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Pyridine nucleotide levels

M. Ju.szczuk and A. M. Rychter, Changes in pyridine nucleotide levels in leaves and roots of bean plants Phaseolus vtilgans L.) during phosphate deficiency. J. Plant Physiol. 151 399 (1997). [Pg.84]

B. Chance, B. Schoener, and S. Elsaesser, Control of the waveform of oscillations of the reduced pyridine nucleotide level in a cell-free extract. Proc. Natl. Acad. Sci. USA 52, 337-341 (1964). [Pg.287]

MAXIMAL FLUORESCENCE, ADENINE AND PYRIDINE NUCLEOTIDE LEVELS IN CHLAMYDOMONAS R. [Pg.2815]

Jacobson EL, Jacobson MK (1976) Pyridine nucleotide levels as a function of growth in normal and transformed 3T3 cells. Arch Biochem Biophys 175 627-634... [Pg.128]

DCMU inhibitory effect on linoleate desaturation appeared in 24 hours after the beginning of pea shoot incubation with l- C oleate the percentage of C-linolenate decreased twice in the presence of DCMU (Tabl. 1). On the one hand, the li-nolenate percentage decrease may be caused by the decrease of the reduced pyridine nucleotide level in the cells in the presence of DCMU. Besides, the possibility of electron transfer to linoleate desaturase both from NADPH and from H2O may be... [Pg.159]

The rise in liver DPN in the mouse is correlated with the concentration of nicotinamide injected, as illustrated in Fig. 4. High concentrations (2000 mg/kg) of the amide are inhibitory to the synthesis of the DPN. The maximum increase is around tenfold and usually occurs from 8 to 10 hr following the administration of the nicotinamide the DPN level then returns to normal at the end of about 20 to 24 hr after the injection. It is of considerable interest to note that the pyridine nucleotide level always drops to the normal base level and not below the original value. [Pg.649]

The increase in pyridine nucleotide level is largely in the form of oxidized DPN there is little rise in DPNH, TPN, or TPNH. The increase is limited to the soluble fraction of the liver there is no detectable change in the pyridine nucleotide concentration of the mitochondria. [Pg.650]

Fio. 9. Effect of azaeerine on the pyridine nucleotide level of mouse liver. Determinations were made on a 6% (w/w) trichloroacetic acid extract of mouse liver. Each value represents the pooled samples of two mice. Curve 1, saline control curve 2, asaserine-injected animals. From Narrod et al. (ttO). [Pg.659]

R8. Rees, E. D., and Huggins, C., Steroid influences on respiration, glycolysis and levels of pyridine nucleotide linked dehydrogenases of experimental mammary cancers. Cancer Research 20, 963-971 (1960). [Pg.305]

Keilin soon realized that three of the absorption bands, those at 604,564, and 550 nm (a, b, and c), represented different pigments, while the one at 521 nm was common to all three. Keilin proposed the names cytochromes a, b, and c. The idea of an electron transport or respiratory chain followed6 quickly as the flavin and pyridine nucleotide coenzymes were recognized to play their role at the dehydrogenase level. Hydrogen removed from substrates by these carriers could be used to oxidize reduced cytochromes. The latter would be oxidized by oxygen under the influence of cytochrome oxidase. [Pg.1022]

Biological autofluorescence in mammalian cells due to flavin coenzymes (FAD and FMN absorption, 450 nm emission, 515 nm) and reduced pyridine nucleotides (NADH absorption, 340 nm emission, 460 nm) can be problematic in the detection of fluorescence probes in tissues and cells. Fixation with aldehydes, particularly glutaraldehyde, can result in high levels of autofluorescence. This can be minimized in fixed cells by washing with 0.1% sodium borohydride in phosphate-buffered saline (5) prior to antibody incubation. Problems due to autofluorescence can be minimized by selecting probes and optical filters that maximize the fluorescence signal relative to the autofluorescence. Other factors that limit IF include the performance of the detection instrument (i.e. how well the microscope has been calibrated and set), the specificity of the antibodies, and the specimen preparation. [Pg.64]

Isolated lettuce chloroplasts could epoxidize zeaxanthin in the presence of reduced pyridine nucleotides and oxygen and the process was stimulated by bovine serum albumin (which protected the epoxidase system from inhibition by fatty acids). Detailed study led to the conclusion that the epoxidase was an external monoxygenase and that the violaxanthin cycle (of which epoxidation of zeaxanthin is a part) was a trans-membrane system wherein de-epoxidation took place on the loculus side and epoxidation on the stroma side of the membrane. This arrangement requires migration of the carotenoids of the violaxanthin cycle across the membrane in a type of shuttle. The possible role of this cycle in some regulatory mechanism of photosynthesis at the membrane level was also discussed. [Pg.217]

Nicotinamide adenine dinucleotide (NAD and its reduced form dihydronicotinamide adenine dinucleotide (NADH)) as well as nicotinamide adenine dinucleotide phosphate (NADP and its reduced form nicotinamide adenine dinucleotide phosphate hydrogen (NADPH)) are essential co-factors for many dehydrogenases. The presence of NAD was first demonstrated in P. gallinaceum (Speck and Evans, 1945) and later studies showed increased levels of these pyridine nucleotides in P. lophurae, P. berghei and P. falciparum. Trager (1977) reported that high levels of... [Pg.258]

Sherman, I. W. (1966c). Levels of oxidized and reduced pyridine nucleotides in avian malaria (Plasmodium lophurae). Am. J. Trop. Med. Hyg. 15,814-817. [Pg.377]

It is possible that the apparent lack of pyridine nucleotide specificity exhibited by the angiosperm enzyme could be explained by the conversion of NADPH to NADH by transdehydrogenase or phosphatase. However these would have to be absent or at least present at very low levels in root nodules and also from bacteria and fungi. Further work is necessary to establish whether the dual specificity of the angiosperm enzyme is an artifiict or, if real, is indicative of two forms of the enzyme or a single form with dual specificity. [Pg.313]

Deoxy sugars may be formed by direct reduction at the level of nucleotides by pyridine nucleotide-dependent... [Pg.250]

Release of Ca from intact rat liver mitochondria can be induced by oxidation of mitochondrial pyridine nucleotides. This was first shown by the group of Lehninger [8] who oxidized mitochondrial pyridine nucleotides with acetoacetate or oxaloacetate at the level of the citric add cycle. Our group [9 used hydroperoxides, known to be produced by the respiratory chain of mitochondria and to be linked to pyridine nucleotides by glutathione peroxidase and reductase, to induce Ca release and oxidation of pyridine nucleotides. Orrenius and co-workers employed [10] menadione (2-methyl-l, 4-naphthoquinone) to induce pyridine nucleotide oxidation and Ca release. The latter... [Pg.531]

Why might it be desirable to coordinately lower the levels of nicotinamide deamidase The 8-fold depression in nicotinamide deamidase activity causes excretion of nicotinamide xthR mutants have shown to be "feeders" for nicotinamide auxotrophs, indicating that these strains continuously excrete nicotinamide into the medium. This is presumably a consequence of the pyridine nucleotide cycle, shown in Fig. 2. Nicotinamide deamidase is not only an enzyme for the salvage of exogenous pyridine, but it is part of a NAD recycling pathway, i.e., a "pyridine nucleotide cycle"... [Pg.356]


See other pages where Pyridine nucleotide levels is mentioned: [Pg.39]    [Pg.659]    [Pg.39]    [Pg.659]    [Pg.385]    [Pg.56]    [Pg.86]    [Pg.357]    [Pg.243]    [Pg.219]    [Pg.5]    [Pg.91]    [Pg.56]    [Pg.298]    [Pg.110]    [Pg.158]    [Pg.281]    [Pg.285]    [Pg.110]    [Pg.158]    [Pg.36]    [Pg.387]    [Pg.252]    [Pg.91]    [Pg.712]    [Pg.358]    [Pg.382]    [Pg.62]    [Pg.271]    [Pg.311]    [Pg.2783]   
See also in sourсe #XX -- [ Pg.38 , Pg.39 ]




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