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

The debromination pathways of seven polybrominated diphenyl ethers (PBDEs) by three different cultures of anaerobic dehalogenating bacteria were investigated using comprehensive two-dimensional gas chromatography (GC x GC). The congeners analyzed were the five major components of the industrially used octa-BDE mixture (octa-BDEs 196, 203, and 197, hepta-BDE 183, and hexa-BDE 153) as well as the two most commonly detected PBDEs in the environment, penta-BDE 99 and tetra-BDE 47. Among the dehalogenating cultures evaluated in this study were a trichloroethene-enriched consortium containing multiple Dehalococcoides species, and two pure cultures, Dehalobacter restrictus PER-K23 and Desulfitobacterium hafniense PCP-1. PBDE samples were analyzed by GC x GC coupled to an electron capture detector to maximize separation and identification of the product congeners. All studied congeners were debrominated to some extent by the three cultures and all exhibited similar debromination pathways with preferential removal of para and meta bromines. Debromination of the highly brominated congeners was extremely slow, with usually less than 10% of nM concentrations of PBDEs transformed after three months. In contrast, debromination of the lesser brominated congeners, such as penta 99 and tetra 47, was faster, with some cultures completely debrominating nM levels of tetra 47 within weeks.
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PMID:Pathways for the anaerobic microbial debromination of polybrominated diphenyl ethers. 1849 33

Bi-acetylated l-stepholidine (l-SPD-A), a novel derivate of l-stepholidine (l-SPD), possesses a pharmacological profile of D(1)/5-HT(1A) agonism and D(2) antagonism. In the present study, we examined the potential antipsychotic effect of l-SPD-A in a phencyclidine (PCP)-induced rat model of schizophrenia. Pretreatment with l-SPD-A blocked acute PCP-induced hyperlocomotion and reversed prepulse inhibition (PPI) deficits. Chronic l-SPD-A administration (i.p., 10mg/kg/day for 14 days) improved social interaction and novel object recognition impairments in rats that were pretreated with PCP (i.p., 5mg/kg/day for 14 days). Moreover, in a conditioned avoidance response (CAR) test, l-SPD-A, with either i.p. or oral administration, significantly decreased active avoidance without affecting the escape response of rats. Importantly, compared to that of the parent compound l-SPD, l-SPD-A showed stronger suppression of CARs. Lastly, using a [(35)S]GTPgammaS binding assay, we demonstrated that l-SPD-A improved impaired dopamine D(1) receptor function in the prefrontal cortex (PFC) in chronic PCP-treated rats. Taken together, these results indicate that l-SPD-A was not only effective against the hyperactivity, but also improved the sensorimotor gating deficit, social withdrawal and cognitive impairment in an animal model of schizophrenia. The present data suggest that l-SPD-A, a potential neurotransmitter stabilizer, is a promising novel candidate drug for the treatment of schizophrenia.
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PMID:Evaluation of the antipsychotic effect of bi-acetylated l-stepholidine (l-SPD-A), a novel dopamine and serotonin receptor dual ligand. 1974 33