Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.17 (PCE)
 1,301 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequency of micronucleated polychromatic erythrocytes (MPCE) and normochromatic erythrocytes (MNCE) was studied in Swiss albino mice treated with 0, 0.025, 0.05, 0.1, 0.25, 0.5, 1 and 2 mg/kg body weight of cadmium chloride. It was observed that cadmium chloride induced a dose-dependent increase in the frequency of MPCE and MNCE. However, this increase was significant only after treatment with 0.05 mg/kg of CdCl2 (MPCE). The polychromatic and normochromatic erythrocyte ratio (PCE/NCE ratio) declined with the increase in CdCl2 dose and this depletion was dose-dependent. A significant decline was observed only after 0.25 mg/kg CdCl2. The dose-response relationship for all three parameters was linear-quadratic.
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PMID:Cadmium chloride induces dose-dependent increases in the frequency of micronuclei in mouse bone marrow. 751 6

The genotoxicity of human fetal cell extract (HFCE) and its effect on the frequency of micronucleated polychromatic erythrocytes (PCE-MNF) in mice induced by cyclophosphamide (CP) were studied. Statistically significant differences were not found between the control group and each group treated with HFCE (0.3, 3, 30 mg/kg bw). CP (200 mg/kg bw) induced a marked increase in MNF (P < 0.01). Administered together with CP, HFCE suppressed the increase of MNF induced by CP. The reduction effect is dependent on the dose of HFCE. At doses of 3 and 30 mg/kg bw HFCE, MNF decreased markedly (P < 0.05 and < 0.01, respectively). It showed that HFCE did not induce micronucleus formation, while it could suppress the micronucleus formation induced by CP in mice. The results suggested that HFCE might be antimutagenic and have potential value in clinical application.
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PMID:Suppressing effects of human fetal cell extract on micronuclei induced by cyclophosphamide in mice. 752 74

Phenolphthalein was tested for the induction of micronucleated erythrocytes in mice. Results of an initial investigation revealed significant, dose-related increases in micronucleated polychromatic erythrocytes (MN-PCE) and normochromatic erythrocytes (MN-NCE) in peripheral blood samples of male and female mice exposed to 0.6% to 5% phenolphthalein (approximately 1100 to 10,000 mg/kg/day) in feed for 90 days (Dietz et al., 1992). Results from a second long-term feed study with Swiss CD-1 mice confirmed this effect. However, administration of comparable doses of phenolphthalein by corn oil gavage on two consecutive days gave negative results in a mouse bone marrow micronucleus test. Subsequent tests were performed to clarify the conflicting results seen in the chronic exposure, dosed-feed, peripheral blood studies and the acute, corn oil gavage, bone marrow studies. Phenolphthalein was administered to male B6C3F1 mice in feed (3%) for 14 days. Peripheral blood samples taken at 4, 7, and 14 days all showed significant increases in micronucleated PCE; bone marrow samples taken on days 7 and 14 also were clearly positive for micronucleus induction. Therefore, comparable results were obtainable from both bone marrow and peripheral blood analyses. Because of the negative results in the two-exposure gavage test, additional tests were then designed to investigate the effects of bolus vs continuous dosing, feeding vs gavage administration, and corn oil vs feed as a carrier for phenolphthalein. Results of these tests indicated that the rate of exposure to phenolphthalein affects the frequency of induced MN-PCE and that micronucleated erythrocytes can be induced by phenolphthalein either by feeding or by corn oil gavage administration. In all the acute exposure studies, relatively high doses of phenolphthalein (2000-6000 mg/kg/day for at least 2 days) were required to induce micronuclei. The positive results obtained with phenolphthalein in vivo were consistent with the results of an in vitro chromosomal aberration test in Chinese hamster ovary cells, where dose-related increases in aberrations were noted only in cells treated in the presence of induced rat liver S9.
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PMID:Phenolphthalein: induction of micronucleated erythrocytes in mice. 752 56

Degradation of tetrachloroethene (perchloroethylene, PCE) was investigated by combining the metabolic abilities of anaerobic bacteria, capable of reductive dechlorination of PCE, with those of aerobic methanotrophic bacteria, capable of co-metabolic degradation of the less-chlorinated ethenes formed by reductive dechlorination of PCE. Anaerobic communities reductively dechlorinating PCE, trichloroethene (TCE) and dichloroethenes were enriched from various sources. The maximum rates of dechlorination observed for various chloroethenes in these batch enrichments were: PCE to TCE (341 mumol l-1 day-1), TCE to cis-dichloroethene (159 mumol l-1 day-1), cis-dichloroethene to chloroethene (99 mumol l-1 day-1) and trans-dichloroethene to chloroethene (22 mumol l-1 day-1). A mixture of these enrichments was inoculated into an anoxic fixed-bed upflow column. In this column PCE was converted mainly into cis-1,2-dichloroethene, small amounts of TCE and chloroethene, and chloride. Enrichments of aerobic methanotrophic bacteria were grown in an oxic fixed-bed downflow column. Less-chlorinated ethenes, formed in the anoxic column, were further metabolized in this oxic methanotrophic column. On the basis of analysis of chloride production and the disappearance of chlorinated ethenes it was demonstrated that complete degradation of PCE was possible by combining these two columns. Operation of the two-column system under various process conditions indicated that the sensitivity of the methanotrophic bacteria to chlorinated intermediates represented the bottle-neck in the sequential anoxic/oxic degradation process of PCE.
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PMID:Complete degradation of tetrachloroethene by combining anaerobic dechlorinating and aerobic methanotrophic enrichment cultures. 757 59

1. We have studied the effects of tetrachloroethylene (PCE) on the kinetics of the P450-dependent monooxygenases in rat liver microsomes. 2. 7-Pentoxyresorufin O-depentylase (PROD) and 7-benzyloxyresorufin O-debenzylase (BROD) activities in phenobarbital (PB)-treated rat liver microsomes were substantially inhibited by PCE. The inhibition profiles were non-competitive for both enzyme activities; Ki's from Eadie-Hofsee plots were 0.16 and 0.29 mM for PROD and BROD respectively. In contrast, the enzyme activities in untreated, beta-naphthoflavone (BNF)-, isoniazid (ISN)- and pregnenolone-16 alpha-carbonitrile (PCN)-induced microsomes were not affected by PCE. 3. 7-Ethoxycoumarin O-deethylase (ECOD) activity in PB-induced microsomes was competitively inhibited by PCE, with a Ki that was lower than those of other microsomes. 4. PCE inhibited 7-ethoxyresorufin O-deethylase (EROD) activities in some microsomes slightly. The Ki for PCE was the lowest in untreated, followed by ISN-treated microsomes. 5. No effect of PCE upon aniline 4-hydroxylase (AN4H) and testosterone 6 beta-hydroxylase (TS6BH) activities was evident in any microsomal preparation. 6. These results indicate that PCE inhibits PB-inducible, P450-dependent monooxygenases in vitro non-competitively or competitively, and that the P450 enzymes of the P4502B subfamily may contribute to PCE toxicity.
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PMID:Interaction of tetrachloroethylene with rat hepatic microsomal P450-dependent monooxygenases. 761 43

A 3.5-kb genomic DNA fragment containing the X1R chromosome-linked retina-specific Arrestin B gene (also called Arrestin 2) of Drosophila miranda (ArrB-mr) was introduced into the Drosophila melanogaster genome via germ-line transformation. The results showed that the ArrB-mr transgene was expressed only in the retina of the transformed flies. The transgene also showed male-specific transcriptional hyperactivation or dosage compensation, but the level was found to be 71-79% of the expected value. The endogenous autosomal ArrB-ml gene of D. melanogaster, as expected, was not found to be dosage compensated in the transformants. Thus, while the cis-regulatory elements for retina-specific expression are fully present in the 3.5-kb DNA, part of the sequences needed for full dosage compensation are missing in this DNA. Nucleotide (nt) sequence comparison of the upstream DNA revealed that both ArrB-mr and ArrB-ml possess a putative TATA box at -32 nt. They also have an 11-bp motif (5'-AATCCAGTTAG) similar to the photoreceptor conserved element I (PCE I) believed to play an important role in retina-specific expression of the D. melanogaster opsin and mouse Arr genes. In addition, both genes contain a TGACCT motif which is known to bind a transcription factor activated by retinoic acid and vitamin D3. However, five tandem repeats of a heptanucleotide sequence (TGGGCNR) and a 29-bp sequence with the potential to form a stem-loop structure, are found only in the ArrB-ml gene. These sequences may play an important role in dosage compensation of the X1R-linked ArrB-mr gene.
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PMID:A 3.5-kb DNA fragment contains the cis-regulatory elements for retina-specific expression and partial dosage compensation of the Arrestin B (ArrB) gene of Drosophila miranda. 764 93

Observation of a patient with a history of asthma who presented a lung pathology in a context linked with the general condition, radiology of a biological inflammatory syndrome and hypereosinophilia, suggested a diagnosis of Chronic Pneumopathy of Eosinophils (PCE). The chronology of the symptomatology favours an occupational role of sulphites, to which the patient is exposed by the respiratory pathway and the reproduction of the symptoms in an identical exposure confirmed the hypothesis.
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PMID:[Occupational eosinophilic lung in a grape grower: role of sulfites]. 766 4

Micronucleus induction in peripheral blood was examined during carcinogenicity assays of the genotoxic carcinogens 2-acetylaminofluorene (2-AAF), benzene, diethylnitrosamine (DEN) and 1,2-dichloroethane (1,2-DCE) in lymphoma prone E mu-PIM-1 transgenic mice. In both sexes, micronuclei were increased in polychromatic (PCE) and normochromatic (NCE) erythrocytes after 14 weeks of oral treatment with 75 mg/kg 2-AAF or 50 and 100 mg/kg benzene. The micronucleus frequencies induced by benzene were higher in males than in females. There was no apparent treatment related suppression of erythropoiesis by 2-AAF or by benzene. Blood micronucleus frequencies induced by benzene were similar in transgenic mice and their non-transgenic litter mates. There was no micronucleus induction or PCE suppression detected in the blood of either sex after treatment with 1 and 3 mg/kg DEN or 100 to 300 mg/kg 1,2-DCE. At 40 weeks bone marrow was sampled from mice given 100 mg/kg benzene, and it was confirmed that micronucleated PCE frequencies in blood were an accurate reflection of those induced in bone marrow. However, the spontaneous and induced frequencies of micronucleated cells in blood were slightly higher in PCE than in NCE suggesting that a small degree of selective removal of micronucleated cells occurs in this mouse strain. Control micronucleus frequencies in E mu-PIM-1 mice appeared comparable to those in other, non-transgenic mouse strains. Thus micronuclei are readily detectable in blood during chronic exposure to the bone-marrow clastogens 2-AAF and benzene, but not to DEN and 1,2-DCE, probably because active species do not reach the bone marrow in sufficient concentrations to induce increases in micronuclei.
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PMID:Micronuclei induced in peripheral blood of E mu-PIM-1 transgenic mice by chronic oral treatment with 2-acetylaminofluorene or benzene but not with diethyl-nitrosamine or 1,2-dichloroethane. 768 8

Recent reports reveal that the C-terminal half of the neuroendocrine polypeptide 7B2 selectively inhibits and binds PC2, a mammalian prohormone converting enzyme that is homologous to the yeast pro-alpha-factor processing protease Kex2. During attempted secretion of the 185 amino-acid human 7B2 in Saccharomyces cerevisiae, we observe that the protein is mostly retained inside the cell. However a mutant polypeptide (7B2 delta 1), where the C-terminal 48 amino acids of 7B2 are deleted, is efficiently secreted. Two shorter C-terminal truncations either permit poor secretion or no secretion at all. Surprisingly, full-length 7B2 but not 7B2 delta 1 abolishes the catalytic activity of Kex2, indicating that C-terminal residues of 7B2 might also be important for inhibition of the yeast protease. When the KEX2 gene is disrupted, yeast cells unexpectedly secrete a 7B2 variant similar in size to 7B2 delta 1, suggesting involvement of the alternate yeast prohormone convertase Yap3 in processing. Secretion is enhanced by overexpression of Yap3 and by the presence of a Lys-Arg residue at the processing site of precursor 7B2. These results purport that, in neuroendocrine cells too, secretion of 7B2 could be mediated by a homologue of Yap3.
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PMID:A C-terminal domain, which prevents secretion of the neuroendocrine protein 7B2 in Saccharomyces cerevisiae, inhibits Kex2 yet is processed by the Yap3 protease. 775 May 51

Desulfomonile tiedjei, a strict anaerobe capable of reductively dechlorinating 3-chlorobenzoate, also dechlorinates tetrachloroethene and trichloroethene. It is not known, however, if the aryl and aliphatic dechlorination activities are catalyzed by the same enzymatic system. Cultures induced for 3-chlorobenzoate activity dechlorinated tetrachloroethene and trichloroethene to lower chlorinated products while uninduced parallel cultures did not dechlorinate either substrate. The observed rate of PCE dechlorination in induced cultures was 22 mumol h-1 g protein-1, which is considerably faster than previous rates obtained with defined cultures of this organism. These results show that both dechlorination activities are co-induced and therefore, that the dechlorination mechanisms may share at least some components.
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PMID:Tetrachloroethene and 3-chlorobenzoate dechlorination activities are co-induced in Desulfomonile tiedjei DCB-1. 777 42


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