INCORPORATION OF RADIOACTIVE PHOSPHATE INTO NON-NUCLEOTIDE PROTEIN-BOUND PHOSPHORUS FRACTIONS OF RESPIRING CAT BRAIN SLICES

1954 ◽  
Vol 32 (5) ◽  
pp. 504-514 ◽  
Author(s):  
Muriel Findlay ◽  
K. P. Strickland ◽  
R. J. Rossiter

Slices of cat brain respiring in a Krebs–Ringer bicarbonate medium were found to incorporate inorganic phosphate labelled with P32 into two non-nucleotide protein-bound phosphorus fractions, which are referred to as the residue organic phosphorus (ROP) and the "phosphoprotein" (PP), respectively. The addition of glucose or mannose to the medium increased the incorporation into both fractions. The addition of fructose, galactose, pyruvate, lactate, succinate, or L-glutamate failed to increase the incorporation into either fraction.Anaerobic conditions, homogenization of the tissue, or the addition of a wide range of metabolic inhibitors (cyanide, azide, iodoacetate, fluoride, nembutal, malononitrile, chloretone) inhibited the incorporation. The incorporation was also inhibited by 2,4-dinitrophenol in concentrations that do not inhibit oxygen consumption.These results are compared and contrasted with previous findings on the incorporation of P32 into the lipid phosphorus and pentosenucleic acid of brain slices.

1954 ◽  
Vol 32 (1) ◽  
pp. 504-514
Author(s):  
Muriel Findlay ◽  
K. P. Strickland ◽  
R. J. Rossiter

Slices of cat brain respiring in a Krebs–Ringer bicarbonate medium were found to incorporate inorganic phosphate labelled with P32 into two non-nucleotide protein-bound phosphorus fractions, which are referred to as the residue organic phosphorus (ROP) and the "phosphoprotein" (PP), respectively. The addition of glucose or mannose to the medium increased the incorporation into both fractions. The addition of fructose, galactose, pyruvate, lactate, succinate, or L-glutamate failed to increase the incorporation into either fraction.Anaerobic conditions, homogenization of the tissue, or the addition of a wide range of metabolic inhibitors (cyanide, azide, iodoacetate, fluoride, nembutal, malononitrile, chloretone) inhibited the incorporation. The incorporation was also inhibited by 2,4-dinitrophenol in concentrations that do not inhibit oxygen consumption.These results are compared and contrasted with previous findings on the incorporation of P32 into the lipid phosphorus and pentosenucleic acid of brain slices.


1954 ◽  
Vol 32 (1) ◽  
pp. 50-59 ◽  
Author(s):  
K. P. Strickland

Slices of cat brain respiring in a Krebs–Ringer bicarbonate medium were found to incorporate radioactive inorganic phosphate (P32) into the phospholipid fraction. The addition of glucose or mannose increased the incorporation of P32 into the phospholipids. Fructose caused a small increase, whereas galactose was without effect. Pyruvate and lactate increased the incorporation of P32 into the phospholipids. Succinate, L (+)-glutamate, D (−)-glutamate, α keto-glutarate, citrate, and L-malate failed to support the incorporation.Anaerobic conditions and homogenization of the tissue prevented the in vitro incorporation of P32 into the phospholipids of cat brain. A wide range of metabolic inhibitors (cyanide, azide, malononitrile, chloretone, nembutal, iodoacetate, and fluoride), in concentrations that inhibit the oxygen consumption of brain slices, inhibited the incorporation. The incorporation was also inhibited by 2,4-dinitrophenol in concentrations that do not decrease the oxygen consumption of brain slices.These findings indicated that the incorporation of P32 into the phospholipids of slices of cat brain is a metabolic phenomenon and is dependent upon the maintenance of an adequate phosphorylating mechanism within the slice.


1954 ◽  
Vol 32 (1) ◽  
pp. 50-59 ◽  
Author(s):  
K. P. Strickland

Slices of cat brain respiring in a Krebs–Ringer bicarbonate medium were found to incorporate radioactive inorganic phosphate (P32) into the phospholipid fraction. The addition of glucose or mannose increased the incorporation of P32 into the phospholipids. Fructose caused a small increase, whereas galactose was without effect. Pyruvate and lactate increased the incorporation of P32 into the phospholipids. Succinate, L (+)-glutamate, D (−)-glutamate, α keto-glutarate, citrate, and L-malate failed to support the incorporation.Anaerobic conditions and homogenization of the tissue prevented the in vitro incorporation of P32 into the phospholipids of cat brain. A wide range of metabolic inhibitors (cyanide, azide, malononitrile, chloretone, nembutal, iodoacetate, and fluoride), in concentrations that inhibit the oxygen consumption of brain slices, inhibited the incorporation. The incorporation was also inhibited by 2,4-dinitrophenol in concentrations that do not decrease the oxygen consumption of brain slices.These findings indicated that the incorporation of P32 into the phospholipids of slices of cat brain is a metabolic phenomenon and is dependent upon the maintenance of an adequate phosphorylating mechanism within the slice.


1989 ◽  
Vol 256 (4) ◽  
pp. H1165-H1175 ◽  
Author(s):  
J. N. Weiss ◽  
S. T. Lamp ◽  
K. I. Shine

It has been suggested that increased K+ efflux during myocardial hypoxia and ischemia may result from efflux of intracellularly generated anions such as lactate and inorganic phosphate (Pi) as a mechanism of balancing transsarcolemmal charge movement. To investigate this hypothesis cellular K+ loss using 42K+ and K+-sensitive electrodes, intracellular potential, venous lactate and Pi, and tissue lactate and high-energy phosphates were measured in isolated arterially perfused rabbit interventricular septa during exposure to metabolic inhibitors, hypoxia, and ischemia. Selective inhibition of glycolysis caused a marked increase in K+ efflux despite a fall in lactate production and maintenance of normal cellular high-energy phosphate content. During ischemia and hypoxia net loss of lactate and Pi exceeded K+ loss by a factor of 2-6. However, removal of glucose prior to ischemia or during hypoxia increased K+ loss but reduced lactate loss without affecting Pi loss. During hypoxia, 30 mM exogenous lactate did not alter K+ loss in a manner consistent with changes in passive electrodiffusion of lactate ion. These findings inhibition which is not related to anion efflux assumes greater importance under conditions in which glycolysis is inhibited, e.g., ischemia. Under conditions in which glycolysis is not inhibited, e.g., hypoxia, K+ efflux does not parallel passive electrodiffusion of lactate ions. However, this finding does not exclude the possibility that K+ loss could be coupled to carrier-mediated lactate ion efflux.


1969 ◽  
Vol 20 (4) ◽  
pp. 653 ◽  
Author(s):  
OL Jones ◽  
SM Bromfield

Ground samples of hayed-off pasture plants were decomposed in the laboratory under continuously moist, and intermittently moist and dry, conditions. During the course of decomposition they were leached at different frequencies and the resulting changes in inorganic and organic phosphorus measured. The dissolution of superphosphate and its conversion to organic phosphorus were also studied under some of these conditions.Inorganic phosphate was readily leached from the samples when microbes were inhibited. Microbial activity, on the other hand, largely prevented the loss of inorganic phosphate by leaching from a phalaris sample over a period of 3 months. Intermittent drying increased the amount of phosphate leached from decomposing plants but the leaching frequencies examined had little effect. The percentage of the phosphorus leached from plants varied with the type of material. In all cases less than half was recovered as inorganic phosphate, even after decomposition and leaching for 6 months. When superphosphate granules were leached in the presence of decomposing plants the conversion of fertilizer phosphate to organic phosphorus was small, but the dissolution of phosphate was sometimes retarded. The recycling of phosphate in hayed-off pastures is discussed in the light of these results.


2019 ◽  
Vol 7 (4) ◽  
pp. 96 ◽  
Author(s):  
Senjie Lin ◽  
Liying Yu ◽  
Huan Zhang

Coral reef-associated Symbiodiniaceae live in tropical and oligotrophic environments and are prone to heat and nutrient stress. How their metabolic pathways respond to pulses of warming and phosphorus (P) depletion is underexplored. Here, we conducted RNA-seq analysis to investigate transcriptomic responses to thermal stress, phosphate deprivation, and organic phosphorus (OP) replacement in Fugacium kawagutii. Using dual-algorithm (edgeR and NOIseq) to remedy the problem of no replicates, we conservatively found 357 differentially expressed genes (DEGs) under heat stress, potentially regulating cell wall modulation and the transport of iron, oxygen, and major nutrients. About 396 DEGs were detected under P deprivation and 671 under OP utilization, both mostly up-regulated and potentially involved in photosystem and defensome, despite different KEGG pathway enrichments. Additionally, we identified 221 genes that showed relatively stable expression levels across all conditions (likely core genes), mostly catalytic and binding proteins. This study reveals a wide range of, and in many cases previously unrecognized, molecular mechanisms in F. kawagutii to cope with heat stress and phosphorus-deficiency stress. Their quantitative expression dynamics, however, requires further verification with triplicated experiments, and the data reported here only provide clues for generating testable hypotheses about molecular mechanisms underpinning responses and adaptation in F. kawagutii to temperature and nutrient stresses.


Genetics ◽  
1975 ◽  
Vol 80 (2) ◽  
pp. 239-250
Author(s):  
R F Matagne ◽  
R Loppes

ABSTRACT In the green alga Chlamydomonas reinhardi, removal of inorganic phosphate from the culture medium results in the increase of phosphatase activity (derepression) in the wild-type (WT) strain as well as in a double mutant (P2Pa) lacking the two main constitutive acid phosphatases. Following treatment of WT and P2Pa with N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), mutants were recovered which display very low phosphatase activities when grown in the absence of phosphate; as shown by electrophoresis, they lack one non-migrating phosphatase (PD mutants). This enzyme is active over a wide range of pH with an optimum at pH 7.5. The comparison of electropherograms from WT and mutants grown on media with or without phosphate allowed us to provide a tentative definition of the pool of derepressible phosphatases in Chlamydomonas : in addition to the neutral phosphatase lacking in PD mutants, Chlamydomonas produces two electrophoretic forms of alkaline phosphatase showing an optimal activity at pH 9.5.


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