Effect of idebenone on adenosine outflow and adenine nucleotide level in hippocampal slices under ischemia-like conditions

1993 ◽  
Vol 249 (1-2) ◽  
pp. 65-70 ◽  
Author(s):  
Serena Latini ◽  
Felicita Pedata ◽  
Giancarlo Pepeu
Hepatology ◽  
1988 ◽  
Vol 8 (3) ◽  
pp. 471-475 ◽  
Author(s):  
Amos Lanir ◽  
Roger L. Jenkins ◽  
Cary Caldwell ◽  
Robert G. L. Lee ◽  
Urmila Khettry ◽  
...  

2005 ◽  
Vol 30 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Rafael Nicolaidis ◽  
Alessandra Nejar Bruno ◽  
João José Freitas Sarkis ◽  
Diogo Onofre Souza

1984 ◽  
Vol 247 (3) ◽  
pp. H380-H386 ◽  
Author(s):  
H. Meno ◽  
H. Kanaide ◽  
M. Okada ◽  
M. Nakamura

We studied the relation between the contractility and metabolic changes in reperfusion after ischemia, and the effect of diltiazem on these changes, in an isolated rat heart perfused using the Langendorff method. After aerobic perfusion at 80 cmH2O, the perfusion pressure was reduced to 10 cmH2O to induce global ischemia. Substrate was removed from the perfusate during ischemia. After 30 or 60 min of ischemia, the heart was reperfused in an aerobic condition. During ischemia, the total adenine nucleotide level (TAN: sum of ATP, ADP, and AMP) was progressively reduced and the ATP-to-ADP ratio was one-third of the value obtained in an aerobic condition. With 30 min of subsequent reperfusion, ATP increased, and the shorter the duration of ischemia, the closer ATP/ADP approached the value of an aerobic condition, whereas TAN was equivalent to the value shown immediately before reperfusion. Thus the degree of ATP recovery by reperfusion mainly depends on the amount of TAN immediately before reperfusion and the mitochondrial function of oxidative phosphorylation that determines ATP/ADP. The calcium transport activity of the sarcoplasmic reticulum of myocardial cells was affected by ischemia and showed no amelioration or further deterioration by subsequent reperfusion. When diltiazem (10(-5)M) was added to the perfusate continuously from 5 min before ischemia, during ischemia, and until 10 min of reperfusion, the amount of TAN in ischemia and reperfusion and the calcium transport activity during reperfusion were maintained at relatively high levels. The degree of contractility recovery by reperfusion showed direct correlations with both the tissue ATP amount and the level of calcium transport activity in the sarcoplasmic reticulum.


Author(s):  
C.A. Mannella ◽  
K.F. Buttle ◽  
K.A. O‘Farrell ◽  
A. Leith ◽  
M. Marko

Early transmission electron microscopy of plastic-embedded, thin-sectioned mitochondria indicated that there are numerous junctions between the outer and inner membranes of this organelle. More recent studies have suggested that the mitochondrial membrane contacts may be the site of protein complexes engaged in specialized functions, e.g., import of mitochondrial precursor proteins, adenine nucleotide channeling, and even intermembrane signalling. It has been suggested that the intermembrane contacts may be sites of membrane fusion involving non-bilayer lipid domains in the two membranes. However, despite growing interest in the nature and function of intramitochondrial contact sites, little is known about their structure.We are using electron microscopic tomography with the Albany HVEM to determine the internal organization of mitochondria. We have reconstructed a 0.6-μm section through an isolated, plasticembedded rat-liver mitochondrion by combining 123 projections collected by tilting (+/- 70°) around two perpendicular tilt axes. The resulting 3-D image has confirmed the basic inner-membrane organization inferred from lower-resolution reconstructions obtained from single-axis tomography.


1980 ◽  
Vol 43 (02) ◽  
pp. 099-103 ◽  
Author(s):  
J M Whaun ◽  
P Lievaart ◽  

SummaryBlood from normal full term infants, mothers and normal adults was collected in citrate. Citrated platelet-rich plasma was prelabelled with 3H-adenine and reacted with release inducers, collagen and adrenaline. Adenine nucleotide metabolism, total adenine nucleotide levels and changes in sizes of these pools were determined in platelets from these three groups of subjects.At rest, the platelet of the newborn infant, compared to that of the mother and normal adult, possessed similar amounts of adenosine triphosphate (ATP), 4.6 ± 0.2 (SD), 5.0 ± 1.1, 4.9 ± 0.6 µmoles ATP/1011 platelets respectively, and adenosine diphosphate (ADP), 2.4 ± 0.7, 2.8 ± 0.6, 3.0 ± 0.3 umoles ADP/1011 platelets respectively. However the marked elevation of specific radioactivity of ADP and ATP in these resting platelets indicated the platelet of the neonate has decreased adenine nucleotide stores.In addition to these decreased stores of adenine nucleotides, infant platelets showed significantly impaired release of ADP and ATP on exposure to collagen. The release of ADP in infants, mothers, and other adults was 0.9 ± 0.5 (SD), 1.5 ± 0.5, 1.5 ± 0.1 umoles/1011 platelets respectively; that of ATP was 0.6 ± 0.3, 1.0 ± 0.1,1.3 ± 0.2 µmoles/1011 platelets respectively. With collagen-induced release, platelets of newborn infants compared to those of other subjects showed only slight increased specific radioactivities of adenine nucleotides over basal levels. The content of metabolic hypoxanthine, a breakdown product of adenine nucleotides, increased in both platelets and plasma in all subjects studied.In contrast, with adrenaline as release inducer, the platelets of the newborn infant showed no adenine nucleotide release, no change in total ATP and level of radioactive hypoxanthine, and minimal change in total ADP. The reason for this decreased adrenaline reactivity of infant platelets compared to reactivity of adult platelets is unknown.Infant platelets may have different membranes, with resulting differences in regulation of cellular processes, or alternatively, may be refractory to catecholamines because of elevated levels of circulating catecholamines in the newborn period.


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