Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Potential sites of action

Eliminating a compound quickly from an organism can minimize the toxicity through the simple act of removing the compound away from the potential site of action. Chemicals that are hydrophilic are more easily eliminated from living systems so either the parent compound or a metabolite that is quickly eliminated is preferred to a slowly excreted compound. [Pg.34]

It is quite possible that phenolic acids may produce more than one effect on the cellular processes responsible for mineral absorption. The potential sites of action discussed above all involve cellular membranes in some way. Which mechanism of action is predominant in a given situation may depend upon the concentration of allelochemicals present and the conditions (e.g. pH) of the plant/chemical interaction. [Pg.176]

Most biologically active purines or purine nucleosides must be anabolized to 5 -nucleotides to exert their effects. "The 5 -nucleotides are in some cases further phosphorylated to the di- and triphosphates and the number of potential sites of action of these compounds is obviously greater than the number of potential sites of action of compounds metabolized only to the monophosphate level. But even... [Pg.91]

Figure 1 Diagrammatic representation of the putative pathophysiological mechanisms involved in the development of migraine headache and the potential sites of action of NKi receptor antagonists (adapted from Longmore et al., 1997). Figure 1 Diagrammatic representation of the putative pathophysiological mechanisms involved in the development of migraine headache and the potential sites of action of NKi receptor antagonists (adapted from Longmore et al., 1997).
Schematic diagram showing some of the potential sites of action of antidepressant drugs. Chronic therapy with these drugs has been proved to reduce reuptake of norepinephrine or serotonin (or both), reduce the number of postsynaptic Preceptors, and reduce the generation of cAMP. The MAO inhibitors act on MAO in the nerve terminals and cause the same effects on Preceptors and cAMP generation. Schematic diagram showing some of the potential sites of action of antidepressant drugs. Chronic therapy with these drugs has been proved to reduce reuptake of norepinephrine or serotonin (or both), reduce the number of postsynaptic Preceptors, and reduce the generation of cAMP. The MAO inhibitors act on MAO in the nerve terminals and cause the same effects on Preceptors and cAMP generation.
Potential Sites of Action for CFTR Potentiators Identified by HTS. Ill... [Pg.91]

Figure 1 Illustration of potential sites of action of inhibitors of chemical... Figure 1 Illustration of potential sites of action of inhibitors of chemical...
Although mesalamine is a salicylate, its therapeutic effect does not appear to be related to cyclooxygenase inhibition indeed, traditional nonsteroidal antiinflammatory drugs actually may exacerbate IBD. Many potential sites of action have been demonstrated in vitro for either sulfasalazine or mesalamine inhibition of the production of IL-1 and TNF-a, inhibition of the lipoxygenase pathway, scavenging of free radicals and oxidants, and inhibition of NF-Kp, a transcription factor pivotal to production of inflammatory mediators. Specific mechanisms of action of these drugs have not been identified. [Pg.416]

DIRECTIONS (Items 15-16) Different diuretic drugs act at different sites in the nephron. The diagram below denotes such potential sites of action with the letters A-E. For questions 15 and 16, select the lettered site of action that applies to the description given. [Pg.154]

B. Mechanisms of Antidepressant Action Potential sites of action of antidepressants at central nervous system synapses are shown in Figure 30-2. By means of several mechanisms, almost all antidepressants result in a potentiation of the neurotransmitter actions of norepinephrine, serotonin, or both. The only exception is bupropion, which has an unknown mechanism of action. Long-term use of tricyclics and MAOIs, but not SSRIs, leads to down-regulation of beta receptors. [Pg.270]

The triazoles and related growth retardants are not general inhibitors of plant cytochrome P-450 monooxygenases [39]. Their action appears to be confined to methyl hydroxylases, with which they interact to differing extents depending on structure. Apart from e f-kaurene oxidase, there are several other such enzymes that are involved in important metabolic pathways (Fig. 5), the products of which may influence growth. These are potential sites of action and will be considered below. [Pg.328]

The metabolism of ABA to phaseic acid is initiated by hydroxylation at C-8 (Fig. 5). The enzyme catalyzing this reaction in Echinocystis lobata was found to be microsomal and to require O2 and NADPH [18]. Although it was not fully characterized, the enzyme has properties consistent with a monooxygenase which, as a methyl hydroxylase, is a potential site of action of the N-heterocyclics. There is evidence that this reaction may indeed be inhibited in some cases, leading to increased ABA levels [49] and therefore reduced transpiration [2]. Although there is little information on the structural requirements for inhibitors of ABA metabolism, it is of interest to note that inhibition of both this reaction and e/z kaurene oxidation would result in growth retardation. [Pg.330]

Figure 5 The potential sites of action of flavonoids in the prevention of cell damage. Oxidative stress results in the oxidation of lipids, proteins, and deoxyribonucleic acid (DNA), which is in turn sensed by signaling pathways, such as the MARK signaling cascade and mitochondria. These events interlink to cause induction of apoptosis/necrosis in response to the initial oxidative insult. Flavonoids may act by direct scavenging of the oxidizing species or intermediate, by direct protein interactions with signaling molecules, or by interaction with mitochondria. MARK, mitogen-activated protein kinase. Figure 5 The potential sites of action of flavonoids in the prevention of cell damage. Oxidative stress results in the oxidation of lipids, proteins, and deoxyribonucleic acid (DNA), which is in turn sensed by signaling pathways, such as the MARK signaling cascade and mitochondria. These events interlink to cause induction of apoptosis/necrosis in response to the initial oxidative insult. Flavonoids may act by direct scavenging of the oxidizing species or intermediate, by direct protein interactions with signaling molecules, or by interaction with mitochondria. MARK, mitogen-activated protein kinase.
Rooke N, Li DJ, Li J, Keung WM. The mitochondrial monoamine oxidase-aldehyde dehydrogenase pathway a potential site of action of daidzin. J Med Chem. 2000 43 4169-79. [Pg.545]


See other pages where Potential sites of action is mentioned: [Pg.112]    [Pg.40]    [Pg.6]    [Pg.352]    [Pg.244]    [Pg.731]    [Pg.27]    [Pg.71]    [Pg.245]    [Pg.704]    [Pg.49]    [Pg.60]    [Pg.893]    [Pg.366]    [Pg.370]    [Pg.1072]    [Pg.507]    [Pg.91]    [Pg.370]    [Pg.94]    [Pg.271]    [Pg.203]    [Pg.408]   
See also in sourсe #XX -- [ Pg.91 ]




SEARCH



Action sites

© 2024 chempedia.info