scholarly journals The effect of lead on the calcium-handling capacity of rat heart mitochondria

1976 ◽  
Vol 158 (2) ◽  
pp. 289-294 ◽  
Author(s):  
D R Parr ◽  
E J Harris
Keyword(s):  
Rat Heart ◽  
Heart Tissue ◽  
Calcium Handling ◽  
Primary Effect ◽  
Heart Mitochondria ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Low Concentrations ◽  
Rat Heart Mitochondria

1. Very low concentrations of Pb2+ decrease the capacity of rat heart mitochondria, oxidizing pyruvate plus malate, to remove Ca2+ from the medium. 2. The primary effect is on the rate of Ca2+ sequestration; this is reflected in the overall extent of Ca2+ removal. 3. Pb2+ has at least two separate actions. Below about 0.5 nmol/mg of protein, it acts solely by competing with Ca2+ (Ki = 0.4 muM); above this concentration it also inhibits the production or use of respiratory energy, so that at 1 nmol of Pb2+/mg of protein, Ca2+ removal is almost completely abolished. 4. Pb2+ inhibits coupled and uncoupled respiratory O2 use by mitochondria oxidizing pyruvate plus malate, but at higher concentrations than those that affect Ca2+ removal; similar concentrations of Pb2+ inhibit pyruvate uptake, but not malate uptake, by the mitochondria. 5. Mg2+ only decreases Ca2+ removal by competition, and is a far-less effective competitor than Pb2+ (Ki = 0.15 mM). It is possible that the primary cause of the second effect of Pb2+ is displacement of membrane Mg2+. 6. The consequences of these results are discussed in terms of the possible involvement of heart mitochondria in excitation-contraction coupling, and the Pb2+ levels that might occur in heart tissue in vivo.

Reactive Nitrogen and Oxygen Species Metabolism in Rat Heart Mitochondria under Administration of Nitric Oxide Donor in Vivo

2012 ◽  
Vol 3 (4) ◽  
pp. 327-340
Author(s):  
Olga V. Akopova ◽  
Yulia P. Korkach ◽  
Anatolii V. Kotsuruba ◽  
Lyudmila I. Kolchinskaya ◽  
Vadim F. Sagach
Keyword(s):  
Nitric Oxide ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Nitric Oxide Donor ◽  
Reactive Nitrogen ◽  
Oxygen Species ◽  
Rat Heart Mitochondria

scholarly journals The uptake and release of calcium by heart mitochondria

1977 ◽  
Vol 168 (3) ◽  
pp. 447-456 ◽  
Author(s):  
Eric J. Harris
Keyword(s):  
Local Anaesthetics ◽  
Inhibitory Effect ◽  
Heart Mitochondria ◽  
Rate Coefficients ◽  
Mitochondrial Activity ◽  
Low Concentrations ◽  
Spontaneous Action ◽  
Rat Heart Mitochondria ◽  
Kinetics Of Uptake

The kinetics of uptake of Ca2+ by rat heart mitochondria were studied by a spectrophotometric method with Arsenazo III indicator. The exponential rate coefficients measured with or without added phosphate increase with the amount of Ca2+ added up to about 24μm. Evidence is given that the effect is attributable to a combination of formation of chelates at low concentrations to act as Ca2+ buffers, with co-transport of substrate to provide more respiratory fuel. The inhibitory effect of Mg2+ depends on the Ca2+ concentration, so with a constant [Mg2+] the low concentrations of Ca2+ are most inhibited, and the rate coefficients are still more Ca2+-dependent. Ca2+ uptake is slowed by local anaesthetics such as butacaine and dibucaine, and also by propranolol and palmitoyl-CoA. After an uptake, the release of Ca2+ was investigated. The spontaneous release involves an initially slow and small appearance of free Ca2+ and is followed by an auto-accelerated phase. The release is accompanied by a gradual decrease in internal ATP; it is initiated by palmitoyl-CoA (reversed by carnitine), by lysophosphatidylcholine, by Na+ salts (reversed by oligomycin) and by K+ salts added to a K+-free medium containing valinomycin. The process is probably a response to an increased energy load imposed on the mitochondria by the various conditions, which include the spontaneous action of phospholipase activated by traces of Ca2+. The problem of how much mitochondrial activity is participating in normal heart Ca2+ turnover is discussed, and experiments showing only 7–14% exchange of the mitochondrial Ca2+ occurring in vivo in 10 or 20min are reported.

scholarly journals The effect of respiratory chain impairment of β-oxidation in rat heart mitochondria

1996 ◽  
Vol 319 (2) ◽  
pp. 633-640 ◽  
Author(s):  
Simon EATON ◽  
Morteza POURFARZAM ◽  
Kim BARTLETT
Keyword(s):  
Respiratory Chain ◽  
Rat Heart ◽  
Redox State ◽  
Complex Iii ◽  
Heart Mitochondria ◽  
Cardiac Ischaemia ◽  
Low Concentrations ◽  
Rat Heart Mitochondria ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
14Co2 Release

Cardiac ischaemia leads to an inhibition of β-oxidation flux and an accumulation of acyl-CoA and acyl-carnitine esters in the myocardium. However, there remains some uncertainty as to which esters accumulate during cardiac ischaemia and therefore the site of inhibition of β-oxidation [Moore, Radloff, Hull and Sweely (1980) Am. J. Physiol. 239, H257-H265; Latipää (1989) J. Mol. Cell. Cardiol. 21, 765–771]. When β-oxidation of hexadecanoyl-CoA in state III rat heart mitochondria was inhibited by titration of complex III activity, flux measured as 14CO2 release, acid-soluble radioactivity or as acetyl-carnitine was progressively decreased. Low concentrations of myxothiazol caused reduction of the ubiquinone pool whereas the NAD+/NADH redox state was less responsive. Measurement of the CoA and carnitine esters generated under these conditions showed that there was a progressive decrease in the amounts of chain-shortened saturated acyl esters with increasing amounts of myxothiazol. The concentrations of 3-hydroxyacyl and 2-enoyl esters, however, were increased between 0 and 0.2 µM myxothiazol but were lowered at higher myxothiazol concentrations. More hexadecanoyl-CoA and hexadecanoyl-carnitine were present with increasing concentrations of myxothiazol. We conclude that 3-hydroxyacyl-CoA dehydrogenase and acyl-CoA dehydrogenase activities are inhibited by reduction of the ubiquinone pool, and that this explains the confusion over which esters of CoA and carnitine accumulate during cardiac ischaemia. Furthermore these studies demonstrate that the site of the control exerted by the respiratory chain over β-oxidation is shifted depending on the extent of the inhibition of the respiratory chain.

scholarly journals Reactive nitrogen and oxygen species metabolism in rat heart mitochondria upon administration of NO donor in vivo

2012 ◽  
Vol 58 (2) ◽  
pp. 3-15 ◽  
Author(s):  
OV Akopova ◽  
◽  
IuP Korkach ◽  
AV Kotsiuruba ◽  
LI Kolchyns'ka ◽  
...  
Keyword(s):  
Rat Heart ◽  
Heart Mitochondria ◽  
Reactive Nitrogen ◽  
Oxygen Species ◽  
No Donor ◽  
Rat Heart Mitochondria

Increased uncoupling proteins and decreased efficiency in palmitate-perfused hyperthyroid rat heart

2001 ◽  
Vol 280 (3) ◽  
pp. H977-H983 ◽  
Author(s):  
Ernest A. Boehm ◽  
Barney E. Jones ◽  
George K. Radda ◽  
Richard L. Veech ◽  
Kieran Clarke
Keyword(s):  
Rat Heart ◽  
Physiological Role ◽  
Physiological Effect ◽  
Uncoupling Proteins ◽  
Heart Mitochondria ◽  
Acid Oxidation ◽  
Mitochondrial Uncoupling ◽  
Myocardial Efficiency ◽  
Rat Heart Mitochondria

The physiological role of mitochondrial uncoupling proteins (UCPs) in heart and skeletal muscle is unknown, as is whether mitochondrial uncoupling of oxidative phosphorylation by fatty acids occurs in vivo. In this study, we found that UCP2 and UCP3 protein content, determined using Western blotting, was increased by 32 and 48%, respectively, in hyperthyroid rat heart mitochondria. Oligomycin-insensitive respiration rate, a measure of mitochondrial uncoupling, was increased in all mitochondria in the presence of palmitate: 36% in controls and 71 and 100% with 0.8 and 0.9 mM palmitate, respectively, in hyperthyroid rat heart mitochondria. In the isolated working heart, 0.4 mM palmitate significantly lowered cardiac output by 36% and cardiac efficiency by 38% in the hyperthyroid rat heart. Thus increased mitochondrial UCPs in the hyperthyroid rat heart were associated with increased uncoupling and decreased myocardial efficiency in the presence of palmitate. In conclusion, a physiological effect of UCPs on fatty acid oxidation has been found in heart at the mitochondrial and whole organ level.

Magnolol and honokiol isolated from magnolia officinalis protect rat heart mitochondria against lipid peroxidation

1994 ◽  
Vol 47 (3) ◽  
pp. 549-553 ◽  
Author(s):  
Yu-Chiang Lo ◽  
Teng Che-Ming ◽  
Chen Chieh-Fu ◽  
Chen Chien-Chih ◽  
Hong Chuang-Ye
Keyword(s):  
Lipid Peroxidation ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Rat Heart Mitochondria ◽  
Magnolia Officinalis

Involvement of SH-groups during interaction of diazoxide with the inner membrane of rat heart mitochondria

2007 ◽  
Vol 415 (1) ◽  
pp. 206-210 ◽  
Author(s):  
S. M. Korotkov ◽  
V. P. Nesterov ◽  
L. V. Emel’yanova ◽  
N. N. Ryabchikov
Keyword(s):  
Rat Heart ◽  
Heart Mitochondria ◽  
Inner Membrane ◽  
Sh Groups ◽  
Rat Heart Mitochondria
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