Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.4.1 (myosin ATPase)
 1,140 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of oxygenation (95% O2 + 5% CO2) and/or SOD (400 mg/l) on addition to St. Thomas' Hospital cardioplegic solution were examined by hemodynamic, cytochemical and biophysical assessments in the isolated working rat heart subjected to hypothermic ischemic arrest (22 degrees C in temperature, 180 min in ischemic time) with multidose cardioplegic infusion. According to the feature of used cardioplegic solution, thirty-two rats were divided into four groups (8 animals per group): That is, Group I; O2 (+) SOD (+), Group II; O2 (-) SOD (+), Group III; O2 (+) SOD (-), Group IV (control); O2 (-), SOD (-). Aortic flow (AF) recovery, expressed as a percent of pre-arrest AF, was 76.7 +/- 11.7% in Group I, 66.9 +/- 7.1% in Group II, 73.9 +/- 11.6% in Group III and 57.7 +/- 12.9% in Group IV (mean +/- SD). Differences in recovery between Group I vs III and Group III vs IV approached statistically significance (respectively, p < 0.01, p < 0.05). The birefringence ratio (ATP value/air value) of the biopsy specimen was 2.49 +/- 0.53 in Group I, 1.96 +/- 0.44 in Group II, 2.04 +/- 0.29 in Group III and 1.65 +/- 0.39 in Group IV (mean +/- SD). Difference between Group I and Group IV indicated statistically significance (p < 0.05). The birefringence ratio (X) had good correlation with the AF recovery ratio (Y): Y = 29.7 + 19.1X (R = 0.74). No statistical difference was seen from cytochemical assessment (myosin ATPase stain) in four groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of oxygenation and/or SOD on addition to St. Thomas' Hospital cardioplegic solution]. 847 61

Treatment of F-actin with the peroxynitrite-releasing agent 3-morpholinosydnonimine (SIN-1) produced a dose-dependent F-actin depolymerization. This is due to released peroxynitrite because it is not produced by 'decomposed SIN-1', and it is prevented by superoxide dismutase concentrations efficiently preventing peroxynitrite formation. F-actin depolymerization has been found to be very sensitive to peroxynitrite, as exposure to fluxes as low as 50-100nM peroxynitrite leads to nearly 50% depolymerization in about 1h. G-actin polymerization is also impaired by peroxynitrite although with nearly 2-fold lower sensitivity. Exposure of F-actin to submicromolar fluxes of peroxynitrite produced cysteine oxidation and also a blockade of the ability of actin to stimulate myosin ATPase activity. Our results suggest that an imbalance of the F-actin/G-actin equilibrium can account for the observed structural and functional impairment of myofibrils under the peroxynitrite-mediated oxidative stress reported for some pathophysiological conditions.
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PMID:Peroxynitrite induces F-actin depolymerization and blockade of myosin ATPase stimulation. 1648 Jun 85