Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 5-(4'-chlorobutyl)-picolinic acid (FD-008), a new dopamine beta-hydroxylase inhibitor of fusaric acid derivatives, on the central nervous system in mice and rats were investigated. FD-008 and fusaric acid did not show marked effects on spontaneous movement, convulsion, sleeping time, tremor and conditioned avoidance response but lowered the body temperature of rats at 100 mg/kg p.o. FD-008 potentiated the depressive action of ethanol on conditioned avoidance response in spite of the lack of aldehyde dehydrogenase inhibition. FD-008 markedly depressed the performance on a shuttle box and lowered the body temperature in rats after reserpine treatment at a dose at which FD-008 per se had no effect.
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PMID:Pharmacological action of FD-008, a new dopamine-beta-hydroxylase inhibitor. 117 34

The effects of some tremor-producing and antitremor agents on the enzymes sequentially metabolizing ethanol and acetaldehyde in addition to biogenic-amine-derived aldehyde intermediates were studied in mouse liver preparations. Aldehyde but not alcohol dehydrogenase was differentially stimulated by the compounds studied in vitro. This effect was confined to the mitochondrial enzyme and was isoenzyme-dependent. The results indicate difference between in vitro and in vivo effects and suggest a role for mitochondrial aldehyde dehydrogenase in metabolic detoxification of endogenous biogenic aldehydes in the presence of alcohol which may explain the worsening of drug-induced tremor by ethanol.
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PMID:Effect of tremorogenic and antitumor agents on enzymes regulating a minor metabolic pathway of biogenic amines: an hypothesis for the underlying mechanism. 182 23

2-Propyl-1-aminopentane (2-PAPN), a branched aliphatic amine, was found to be readily deaminated by monoamine oxidase B in the liver of the rat and semicarbazide-sensitive amine oxidase in the aorta of the rat. The deaminated product, 2-propyl-1-pentaldehyde, could be subsequently converted to valproic acid in the presence of aldehyde dehydrogenase and beta-NAD cofactor in vitro as well as in vivo. Valproic acid was identified after derivatization with 4-bromomethyl-6,7-dimethoxycoumarin, followed by HPLC-fluorometric assessment. Absorption and biotransformation of a single intraperitoneal dose of 2-PAPN resulted in the rapid appearance of the drug and its metabolite in the blood and in the brain. The formation of valproic acid from 2-PAPN in vivo, however, was insufficient to facilitate anticonvulsant action. In fact, 2-PAPN itself, at relatively small doses, exhibited distinct tremor effects. Such tremor effects could be prevented by valproic acid. However, 2-PAPN was also found to potentiate the convulsant effect induced by mercaptopropionic acid (MPA) and, in addition, the 2-PAPN-induced tremor could be potentiated by MPA in mice.
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PMID:2-propyl-1-aminopentane, its deamination by monoamine oxidase and semicarbazide-sensitive amine oxidase, conversion to valproic acid and behavioral effects. 186 97

Disulfiram (Antabuse) is used for aversive treatment of alcohol dependence with good effects. Through inhibition of aldehyde dehydrogenase, disulfiram heightens serum aldehyde concentration after alcohol ingestion and causes aversive disulfiram-ethanol reaction. Typical symptoms of this reaction include flushing, nausea, dyspnea, tremor, and confusion, which are usually self-limiting. However, severe life-threatening arterial hypotension sometimes develops. We report here a patient with generalized flushing, tremor, and refractive hypotension after ingestion of alcohol 18 hours after disulfiram treatment. Initial volume resuscitation and dopamine infusion failed to restore the blood pressure. Noradrenaline was given and the blood pressure returned to normal range. This case illustrates the intensity of disulfiram-ethanol reaction and underscores the advantageous use of noradrenaline in patients in such a critical condition.
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PMID:Refractive hypotension in a patient with disulfiram-ethanol reaction. 1722 Jun 94

The senescence-accelerated SAMP8 mouse is considered a useful non-transgenic model for studying aspects of progressive cognitive decline and Alzheimer's disease (AD). Using SAMR1 mice as controls, here we explored the effects of 6 months of voluntary wheel running in 10-month-old female SAMP8 mice. Exercise in SAMP8 mice improved phenotypic features associated with premature aging (i.e., skin color and body tremor) and enhanced vascularization and BDNF gene expression in the hippocampus compared with controls. With the aim of identifying genes involved in brain aging responsive to long-term exercise, we performed whole genome microarray studies in hippocampus from sedentary SAMP8 (P8sed), SAMR1 (R1sed), and exercised SAMP8 (P8run) mice. The genes differentially expressed in P8sed versus R1sed were considered as putative aging markers (i) and those differentially expressed in P8run versus P8sed were considered as genes modulated by exercise (ii). Genes differentially expressed in both comparisons (i and ii) were considered as putative aging genes responsive to physical exercise. We identified 34 genes which met both criteria. Gene ontology analysis revealed that they are mainly involved in functions related to extracellular matrix maintenance. Selected genes were validated by real-time quantitative PCR assays, i.e., collagen type 1 alpha 1 (col1a1), collagen type 1 alpha 2 (col1a2), fibromodulin (fmod), prostaglandin D(2) synthase (ptgds), and aldehyde dehydrogenase (Aldh1a2). As a whole, our study suggests that exercise training during adulthood may prevent or delay gene expression alterations and processes associated with hippocampal aging in at-risk subjects.
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PMID:Long-term exercise modulates hippocampal gene expression in senescent female mice. 2316 50