Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

d-2-(6'Methoxy-2'-naphthyl)-propionic acid (naproxen) in different concentrations was investigated as to its influence on the semiconservative DNA synthesis and DNA repair of human lymphocytes and mouse speen cells. As could be shown, there was a slight diminuation of the DNA synthesis. In view of a desired antiproliferating effect in the treatment of rheumatic diseases this fact could certainly prove useful. Additionally, with a naproxen concentration of 30 ppm, a diminuation of the endonuclease activity in mouse spleen cells could be shown. With naproxen concentrations higher than 60 ppm a slight lowering of the exonuclease and polymerase activities in mouse spleen cells as well as in human lymphocytes were observed. With naproxen in a concentration of 120 ppm, all three enzymes of the excision repair investigated showed a distinct loss of activity. Results of investigations on ligase activity will be presented separately. Under the administration of naproxen, late effects on the genetic material are rather improbable, as long as the substance is not admininstered concomitantly with agents which have a direct effect on the DNA.
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PMID:[Effect of naproxen on the semiconservative DNA synthesis and DNA repair of various cell systems]. 117 75

Inhibition of endonuclease by d-2-(6'-methoxy-2'-naphthyl)-propionic acid (naproxen) is discussed as a possible therapeutic principle of the antiinflammatory action in polyarthritis. Infections by 'slow viruses" and mycoplasma have to be considered as possible etiologic factors for rheumatoid arthritis. The incorporation of the viral or mycoplasmatic DNA into the genetic material of the host cell depends on the function of endonucleases, which can be inhibited by naproxen. The advantages and the drawbacks of this type of mechanism of action are discussed.
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PMID:[Naproxen, a 'specific" antirheumatic drug?]. 117 77

In this study, the endonuclease inhibitor aurintricarboxylic acid (ATA) was examined for its ability to attenuate both acute and delayed excitotoxicity mediated through NMDA and non-NMDA glutamate receptors. Ex vivo embryonic chick retina, a model system frequently used for studies of excitotoxicity, was exposed to either 100 microM NMDA or kainate (KA) +/- various concentrations of ATA for 60 min, then allowed to recover for 24 h. Lactate dehydrogenase release into the medium and histology were assessed as measures of delayed toxicity. ATA attenuated lactate dehydrogenase release due to NMDA or KA in a dose-dependent manner. Histology revealed that ATA decreased the number of pyknotic profiles in response to either glutamate agonist. The mechanism of ATA protection was addressed. ATA was found to block NMDA- but not KA-mediated 22Na+ influx and cyclic GMP formation. In membrane binding studies, ATA was relatively selective for displacement at the NMDA receptor. The IC50 values for displacement of [3H]CGS 19755, alpha-[3H]amino-3-hydroxy-5-methylisoxazole-4-propionic acid ([3H]AMPA), or [3H]KA were 29.9 +/- 1.3, 313 +/- 46, and > 1,000 microM +/- SEM, respectively. ATA also fully attenuated NMDA-induced and partially attenuated KA-induced acute excitotoxicity as monitored histologically by tissue swelling and by the increase in GABA in the medium. Temporal studies of ATA efficacy indicated that ATA needed to be present during NMDA exposure to afford protection but, versus KA, was equally effective if administered immediately after KA exposure. Questions regarding the cellular penetration of ATA were raised because incubation with 100 microM ATA for 60 min had no effect on lactate formation or [3H]leucine incorporation into trichloroacetic acid-precipitable material, even though, in cell-free systems, ATA is a potent inhibitor of phosphofructokinase activity and protein synthesis. These studies demonstrate that ATA can protect against excitotoxicity mediated through NMDA or non-NMDA glutamate receptors. The mechanism of protection versus NMDA is through interruption of NMDA receptor interactions. ATA has no direct effect at the KA receptor; thus, its mechanism of protection versus KA is distinct from that versus NMDA and is, at present, unknown.
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PMID:Excitotoxicity at both NMDA and non-NMDA glutamate receptors is antagonized by aurintricarboxylic acid: evidence for differing mechanisms of action. 789 Nov 4

The degradation of the aromatic carboxylic acids 3-phenylpropionic acid, cinnamic acid and L-phenylalanine was investigated in several strains of Acinetobacter calcoaceticus var. lwoffii. Evidence is presented for the conversion of 3-phenylpropionic acid into the cis-2,3-dihydrodihydroxy-derivative, which is further metabolized to 3-(2,3-dihydroxyphenyl-)propionic acid, followed by cleavage of the aromatic ring in meta-proximal position. When pre-grown on 3-phenylpropionic acid, cinnamic acid as well as L-phenylalanine were metabolized under resting cell conditions via the same degradation pathway. When cultivated with cinnamic acid as sole carbon source 4-hydroxycinnamate, together with 4-hydroxybenzoate and protocatechuate were found as metabolites. L-phenylalanine, when provided as the only carbon source, is converted via phenylacetic acid to 2-hydroxyphenyl-acetic acid. All metabolites were identified by conventional chemical techniques. Enzymatic studies yielded further support for the proposed pathways. In 14 of 15 Acinetobacter strains the presence of plasmid DNA could be detected. The number of plasmids varied between 1 and 7. Regarding the number and size of the plasmids considerable variations within the different bacterial strains were observed. No extended homology among the plasmids could be shown by restriction endonuclease digestion. One strain exhibiting a high spontaneous mutation rate to the 3-phenylpropionic acid-negative phenotype did not show any change in its plasmid pattern. The results lead us to conclude that a correlation between the degradative properties of these strains and the presence of plasmid DNA is unlikely.
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PMID:Degradation of aromatic carboxylic acids by acinetobacter. 2319 32