Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pro- and anticonvulsant effects of phencyclidine (1-[1-phenylcyclohexyl]piperidine HCl, PCP), a number of its analogues, and SKF 10047 were investigated in rats. The PCP analogues were compounds produced by substitutions for the phenyl and piperidine rings of PCP and were selected to elucidate the structure-activity relationships existing between PCP and its pro- and/or anticonvulsant effects. All of the compounds, except ketamine, induced convulsions at high (12.8-25.6 mg/kg, i.v.), yet almost always sublethal doses. Ketamine failed to induce convulsions, even at lethal doses (51.2 mg/kg, i.v.). The acute pro- or anticonvulsant actions of PCP were then investigated. Rats were subjected to transorbital electroconvulsive shock subsequent to i.p. injections of saline or 0.625, 2.5, 5.0, 10.0 or 20.0 mg/kg PCP. It was found that PCP induced an acute, dose-dependent anticonvulsant effect. The acute pro- and/or anticonvulsant actions of the remaining compounds were then investigated by administration of electroconvulsive shock subsequent to i.p. injections of saline or one of two doses of each compound. The low and high doses of each compound were selected to be behaviorally equivalent to 2.5 and 10.0 mg/kg PCP i.p., respectively. With one exception, each dose of each drug induced an acute anticonvulsant action, with no difference in efficacy between the compounds tested. However, PCA (produced by substitution of an amine for the piperidine ring of PCP) induced a statistically greater anticonvulsant action at the higher, compared to the lower, dose. In addition, PCA was the only compound to eliminate all motor signs of the electrically induced seizure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The convulsant and anticonvulsant effects of phencyclidine (PCP) and PCP analogues in the rat. 396 7

Mill process changes and source controls instituted in the late 1980s at pulp and paper mills along the British Columbia (BC) coast produced dramatic reductions in both the concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and the TEQ (2,3,7,8-TCDD toxic equivalents). Nevertheless, questions remained as to whether the sediments were acting as contaminant sources or sinks, whether crab uptake pathways have stayed the same since the mills ceased producing PCDD/Fs, and whether improvement was faster at some sites than others. To examine the processes governing the changes in PCDD/F composition, PCDD/F sources and compositional trends for the coastal BC sites were interpreted using sediment and crab PCA (principal components analysis) models and two indices based on the three main groups of PCDD/Fs that covary in all PCA models. One index measured the relative inputs of chlorine bleaching PCDFs and PCP (pentachlorophenol)-related PCDDs at each mill and harbor site whereas the other measured the relative inputs of PCP wood preservatives and pulp mill effluents. Results indicated that PCDFs produced during chlorine bleaching accumulate from sediments to crabs more readily than the PCDDs but that the chlorine bleaching TCDFs have generally decreased in importance at all mill sites. In the years just before 1995, little change was observed in either the proportion of toxic 2,3,7,8-chlorinated congeners or the PCDD/F concentrations, and the improvements seemed to have largely ceased by 1995. The lack of change in PCA composition for the harbors provided a further, disturbing indication that ecosystem recovery may have stalled. Results also implied that the main route of PCDD/Fs into crabs shifted from uptake via a pelagic food web incorporating effluent-borne PCDD/Fs associated with suspended particulate matter to uptake via a benthic food web.
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PMID:Assessment of chlorinated dibenzo-p-dioxin and dibenzofuran trends in sediment and crab hepatopancreas from pulp mill and harbor sites using multivariate- and index-based approaches. 1202 64