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)

Prostitution among female street youths represents an important risk factor for several health problems. Little is known about the incidence and determinants of prostitution in this vulnerable population, and no data have been previously reported based on a longitudinal follow-up study. The objective of this study was to determine predictors of initiation into prostitution among female street youths. Female youths aged 14 to 25 years were enrolled in the Montreal Street Youth Cohort. They completed a baseline and at least one follow-up questionnaire between January 1995 and March 2000. Girls who reported never having engaged in prostitution at baseline were followed prospectively to estimate the incidence and predictors of prostitution. Of the 330 female street youths enrolled as of September 2000 in the cohort, 148 reported no history of involvement in prostitution at baseline and completed at least one follow-up questionnaire. Of these 148 girls, 33 became involved in prostitution over the course of the study (mean follow-up 2.4 years), resulting in an incidence rate of 11.1/100 person-years. Multivariate Cox regression analysis revealed having a female sex partner (adjusted hazard ratio [AHR] 3.8; 95% confidence interval [CI] 1.6-9.1) was an independent predictor of initiation into prostitution after controlling for having been on the street at age 15 years or younger (AHR 1.8, 95% CI 0.9-3.8), using acid or phencyclidine (PCP; AHR 2.0, 95% CI 0.9-4.6), using heroin (AHR 1.9, 95% CI 0.7-5.5), the use of drugs greater than twice per week (AHR 1.9, 95% CI 0.9-4.2), and injection drug use (AHR 0.8, 95% CI 0.3-2.4). The incidence of prostitution in female street youths was elevated. Having a female sex partner was a strong predictor of initiating involvement in prostitution.
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PMID:Predictors of initiation into prostitution among female street youths. 1546 40

Cultured rat hepatocytes were challenged with benzo[a]pyrene (BaP; 0.3-30 mum), naphthalene (NAPH; 0.1-100 mum), 2-methylnaphthalene (2-MNAPH; 0.1-100 mum), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 0.001-1 nM), 2,3,7,8-tetrachlorodibenzofuran (TCDF; 0.005-5 nM) or pentachlorophenol (PCP; 0.1-100 mum) for 4-24 hr to define class-specific differences in hepatotoxic potential. Mitochondrial fragility and GSH status were monitored as indices of hepatocyte injury. A 4-hr challenge with BaP and PCP increased mitochondrial fragility in a concentration-dependent manner, while TCDD and TCDF elicited erratic increases, and NAPH and 2-MNAPH were without effect. Pretreatment of hepatocytes with 250 muM diamide enhanced the mitochondrial toxicity of BaP. The aryl hydrocarbon receptor agonists upregulated hepatocyte GSH levels by 24 hr, a response which in the case of BaP was preceded by varying degrees of GSH depletion between 6 to 16 hr. NAPH and 2-MNAPH transiently decreased hepatocyte GSH levels at 12 hr, but were without effect at later time points, while PCP did not modulate hepatocyte GSH levels. Modulation of hepatocyte GSH by BaP and TCDD was antagonized by 10 muM alpha-naphthoflavone. These data implicate oxidative mechanisms and aryl hydrocarbon receptor signalling in aromatic hydrocarbon hepatotoxicity.
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PMID:Cytotoxic response profiles of cultured rat hepatocytes to selected aromatic hydrocarbons. 2065 98

The cytotoxic responses of cultured rat renal cortico-tubular epithelial cells (TECs) and glomerular mesangial cells (GMCs) to selected polycyclic and polyhalogenated aromatic hydrocarbons (AHs) were evaluated to further define class specific differences in toxicity potential among these chemicals. Primary cultures of renal cells were exposed to benzo[a]pyrene (BaP, 0.3-30mum); naphthalene (NAPH, 1-1000mum); 2-methylnaphthalene (2-MNAPH, 1-1000mum), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 0.01-1nm); 2,3,7,8-tetrachlorodibenzofuran (TCDF, 0.05-5nm; and pentachlorophenol (PCP, 0.1-10mum for 4 or 24hr. Measurements of mitochondrial membrane fragility in TECs revealed that the polycyclic aromatic hydrocarbons (PAHs) (BaP, NAPH and 2-MNAPH) preferentially injured these cells relative to halogenated aromatic hydrocarbons (HAHs). Extended exposures to all AHs tested were associated with moderate mitochondrial injury in TECs. Challenge of TECs with AHs for 4hr did not modulate GSH levels, although modest increases in this tripeptide occurred on extended exposures. Similar response profiles were observed in GMCs, where PAHs elicited mitochondrial damage by 4hr, while extended challenge was associated with injury in response to all AHs. Only aryl hydrocarbon receptor (AhR) ligands (BaP, TCDD and TCDF) depleted intracellular glutathione (GSH) in GMCs, while extended exposures to BaP and TCDD, as well as NAPH and 2-MNAPH, were associated with rebound increases in cellular GSH content. These data indicate that AHs can compromise renal cell function by interference with mitochondrial function and GSH homeostasis and implicate both epithelial and mesenchymal populations in the nephrotoxic response to this heterogeneous class of chemicals.
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PMID:Cytotoxic Response Profiles of Cultured Renal Epithelial and Mesenchymal Cells toSelected Aromatic Hydrocarbons. 2065 4