scholarly journals Flight-muscle mitochondria of Lucilia cuprina and Musca domestica. Estimation of the pyridine nucleotide content and of the response of respiration to adenosine diphosphate

1961 ◽  
Vol 80 (3) ◽  
pp. 623-631 ◽  
Author(s):  
LM Birt
Keyword(s):  
Musca Domestica ◽  
Flight Muscle ◽  
Adenosine Diphosphate ◽  
Pyridine Nucleotide ◽  
Lucilia Cuprina ◽  
Muscle Mitochondria ◽  
Nucleotide Content

scholarly journals Inability of tributyltin-induced chloride/hydroxyl exchange to stimulate calcium transport in mitochondria isolated from flight muscle of the sheep blowfly Lucilia cuprina

1978 ◽  
Vol 174 (3) ◽  
pp. 1075-1077 ◽  
Author(s):  
Fyfe L. Bygrave ◽  
Robyn L. Smith
Keyword(s):  
Calcium Transport ◽  
Flight Muscle ◽  
Initial Rate ◽  
Mitochondrial Protein ◽  
Lucilia Cuprina ◽  
Muscle Mitochondria ◽  
Transport In Mitochondria

Tributyltin in the concentration range 1–4μm failed to stimulate Ca2+ transport by Lucilia flight-muscle mitochondria in a medium containing KCl and respiratory substrate but devoid of Pi, despite its promotion of a rapid Cl−/OH− exchange. When 2mm-Pi was present, concentrations of tributyltin greater than 1μm inhibited the initial rate of Ca2+ transport and induced efflux of the ion from the mitochondria in Cl−- or NO3−-containing media. Lower concentrations had little effect. Oligomycin added at up to 10μg/mg of mitochondrial protein had no effect on Ca2+ transport. By contrast, approx. 0.3μm-tributyltin completely inhibited respiration supported by α-glycerophosphate in either the presence or absence of added ADP. The data suggest that tributyltin can inhibit Ca2+ transport in Lucilia flight-muscle mitochondria other than by facilitating a Cl−/OH− exchange or producing an oligomycin-like effect.

scholarly journals The effect of the coupled oxidation of substrate on the permeability of blowfly flight-muscle mitochondria to potassium and other cations

1972 ◽  
Vol 126 (3) ◽  
pp. 689-700 ◽  
Author(s):  
R. G. Hansford ◽  
A. L. Lehninger
Keyword(s):  
Light Scattering ◽  
Flight Muscle ◽  
Unit Area ◽  
Membrane Surface ◽  
Mitochondrial Matrix ◽  
Exposed Area ◽  
Muscle Mitochondria ◽  
Area 5 ◽  
Choline Phosphate ◽  
Permeant Anion

1. Blowfly flight-muscle mitochondria respiring in the absence of phosphate acceptor (i.e. in state 4) take up greater amounts of K+, Na+, choline, phosphate and Cl-(but less NH4+) than non-respiring control mitochondria. 2. Uptake of cations is accompanied by an increase in the volume of the mitochondrial matrix, determined with the use of [14C]-sucrose and3H2O. The osmolarity of the salt solution taken up was approximately that of the suspending medium. 3. The [14C]sucrose-inaccessible space decreased with increasing osmolarity of potassium chloride in the suspending medium, confirming that the blowfly mitochondrion behaves as an osmometer. 4. Light-scattering studies showed that both respiratory substrate and a permeant anion such as phosphate or acetate are required for rapid and massive entry of K+, which occurs in an electrophoretic process rather than in exchange for H+. The increase in permeability to K+and other cations is probably the result of a large increase in the exposed area of inner membrane surface in these mitochondria, with no intrinsic increase in the permeability per unit area. 5. No increase in permeability to K+and other cations occurs during phosphorylation of ADP in state 3 respiration.

scholarly journals Impaired erythrocyte phosphoribosylpyrophosphate formation in hemolytic anemia due to pyruvate kinase deficiency

Blood ◽  
1988 ◽  
Vol 72 (2) ◽  
pp. 500-506 ◽  
Author(s):  
CR Zerez ◽  
MD Wong ◽  
NA Lachant ◽  
KR Tanaka
Keyword(s):  
Pyruvate Kinase ◽  
Hemolytic Anemia ◽  
Adenosine Triphosphate ◽  
Pyridine Nucleotide ◽  
Pentose Phosphate ◽  
Atp Depletion ◽  
Pyridine Nucleotides ◽  
Pyruvate Kinase Deficiency ◽  
Nucleotide Content ◽  
Pentose Phosphate Shunt

Abstract RBCs from patients with hemolytic anemia due to pyruvate kinase (PK) deficiency are characterized by a decreased total adenine and pyridine nucleotide content. Because phosphoribosylpyrophosphate (PRPP) is a precursor of both adenine and pyridine nucleotides, we investigated the ability of intact PK-deficient RBCs to accumulate PRPP. The rate of PRPP formation in normal RBCs (n = 11) was 2.89 +/- 0.80 nmol/min.mL RBCs. In contrast, the rate of PRPP formation in PK-deficient RBCs (n = 4) was markedly impaired at 1.03 +/- 0.39 nmol/min.mL RBCs. Impaired PRPP formation in these cells was not due to the higher proportion of reticulocytes. To study the mechanism of impaired PRPP formation, PK deficiency was simulated by incubating normal RBCs with fluoride. In normal RBCs, fluoride inhibited PRPP formation, caused adenosine triphosphate (ATP) depletion, prevented 2,3-diphosphoglycerate (DPG) depletion, and inhibited pentose phosphate shunt (PPS) activity. These results together with other data suggest that impaired PRPP formation is mediated by changes in ATP and DPG concentration, which lead to decreased PPS and perhaps decreased hexokinase and PRPP synthetase activities. Impaired PRPP formation may be a mechanism for the decreased adenine and pyridine nucleotide content in PK-deficient RBCs.

scholarly journals The role of dietary niacin intake and the adenosine-5′-diphosphate-ribosyl cyclase enzyme CD38 in spatial learning ability: is cyclic adenosine diphosphate ribose the link between diet and behaviour?

2008 ◽  
Vol 21 (1) ◽  
pp. 42-55 ◽  
Author(s):  
Genevieve S. Young ◽  
James B. Kirkland
Keyword(s):  
Spatial Learning ◽  
Young Male ◽  
Adenosine Diphosphate ◽  
Pyridine Nucleotide ◽  
Learning Ability ◽  
Learning Performance ◽  
Male Rats ◽  
Current Evidence ◽  
Niacin Deficiency ◽  
The Brain

The pyridine nucleotide NAD+is derived from dietary niacin and serves as the substrate for the synthesis of cyclic ADP-ribose (cADPR), an intracellular Ca signalling molecule that plays an important role in synaptic plasticity in the hippocampus, a region of the brain involved in spatial learning. cADPR is formed in part via the activity of the ADP-ribosyl cyclase enzyme CD38, which is widespread throughout the brain. In the present review, current evidence of the relationship between dietary niacin and behaviour is presented following investigations of the effect of niacin deficiency, pharmacological nicotinamide supplementation and CD38 gene deletion on brain nucleotides and spatial learning ability in mice and rats. In young male rats, both niacin deficiency and nicotinamide supplementation significantly altered brain NAD+and cADPR, both of which were inversely correlated with spatial learning ability. These results were consistent across three different models of niacin deficiency (pair feeding, partially restricted feeding and niacin recovery). Similar changes in spatial learning ability were observed inCd38− / − mice, which also showed decreases in brain cADPR. These findings suggest an inverse relationship between spatial learning ability, dietary niacin intake and cADPR, although a direct link between cADPR and spatial learning ability is still missing. Dietary niacin may therefore play a role in the molecular events regulating learning performance, and further investigations of niacin intake, CD38 and cADPR may help identify potential molecular targets for clinical intervention to enhance learning and prevent or reverse cognitive decline.

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