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At least 19 recordsLinked to original sources

Effect of oral melatonin administration on melatonin, 5-hydroxyindoleacetic acid, indoleacetic acid, and cyclic nucleotides in human cerebrospinal fluid.

Melatonin was given orally to patients undergoing diagnostic pneumoencephalography and various compounds were measured in the lumbar and cisternal CSF. Melatonin markedly increased plasma and CSF melatonin concentrations. The plasma: CSF melatonin ratios were similar in patients who received, and in those who did not receive, melatonin. This supports the idea that melatonin is released from pineal to blood and gets into the CSF via the blood. Melatonin did not affect CSF 5-hydroxyindoleacetic acid, which indicates that it has no effect on 5-hydroxytryptamine metabolism. Melatonin increased CSF indoleacetic acid significantly, indicating increased metabolism of tryptamine. Melatonin did not affect CSF cAMP levels, but increased cGMP levels. The effect on indoleacetic acid and cGMP was seen in both lumbar and cisternal CSF, suggesting that melatonin can have generalized actions throughout the CNS.

Adolescent↗

Effect of abscisic acid, gibberellic acid, indoleacetic acid, and kinetin on selective ribosomal cistron regulation in quiescent and senescent onion leaf base tissue.

Small pieces of tissue from the basal, equatorial, near-apical, and apical regions of the third turgid onion leaf base were treated (3 and 6 h in the dark) with abscisic acid (ABA), gibberellic acid (GA3), indoleacetic acid (IAA), and kinetin (K) and compared with responses in water controls. ABA inhibited the activation (increase in size and changes in morphologies from round or oval to elongated-oval and dumbbell) of major nucleolar organizer regions (NORs) in basal, equatorial, and near-apical tissue. GA3 and K activated the major NORs in the basal, equatorial, and near-apical tissue. IAA stimulated the activation of major NORs in basal tissue but inhibited their activation in equatorial and near-apical tissue. No major nucleoli were activated in control or plant growth regulator-treated apical tissue. Minor NORs were not expressed in the control and plant growth regulator-treated tissue in these four locations. Actinomycin D and cycloheximide inhibited major NOR activation in equatorial control and kinetin-treated tissue. We propose that ABA, GA3, IAA, and K are major NOR regulators. We infer that the basal through near-apical cells were quiescent during post-harvest storage and that the cells in the apical tissue had senesced beyond the point of no return (degeneration of the karyoskeleton) in the cellular senescence pathway.

Abscisic Acid↗

Tryptophan, 5-hydroxyindoleacetic acid and indoleacetic acid in human cerebrospinal fluid: interrelationships and the influence of age, sex, epilepsy and anticonvulsant drugs.

Tryptophan, 5-hydroxyindoleacetic acid and indoleacetic acid were measured in cerebrospinal fluid, taken during pneumoencephalography, from a large series of patients, the majority of whom were epileptics, most of them receiving anticonvulsants. CSF indoleacetic acid reflects CNS tyrptamine metabolism in the same way that CSF 5-hydroxyindoleacetic acid reflects CNS 5-hydroxytryptamine metabolism. Our data suggest that (i) the brain tryptophan content is an important factor in the control of both 5-hydroxytryptamine and tryptamine synthesis (ii) brain 5-hydroxytryptamine metabolism exhibits a U-shaped relationship with age (iii) the mean brain tryptophan content and rate of 5-hydroxytryptamine metabolism are greater for women than men (iv) indoleamine metabolism is unaffected in untreated epileptics compared with non-epileptics, but anticonvulsant drugs decrease the rate of 5-hydrosytryptamine metabolism.

Adult↗

Effect of tryptophan administration on tryptophan, 5-hydroxyindoleacetic acid and indoleacetic acid in human lumbar and cisternal cerebrospinal fluid.

Tryptophan 5-hydroxyindoleacetic acid and indoleacetic acid were measured in cerebrospinal fluid taken during pneumoencephalography from patients, some of whom took a 3 g or 6 g tryptophan load at various times before. Measurements were made on both lumbar and cisternal cerebrospinal fluid and the results showed similarities between indoleamine metabolism in human brain and spinal cord. Our data suggested that (1) the blood-brain barrier active transport system for tryptophan is not far from saturation with tryptophan and the rate-limiting enzyme in 5-hydroxytryptamine (5HT) synthesis, tryptophan hydroxylase, is about half saturated. Therefore, both 3 g and 6 g tryptophan loads produced the same maximum rise in 5HT synthesis of just under 100%, (2) tryptamine differs from 5HT in two respects. It is more sensitive to changes in tryptophan availability than 5HT and the 6 g load increased brain tryptamine metabolism more than the 3 g load; also some of the tryptamine in brain is derived from peripheral sources and diffuses from blood to brain, (3) although the brain tryptamine content is much lower than that of 5HT, its rate of metabolism as indicated by CSF metabolite levels is not. In controls the rate of tryptamine metabolism is 15% of the rate of 5HT metabolism and this can increase to 40% after a 6 g tryptophan load.

Adolescent↗

Involvement of plasmid deoxyribonucleic acid in indoleacetic acid synthesis in Pseudomonas savastanoi.

Olive (or oleander) knot is a plant disease incited by Pseudomonas savastanoi. Disease symptoms consist of tumorous outgrowths induced in the plant by bacterial production of indole-3-acetic acid (IAA). Synthesis of IAA occurs by the following reactions: L-tryptophan leads to indoleacetamide leads to indoleacetic acid, catalyzed by tryptophan 2-monooxygenase and indoleacetamide hydrolase, respectively. Whereas the enzymology of IAA synthesis is well characterized, nothing is known about the genetics of the system. We devised a positive selection for the presence of tryptophan 2-monooxygenase based on its capacity to use as a substrate the toxic tryptophan analogue 5-methyltryptophan. Efficient curing of the bacterium of tryptophan 2-monoxygenase, indoleacetamide hydrolase, and IAA production was obtained by acridine orange treatment. Further, loss of capacity to produce IAA by curing was correlated with loss of a plasmid of 34 X 10(6) molecular weight. This plasmid, here called pIAA1, when reintroduced into Iaa- mutants by transformation, restored tryptophan 2-monooxygenase and indoleacetamide hydrolase activities and production of IAA.

Acridine Orange↗

Interaction of gibberellic acid and indoleacetic acid in Impatiens.

Gibberellic acid promotes doubling, early flowering, and fruiting directly in Impatiens. It also lengthens the stem, probably through a neutralization of auxin inhibitors. Such a mechanism would leave the growth-promoting auxins unchecked to produce the increased elongation characteristic of gibberellin application. It seems that application of additional auxin produces a rapid build-up of the auxin inhibitor(s) in the plant.

Gibberellins↗

Influence of 2,3,5-Triiodobenzoic Acid and 1-N-Naphthylphthalamic Acid on Indoleacetic Acid Transport in Carnation Cuttings: Relationship with Rooting.

(3)H-IAA transport in excised sections of carnation cuttings was studied by using two receiver systems for recovery of transported radioactivity: agar blocks (A) and wells containing a buffer solution (B). When receivers were periodically renewed, transport continued for up to 8 h and ceased before 24 h. If receivers were not renewed, IAA transport decreased drastically due to immobilization in the base of the sections. TIBA was as effective as NPA in inhibiting the basipetal transport irrespective of the application site (the basal or the apical side of sections). The polarity of IAA transport was determined by measuring the polar ratio (basipetal/acropetal) and the inhibition caused by TIBA or NPA. The polar ratio varied with receiver, whereas the inhibition by TIBA or NPA was similar. Distribution of immobilized radioactivity along the sections after a transport period of 24 h showed that the application of TIBA to the apical side or NPA to the basal side of sections, increased the radioactivity in zones further from the application site, which agrees with a basipetal and acropetal movement of TIBA and NPA, respectively. The existence of a slow acropetal movement of the inhibitor was confirmed by using (3)H-NPA. From the results obtained, a methodological approach is proposed to measure the variations in polar auxin transport. This method was used to investigate whether the variations in rooting observed during the cold storage of cuttings might be related to changes in polar auxin transport. As the storage period increased, a decrease in intensity and polarity of auxin transport occurred, which was accompanied by a delay in the formation and growth of adventitious roots, confirming the involvement of polar auxin transport in supplying the auxin for rooting.

Journal Article↗

Urinary 4-hydroxy-3-methoxymandelic (vanillylmandelic) acid, 4-hydroxy-3-methoxyphenylacetic (homovanillic) acid, and 5-hydroxy-3-indoleacetic acid determined by liquid chromatography with electrochemical detection.

We describe a simple liquid-chromatographic assay of urinary 4-hydroxy-3-methoxymandelic (vanillylmandelic) acid, 4-hydroxy-3-methoxyphenylacetic (homovanillic) acid, and 5-hydroxy-3-indoleacetic acid with electrochemical detection, with direct injection of the sample. The first two analytes are measured simultaneously; 5-hydroxy-3-indoleacetic acid is measured separately. Chromatographic conditions for assay of the three were: column temperature, 65 and 60 degrees C; mobile phase, potassium phosphate buffer (0.2 mol/L, pH 3.0) for 6 min, then potassium phosphate buffer plus acetonitrile (9/1 by vol) for 20 min; flow rate, 0.7 mL/min; oxidation potential, 600 and 450 mV vs an Ag/AgCl reference electrode; and sensitivity, 40 and 160 nA at full scale. Values so obtained agreed well with those obtained for samples that were first solvent-extracted.

Chromatography, High Pressure Liquid↗