ◽  
pp. 1459-1464 ◽  
Author(s):  
Ramez Chamine ◽  
Mircea Alexandru Mateescu ◽  
Stéphane Roger ◽  
Nobuharu Yamaguchi ◽  
Jacques de Champlain ◽  
...  

The potentially injurious effects of oxygen-derived free radicals (OFR) on the myocardium can be prevented in part by pretreatment with OFR scavengers or antioxidants. Since ceruloplasmin (CP) has been shown to possess potent antioxidant activity and scavenge a variety of OFR in vitro, we have undertaken to study its protective effects against myocardial injury induced by OFR. CP was freshly purified by a fast method that minimized proteolytic enzyme degradation. Free radicals were generated by the electrolysis (10 mA DC current for 1 min) of a Krebs–Henseleit solution perfusing an isolated rat heart preparation under constant pressure conditions. CP (0.25 μM) afforded 80 and 63% protection (n = 8, p < 0.05), respectively, against the deleterious effects of electrolysis-induced OFR on left ventricular pressure and coronary flow. The increase in left ventricular end diastolic pressure used here as an index of heart failure did not occur in the presence of 0.25 μM CP. Moreover, CP significantly reduced the increase of norepinephrine washout in the effluent perfusate after electrolysis suggesting a protection against free radical-induced injury to sympathetic nerve endings.Key words: oxygen free radicals, heart, ceruloplasmin, superoxide dismutase, norepinephrine.


Author(s):  
T. Oguro ◽  
T. Onodera ◽  
M. Ashraf

Previously we reported that hydrogen peroxide (H2O2) is primarily cytotoxic to the cardiac cell membranes presumably through lipid peroxidation (LP). However, the effect of LP on the altered cell membrane permeability remains unknown. In this study, we evaluated the ultrastructural effects of LP on the sarcolemma of the isolated rat heart using H2O2 and N,N’-diphenyl-p-phenylene diamine (DPPD), an antilipid peroxidative agent.The hearts were perfused with 300 μM H2O2 for 15 minutes. In the other experiment the hearts were perfused with 2.5 μM DPPD for 20 minutes prior to perfusion with H2O2 for 15 minutes. Coronary effluent was collected at the end of the equilibration period and during H2O2 treatment for malondialdehyde (MDA) determination. Two minutes prior to the termination of the experiment, horseradish peroxidase (HRP: 220 U/mg × 55 mg) was perfused to assess the enhanced permeability of the cell membranes. The tissue slices were incubated in Graham-Karnovsky medium for one hour followed by postfixation with buffered 1% OsO4.


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