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Gallic acid has been modified to naphthophenone derivatives with esterified fatty acid side chain. Compound 12, an ethyl crotonate ester of naphthophenone derivative has shown potent auxin like growth promoter activity. This is the first example of naphthophenone derivatives with plant growth promoting activity.
(Neuro-)endocrine tumours of the gastrointestinal tract are also called 'carcinoids'. (Neuro-)endocrine midgut tumours can be categorized according to their clinical behaviour. Most tumours are non-functioning. Functioning tumours are responsible for the carcinoid syndrome. The carcinoid syndrome is almost uniquely associated with midgut carcinoids. Symptoms of the carcinoid syndrome are caused by an excess of biogenic amines, peptides and other factors in the circulation. The typical symptoms of the carcinoid syndrome are diarrhoea, flushing, and carcinoid heart disease. Carcinoid heart disease involves the tricuspid and pulmonary valves and the endocardium. Serum chromogranin A and urinary excretion of 5-hydroxy-indoleacetic acid (5-HIAA) are biochemical markers. Carcinoid tumours express large numbers of high-affinity somatostatin receptors. These can bind the currently available octapeptide somatostatin analogues. In inoperable patients, biotherapy with somatostatin analogues and interferon-alpha is the treatment of choice. Somatostatin analogues and interferon-alpha significantly improve symptoms.
The reported increase in brain-derived neurotrophic factor (BDNF) mRNA expression after antidepressant treatment is a cornerstone of the BDNF hypothesis of antidepressant action. However, if this increase becomes manifest on the BDNF protein level is unknown. In the present study we performed parallel measurements of BDNF mRNA and protein expression in the frontal cortex and hippocampus of the rat after chronic treatment with electroconvulsive seizures (ECS), lithium, desipramine or escitalopram. ECS increased BDNF mRNA and protein in the hippocampus and BDNF protein in the frontal cortex. Desipramine moderately increased BDNF mRNA expression in the dentate gyrus but did not change BDNF protein in neither region. Escitalopram did not affect BDNF mRNA expression, but decreased BDNF protein in the frontal cortex and the hippocampus. Lithium increased BDNF protein levels in the hippocampus and frontal cortex, but overall decreased BDNF mRNA expression. Thus, here we report a striking non-correspondence between changes in BDNF mRNA and protein expression induced by the antidepressant treatments and lithium. Further, increased expression of BDNF mRNA or protein was not a common action of the treatments. We also investigated if treatment-induced modulations of the tissue contents of 5-hydroxytryptamine (5-HT) and its metabolite, 5-hydroxy-indoleacetic acid (5-HIAA), were related to changes in BDNF mRNA or protein expression. No correlation was found. However, all treatments increased 5-HT levels in the hippocampus.
Phytoremediation is a novel cleanup technology for the removal of contaminants from polluted waters and soils. In phytoremediation, the plant uptake capability and the availability of the pollutant in the media are important. Here we show the results of a study on the combined effects of ethylenediaminetetraacetic acid (EDTA) and the phytohormone indole-3-acetic acid (IAA) on Pb uptake by Medicago sativa (alfalfa). Plants were grown in hydroponics media containing a nutrient solution amended with Pb at 0.2mM and different combinations of EDTA, and IAA. After 10d of treatment, the Pb content in plant tissues was quantified using an Inductively Coupled Plasma Optical Emission Spectrometer (ICP/OES). The results showed that the combination of 100 microM IAA/0.2 mM EDTA increased the Pb accumulation in leaves by about 2800% and by about 600%, as compared to Pb content in leaves of plants exposed to Pb alone and those cultivated with Pb/EDTA, respectively. These results indicate that non-metal hyperaccumulator plants could increase their hyperaccumulating potential without genetic manipulation.
Some studies have suggested that disorders in the peripheral and central metabolism of serotonin (5-HT) may play a role in the pathophysiology of autistic disorder. This study examines the whole blood concentrations of 5-HT and 5-hydroxy-indoleacetic acid (5-HIAA) in baseline conditions and during a challenge with L-5-OH-tryptophane (5-HTP; 4 mg/kg in non enteric-coated tablets), the precursor of 5-HT, in a study group of 18 male, post-pubertal, Caucasian autistic patients (age 13-19 y.; I.Q.>55) and 20 matched healthy volunteers. In baseline conditions, no significant differences in 5-HT or 5-HIAA levels could be found between autistic youngsters and normal controls. 5-HTP administration significantly increased the levels of 5-HT in autistic youngsters but not in normal controls. Following 5-HTP challenge the 5-HT levels were significantly higher in autistic patients than in healthy volunteers. After challenge with 5-HTP, no significant differences were found in the concentrations of 5-HIAA or the test substance between autistic youngsters and normal controls. Differences in the peripheral metabolism of 5-HT which may not be observed in baseline conditions but which became clear after loading with 5-HTP, suggest that an increased synthesis of 5-HT from its precursor 5-HTP might be a one factor responsible for differences in the serotonergic system between autistic post-pubertal youngsters and normal controls.
The separation of 5-hydroxyindole-3-acetic acid and indole-3-acetic acid from urine is demonstrated. The urine is injected directly on a liquid chromatographic column which is coupled to a flow-through fluorescence detector or a UV detector. A hydrogen-accepting stationary phase, tributyl phosphate (TBP), which retains carboxylic acid selectivity, was more selective than more common reversed-phase systems with alkyl-bonded stationary phases. The mobile phases were buffers, sometimes buffers containing methanol or acetonitrile. A simple method of removing late peaks in the chromatogram, in order to reduce analysis time, is also presented.
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The brain stems (BS) of streptozotocin (STZ)-diabetic rats were studied to see the changes in neurotransmitter content and their receptor regulation. The norepinephrine (NE) content determined in the diabetic brain stems did not show an increase, while epinephrine (EPI) content increased significantly compared with control. The NE to EPI turnover showed a significant increase. The alpha2 adrenergic receptor kinetics revealed that the receptor affinity was significantly reduced during diabetes. In insulin treated rats the NE content decreased while EPI content remained increased as in the diabetic state. Insulin treatment increased the Bmax for alpha2 adrenergic receptors significantly while the increase in Kd reversed to normal. Unlabelled clonidine inhibited [3H]NE binding in BS of control diabetic and insulin treated diabetic rats showed that alpha2 adrenergic receptors consisted of two populations of binding sites with Hill slopes significantly away from unity. In diabetic animals the ligand bound weaker to the low affinity site than in controls. Insulin treatment reversed this alteration to control levels. The displacement analysis using (-)-epinephrine against [3H]yohimbine in control and diabetic animals revealed two populations of receptor affinity states. In control animals, when GTP analogue added with epinephrine, the curve fitted for a single affinity model; but in the diabetic BS this effect was not observed. In both the diabetic and control BS the effects of monovalent cations on affinity alterations were intact. Our data thus show that alpha2 adrenergic receptors have a reduced affinity due to an altered post receptor affinity regulation The serotonin (5-HT) content in the brain stem increased. Its precursor (5-hydroxy) tryptophan (5-HTP) showed an increase and its breakdown metabolite (5-hydroxy) indoleacetic acid (5-HIAA) showed a significant decrease. This showed that in serotonergic nerves there is a disturbance in both synthetic and breakdown pathways which lead to an increased 5-HT. The high affinity serotonin receptor numbers remained unaltered with a decrease in the receptor affinity. The insulin treatment reversed these altered serotonergic receptor kinetic parameters to control level. Thus our study shows a decreased serotonergic receptor function. These changes in adrenergic and serotonergic receptor function were suggested to be important in insulin function during STZ diabetes.
Adventitious root cultures of Rhus javanica L. produced large amounts of galloylglucoses (gallotannins) and an anthocyanidin, riccionidin A, formerly found only in liverworts. Production of both galloylglucoses and riccionidin A in the adventitious root culture system was suppressed by light. The Rhus root culture showed the highest productivity for those secondary metabolites in a modified Linsmaier-Skoog (LS) liquid medium containing 30 mM NH4+ and 30 mM NO3- as nitrogen sources in the presence of 10(-6) M 3-indoleacetic acid (IAA).
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Learning in male Sprague-Dawley rats was assessed in two types of positively reinforced complex spatial discrimination tasks (Stone 14-unit T-maze and eight-arm radial-arm maze) following cytotoxic lesions of central serotonergic terminal projection fields with p-chloroamphetamine (PCA). Learning, as expressed as mean number of errors per day and mean number of trails required to reach criterion, was significantly enhanced in the PCA-lesioned animals trained in the Stone maze. On the other hand, the performance of the PCA-lesioned animals trained in the eight-arm radial-arm maze was not found to differ significantly from that of saline-injected animals. The improved acquisition of the PCA-lesioned rats trained in the Stone maze was completely abolished following pretreatment with the selective serotonergic reuptake inhibitor norzimeldine. Neurochemical analyses of the brains of representative animals revealed that the levels of serotonin and its major metabolite, 5-hydroxy-3-indoleacetic acid, were both significantly reduced by PCA in all regions examined. While it is clear from these and other studies that the serotonergic nervous system plays an important role in the processes underlying learning and memory, these results further underscore the selective role of this neurotransmitter system in the way information is processed by the brain.
Stomatal movement is governed by osmotic potential, in which K(+) concentration plays the dominant role. Our previous work has shown that both microtubules and microfilaments are involved in regulating stomatal movement. In the present investigation the relationships between cytoskeletal components and K(+) fluxes in stomatal opening were addressed by using fusicoccin (FC), indoleacetic acid (IAA), and cytoskeletal inhibitors to treat both epidermal strips and protoplasts of guard cells. The results revealed that FC and IAA induced stomatal opening with or without KCl in the dark. Also FC or IAA induced guard cell protoplast swelling in the dark even without added KCl. However, the induction was partially suppressed when strips and protoplasts were pretreated with cytochalasin B (CB), an inhibitor of F-actin polymerization, or oryzalin, an inhibitor of plant microtubule polymerization. Thus our preliminary results indicate for the first time that microtubules and microfilaments can affect stomatal opening independently of K(+) fluxes.
It has been proposed that interaction of catecholamines and indoleamines with free radicals may result in the formation of endogenous neurotoxins. In order to better understand the mechanisms involved in neurodegenerative disorders showing evidence of oxidative stress, we have studied the basal concentrations and the turnover rates of dopamine, noradrenaline, serotonin and their metabolites in the prefrontal cortex of rats that were fed on control or low selenium diets. Nutritional deficit of selenium decreases the brain antioxidant protection in experimental conditions by the decrease in glutathione peroxidase activity. The dopamine and serotonin turnover increased and noradrenaline and 5-hydroxy-3-indoleacetic acid turnover decreased compared to experimental control animals. The increase of dopamine turnover in experimental rats was accompanied by an increase in tyrosine hydroxylase activity. These results suggest that the decrease of brain protection against oxidative damage could induce brain damage by disturbing the turnover rate of some monoamines.
Serotonin (5-HT) neurons located in the median raphe nucleus (MRN) may have a role in the development of behavioral changes to stress. The objective of the present work was to investigate the effects of a selective lesion of 5-HT neurons located in the MRN in previously stressed male Wistar rats submitted to the elevated plus maze (EPM). In an initial experiment, the animals (n=20-22) were submitted to one (acute) or seven (chronic) daily restraint stress periods (2 h) and tested in the EPM 24 h later. Results showed that acute restraint caused a significant decrease in the number of entries into the open arms, as compared to nonstressed controls. This effect disappeared when the animals were submitted to chronic restraint. In the next set of experiments, animals (n=6-8) received, 1 week before the behavioral studies, intra-MRN injection of 5,7-dihydroxytryptamine (5,7-DHT; 8 microg/1 microl). Neurochemical analysis showed that this treatment significantly decreases 5-HT and 5-hydroxy-indoleacetic acid (5-HIAA) levels in the hippocampus, but not in the striatum. No difference between lesioned and sham-operated animals in EPM performance was found in nonstressed animals or in those submitted to acute restraint. In chronically restrained animals, however, lesioned rats showed a significant decrease in the number of entries and time spent in the open arms. These results suggest that lesions of 5-HT neurons located in the MRN cause anxiogenic-like behavior in animals that have been chronically restrained.
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T-2 toxin has been shown to affect the central nervous system. Only recently have attempts been made to characterize the neurochemical perturbations associated with T-2 intoxication. To examine the effect of T-2 on regional brain biogenic monoamines and selected metabolites, male rats were dosed orally with T-2 toxin in corn oil at 0.1, 1.0 or 2.5 mg/kg body weight. At 2, 6 and 10 hr post-dosing, rats were killed, brains were collected and stored at -80 degrees until analysed. Brain nuclei, including nucleus raphe magnus, paraventricular nucleus, locus coeruleus, substantia nigra, medial forebrain bundle, nucleus accumbens and olfactory tubercle, were analysed. T-2 treatment increased 5-hydroxy-3-indoleacetic acid and serotonin throughout the brain, and produced a transient increase in norepinephrine in the nucleus raphe magnus and a temporary decrease in the substantia nigra. Regional dihydroxyphenylacetic acid concentration was affected, with increased DOPAC observed in the locus coeruleus, medial forebrain bundle and paraventricular nucleus of the hypothalamus, and decreased DOPAC in the olfactory tubercles. No regional changes in epinephrine or dopamine were observed. Few treatment differences were observed, with the 0.1 mg/kg body weight T-2, 2% of the LD50, significantly affecting brain monoamines. It had been suggested that neurological manifestations of T-2 toxin are the result of brain hypoxia; however, the altered brain monoamine profile observed at doses that do not alter heart function, suggests the brain is a primary site of trichothecene action.
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