Document Detail


Emetine inhibits glycolysis in isolated, perfused rat hearts.
MedLine Citation:
PMID:  14734828     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This work was designed to test whether phosphofructokinase is a target for emetine action on the heart. The effects of 37 microM emetine on the activities of phosphofructokinase and hexokinase were measured in homogenates from perfused hearts. The action of increasing concentrations of emetine was determined in nonperfused heart homogenates. The effect of 37 microM emetine or control solutions on the concentration of fructose-6-phosphate and fructose- 1,6-phosphate was measured. The effect of 37 microM emetine or control perfusion on the utilization of fructose-6-phosphate by phosphofructokinase in centrifugation supernatants of homogenates and in reconstituted 27,000g pellets was measured. Double-reciprocal plots of fructose-6-phosphate concentrations vs phosphofructokinase activities were plotted. Emetine decreased phosphofructokinase activity in homogenates from both perfused and nonperfused hearts. Emetine did not inhibit cardiac hexokinase activity. In homogenates from nonperfused hearts, the maximal inhibition with high concentrations of emetine was approx 50%. Emetine perfusion caused a simultaneous increase in the phosphofructokinase substrate fructose-6-phosphate and a decrease in the phosphofructokinase product fructose-1,6-bisphosphate. Phosphofructokinase and, consequently, glycolytic flux appear to be subcellular targets for emetine in the heart. Homogenate centrifugation studies indicate that emetine acts on bound rather than unbound phosphofructokinase. The inhibition may be uncompetitive in nature.
Authors:
Shujia J Pan; Alan B Combs
Related Documents :
16959758 - Early reperfusion phenomena.
8945998 - H(+)-k(+)-atpase mediates net acid secretion in rat terminal inner medullary collecting...
1691628 - Transmural inhomogeneity of extracellular [k+] and ph and myocardial energy metabolism ...
8475998 - Reversibility of mild to moderate ischemic injuries in the isolated rat heart. a charac...
18097948 - Nasal contribution to breathing and fine particle deposition in children versus adults.
11427778 - Dose-response and coagulation and hemostatic factors.
Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Cardiovascular toxicology     Volume:  3     ISSN:  1530-7905     ISO Abbreviation:  Cardiovasc. Toxicol.     Publication Date:  2003  
Date Detail:
Created Date:  2004-01-21     Completed Date:  2004-07-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  101135818     Medline TA:  Cardiovasc Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  311-8     Citation Subset:  IM    
Affiliation:
Department of Kinesiology, University of Texas at Austin, Austin, TX, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Antidotes / toxicity*
Emetine / toxicity*
Fructosediphosphates / metabolism
Fructosephosphates / metabolism
Glycolysis
Hexokinase / metabolism
Male
Myocardium / metabolism*
Perfusion
Phosphofructokinases / antagonists & inhibitors,  metabolism
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Antidotes; 0/Fructosediphosphates; 0/Fructosephosphates; 483-18-1/Emetine; 488-69-7/fructose-1,6-diphosphate; 6814-87-5/fructose-6-phosphate; EC 2.7.1 -/Phosphofructokinases; EC 2.7.1.1/Hexokinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Increase in cardiovascular pathology in female Sprague-Dawley rats following chronic treatment with ...
Next Document:  Effects of angiotensin-converting enzyme inhibitor on delayed-onset doxorubicin-induced cardiotoxici...