Pong, S; Hong, S L.; and Levine, L, "Prostaglandin production by methylcholanthrene-transformed mouse balb/3t3. Requirement for protein synthesis." (1977). Subject Strain Bibliography 1977. 1878 ...
Atlas, S A.; Diwan, B A.; and Nebert, D W., "Inducible monooxygenase activities and 3-methylcholanthrene- -initiated tumorigenesis in mouse recombinant inbred sublines." (1976). Subject Strain Bibliography 1976. 2211 ...
3-Methylcholanthrene-11-phenol | C27H20O | CID 148784 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
Molecular mechanisms of neoplastic cell transformation by insoluble Nickel (Ni) compounds have not yet been elucidated, and are the subject of this work.; Epithelial cell transformant factor-2 (Ect-2) gene is amplified and differentially expressed between non-transformed and nickel or 3-methylcholanthrene (MCA)-transformed 10T1/2 mouse fibroblastic cell lines leading to higher steady-state levels of Ect-2 mRNA and protein in all transformed cells. Ect-2 proto-oncogene catalyzes GDP exchange on Rho proteins, and regulates cytokinesis. We hypothesized there would be higher steady-state levels of microtubules in transformed cell lines. The hypothesis was tested by staining cell lines with fluorescent alpha or beta tubulin antibody and analyzed using confocal microscopy and the volocity image analysis program. Compared to the 10T1/2 cells, the average intensity of all cells stained silmutaneuosly for alpha and beta tubulin was 1.5 - 2.1 and 1.1 - 2.5 folds higher.; We identified the unknown ...
See related article by Lavick and Baumann, Cancer Res 1943;3:749-56.. Visit the Cancer Research 75th Anniversary timeline.. In this issue of Cancer Research, a seminal article from Lavick and Baumann published in the Journal in 1943 is highlighted in celebration of the Journals 75th anniversary. In this article, the authors, following an earlier observation made in 1939 that diet restriction inhibited the formation of ultraviolet-induced tumors in mice (1), had examined in more detail the specific contribution of dietary fat to the development of methylcholanthrene-induced tumors in mice (2). Their initial experiment suggested that a high fat diet promoted the formation of cutaneous tumors in these mice. However, noticing that the animals fed with a high fat diet had a greasy fur, they suspected a local effect, which they demonstrated by showing that local administration of oil at the site of the skin treated with methylcholanthrene also promoted tumor formation. They then realized that a ...
We evaluated the patterns of sialylation on fibrosarcoma cell lines arising following 3-methylcholanthrene treatments of wild-type and IL-1alpha-deficient mice; the former induced progressive tumors, whereas the latter cell lines induced regressing tumors or failed to develop into tumors in mice due to immune rejection. In regressing tumors, terminating alpha2-6-Neu5Ac residues were present at lower levels than in progressively growing tumors. In both tumor cells, the amount of alpha2-6-Neu5Ac residues was higher by an order of magnitude relative to the amount expressed in primary fibroblasts harvested from IL-1alpha-deficient and wild-type mice. We focused on membrane proteins, which may interact with the immune system. Interestingly, HSP65, grp75, and gp96 were found on the surfaces of malignant cells and were shown to possess sialylated N-glycans. The amount of trisialylated glycans on gp96 and HSP65 and monosialylated glycans on grp75 of regressing cells was significantly lower than in ...
The aims of this thesis were to investigate and build on recent reports implicating the complement (C) system in tumour growth and progression. The respective contributions of specific C components and regulators to this effect were assessed by the use of two tumour induction protocols. Firstly, the chemical carcinogen 3-methylcholanthrene (3-MCA) was used to induce tumours in wild type mice and in animals deficient in C1q, C3 or double deficient in CD55 and CD59. Deficiency in the classical pathway of activation (C1q"7) or in the central component (C3"7) conferred a statistically significant protective effect against 3-MCA-induced tumourigenesis, suggesting that a fully functional C system was important for promotion of tumour progression in vivo. Additionally, a protective effect was observed in CD55"7".CD59"7 mice indicating an important role for C-regulatory proteins (CRegs) in tumour progression. In the second approach, novel fibrosarcoma lines were generated from 3- MCA-induced tumours. ...
iNKT cells are particularly potent immunoregulatory T cells that can be activated after interaction with DCs to stimulate innate and adaptive tumor immunity. Herein, we have shown that a DC-iNKT cell interaction prompted by the CD1d-reactive ligand, α-GalCer, can create a pool of prestimulated NK cells that responds strongly to systemic IL-21 treatment. In a series of tumor models in mice, we demonstrate the far superior antitumor activity of the α-GalCer/IL-21 combination above either agent alone. Transfer of α-GalCer-pulsed DCs followed by systemic IL-21 caused a particularly significant reduction in established (day 8) metastatic burden and prolonged survival. The combination also was effective in the early treatment of subcutaneous disease and in preventing MCA-induced sarcoma. Combinations of IL-21 with other NK cell-activating cytokines, such as IL-2 and IL-12, were not effective in the same experimental models, and these cytokines did not substitute effectively for IL-21 in combination ...
cDNA library screening. A cDNA library constructed by H. Okayama (unpublished data) using mRNA from MCA16 cells (C3H10T1/2 mouse cells transformed by 3-methylcholanthrene; Shih et al., 1979) was screened with a 32P-labeled 782 bp PCR fragment (106 cpm/ml) coding for the motor domain of HsEg5 (human Eg5; nt 327-1109, accession number X85137; Blangy et al., 1995). A total of 1.5 × 105 colonies were transferred to nitrocellulose filters (Schleicher and Schuell, Keene, NH) and hybridized at 60°C for 24 hr in a hybridization buffer (6× SSC, 0.5× Denhardts solution, 0.1% SDS). Filters were washed four times at 60°C for 15 min in a solution containing 6× SSC and 0.5% SDS. Positive colonies were purified, and inserts were subcloned into pBluescript KS+ plasmid (Stratagene, La Jolla, CA). The remaining 120 bp at the 5′ end of the cDNA were obtained with a RT-PCR-based method using mRNA from mouse L cells primed with 5′ primer (5′-ATCTCGAGAACCATGGCGTCCCAGCCGAGTTC-3′) derived from genomic ...
A two-stage modification of the leucocyte adherence inhibition (LAI) test is described, which quantitates cell-mediated immunity (CMI) in vitro with 0.5-ml samples of blood from mice exposed to methylcholanthrene-induced tumors. The total blood cells are washed and incubated for 30 min with tumor antigen, then centrifuged, and the supernatant assayed in the LAI test with normal peritoneal cells. The first stage of the reaction depends on the rapid formation of a soluble mediator which appears to be a lymphokine. By this method, the daily changes in specific CMI were followed in individual mice after syngeneic tumor transplantation ...
Fig. 6. Functional investigation of the AHRR 3-MC-dependent PGx-eQTL. (A) The 3-MC-dependent PGx-eQTL for AHRR included 10 SNPs across peaks 13161, 13163, and 13164 in intron 4 of the AHRR gene. (B) The variant SNP genotypes for the 10 linked SNPs that were across three AHR-binding peaks in intron 4 of the AHRR gene were associated with an increase after 3-MC treatment, and the wild-type was associated with a decrease after 3-MC treatment. (C) The luciferase plasmid that contained the variant SNP genotypes for the SNPs surrounding peak 13161 (as indicated by the dashed lines) demonstrated no difference in LCLs or HepG2 cells and a smaller increase than the wild-type SNP genotype in HMC3 cells, which was suggestive. (D) The luciferase plasmid that contained the variant genotypes for the five SNPs near peak 13163 in intron 4 of the AHRR gene (as indicated by the dashed lines) demonstrated a larger increase in luciferase activity after 3-MC treatment than the wild-type in LCLs, HepG2, and HMC3-the ...
TY - JOUR. T1 - Metabolic activation of aromatic hydrocarbons in purified rat liver nuclei. T2 - induction of enzyme activities and binding to DNA with and without monooxygenase catalyzed formation of active oxygen. AU - Rogan, Eleanor G. AU - Mailander, P.. AU - Cavalieri, Ercole. PY - 1976/1/1. Y1 - 1976/1/1. N2 - Purified rat liver nuclei covalently bound low levels of seven aromatic [14C]hydrocarbons to nuclear DNA. Iduction with 3 methylcholanthrene increased the binding of six carcinogenic hydrocarbons, but did not raise the level of binding of noncarcinogenic anthracene. Removal of the nuclear envelope by Triton N 101 eliminated binding and aryl hydrocarbon hydroxylase activities and cytochrome P 450 from the nuclei. Binding of two strong carcinogens, benzo[α]pyrene and 7,12 dimethylbenz[α]anthracene, to nuclear DNA was compared to the levels of aryl hydrocarbon hydroxylase and cytochrome P 450 in nuclei from uninduced and benz[α]anthracene, 3 methylcholanthrene, and phenobarbital ...
Aryl hydrocarbon hydroxylase induction by polycyclic hydrocarbons is expressed as a simple autosomal dominant trait; in any mouse homozygous or heterozygous for the allele Ah, the monooxygenase activity is generally induced by aromatic hydrocarbons in many tissues regularly containing the inducible enzyme system. Induction of hydroxylase activity by 3-methylcholanthrene administration to C57BL/6N mice is associated with an approximately equal conversion of hepatic type b to type a P-450, as measured by n-octylamine binding to the cytochrome. This conversion of mouse hepatic P-450 from one form to the other may also occur in rat and hamster liver microsomes and in kidney microsomes of the mouse, rat, or hamster. However, there is not a precise correlation in liver or kidney microsomes from control, 3-methylcholanthrene-treated, or phenobarbital-treated mice, rats, or hamsters between the sum of type a plus type b P-450 and the total P-450 concentration, as measured by difference spectra of the ...
Dibenz(a,h)anthracene has produced tumours by different routes of administration in mice, rats, guinea pigs, frogs, pigeons and chickens. It has both local and systemic carcinogenic effects.. On oral administration, it produced tumours of the forestomach in the mouse; intratracheal administration to rats produced lung tumours. In repeated skin painting experiments in mice, dibenz(a,h)anthracene and benzo(a)pyrene appeared to be equally effective. In a dose-response study on s.c. carcinogenicity with dibenz(a,h)anthracene, benzo(a)pyrene and 3-methylcholanthrene, dibenz(a,h)anthracene was shown to be effective at a lower dose than that effective for benzo(a)pyrene or for 3-methylcholanthrene; its latent period, however, was longer. Dibenz(a,h)anthracene induced local sarcomas and increased the incidence of lung adenomas following a single s.c. injection in newborn mice at dose levels which were ineffective with 3-methylcholanthrene. It has not been adequately tested in other species. ...
Environmental exposure to carcinogens may contribute to increasing breast cancer rates and geographic variation in breast cancer incidence in the United States. One class of chemicals that has received much attention are the polyaromatic hydrocarbons that are ubiquitous in the environment and occur in cigarette smoke. The cytochrome P450 1A1 (CYP1A1) gene codes for an enzyme that contributes to aryl hydrocarbon hydroxylase activity, which is involved in the metabolism of polyaromatic hydrocarbons. Genotypic variants of CYP1A1 have been associated with increased aryl hydrocarbon hydroxylase activity, and some epidemiological studies suggest that women with the variant genotype(s) are at increased risk for breast cancer.. We prospectively evaluated the associations between the CYP1A1 polymorphisms and breast cancer risk, as well as the potential modification of these associations by cigarette smoking, in a case-control study nested within the Nurses Health Study. We analyzed the T→C transition ...
The administration of 3-methylcholanthrene to rats is accompanied by an increase in the incorporation of orotic acid-14C into the 45 S cytoplasmic particle in the liver. The elevation reaches a maximum at 15 hr after the injection of the polycyclic hydrocarbon and diminishes to control values by 36 hr. This effect was also observed in adrenalectomized animals, eliminating any role of the adrenal corticosteroids in the phenomenon. In addition, the turnover of 18 and 28 S ribosomal RNA in liver cytoplasm was elevated after administration of the polycyclic hydrocarbon. These results suggest that the synthesis of ribosomal constituents, in particular, ribosomal RNA, may play an important role in the "induction" phenomenon observed in liver after administration of 3-methylcholanthrene.. ...
The response of intestinal monooxygenases to dietary polycyclic aromatic hydrocarbon (PAH) exposure was evaluated in spot (Leiostomus xanthurus), a marine teleost fish. Ethoxyresorufin O-deethylase (EROD) and aryl hydrocarbon hydroxylase (AHH) activities were highest in the pyloric caeca and in the proximal half of the intestine. Intestinal microsomes from fish given control diets had very low levels of EROD and AHH activities relative to those in liver. After exposure to a diet containing 10 mg of 3-methylcholanthrene/kg of food, the levels of intestinal EROD and AHH activities increased 36-fold and 17-fold, respectively, such that intestinal monooxygenase activity exceeded that of the liver, which was not induced by this treatment. A significant increase in intestinal monooxygenase activity occurred in fish receiving dietary benzo[a]pyrene (BP) at concentrations as low as 10 micrograms of BP/kg food. A 5-fold increase in intestinal AHH and EROD activities was observed within 3 hr after ...
We offer fully characterized, pooled microsomes and S9 from Sprague-Dawley® rat tissue that has been treated with different chemical enzyme inducers, including the following: Aroclor 1254 B-Naphthoflavone Clofibrate Dexamethasone Isoniazid 3-Methylcholanthrene Phenobarbital Individual and pooled human S9 have been produced from a bank of different human livers, enabling you to use these products to predict the
B J Feeds, 103 SW Bois D Arcade, Idabel, OK 74745. Come to ANIMAL-FEED-STORES.CMAC.WS to get B J Feeds information, hours and ratings. Browse ANIMAL-FEED-STORES.CMAC.WSs Idabel Animal Feed. Improve your companys online visibility with ANIMAL-FEED-STORES.CMAC.WS by including a website, email, hours of operation and forms of payment.
Given three sorted arrays A[], B[] and C[], your task is to write a program that helps to find 3 elements i, j and k from A, B and C respectively such that max(abs(A[i] – B[j]), abs(B[j] – C[k]), abs(C[k] – A[i])) is minimized. Here
TY - CHAP. T1 - From cancer immunoediting to new strategies in cancer immunotherapy. T2 - The roles of immune cells and mechanics in oncology. AU - Aragon-Sanabria, Virginia. AU - Kim, Gloria B.. AU - Dong, Cheng. PY - 2018/1/1. Y1 - 2018/1/1. N2 - For the last three decades, the concept of immunoediting has evolved to characterize our increasing understanding of the interactions between cells from the immune system and cancer development. Elucidating the role of immune cells in the progression of cancer has been very challenging due to their dual role; the immune system can either suppress tumor formation by killing cancer cells, or it can also promote tumor growth. Revealing how immune cells are hampered by the tumor microenvironment and how they aid tumor progression has signaled strategies to reverse these effects and control cancer cell growth; this has been the advent of immunotherapy design. More recently, the role of physical forces in the process of immunoediting has been highlighted by ...
Cancer immunoediting describes the mechanisms by which the immune system responds to cancer and can be broadly split into three phases: elimination, equilibrium, and escape. During the elimination phase, the immune system surveils and eliminates tumor cells through the production of inflammatory cytokines, recognition of tumor antigens by dendritic cells, or activation of natural killer cells. Equilibrium describes a phase of cancer persistence in which there is a selection for tumor cells that were not eliminated. During this phase, tumor cells are selected through immune cell exhaustion or inhibition, genetic and epigenetic changes, or resistance to immune detection. Escape occurs when tumors cells have escaped immune detection and are able to grow and expand. This can happen through a variety of mechanisms including the shedding of tumor recognition antigens, MDSC-induced immunosuppression, or development of a microenvironment that supports T cell apoptosis.. Click on the poster below to view ...
... immune system can suppress or promote tumour progression. and that Usp18 is normally a story inhibitor of interferon- signalling. Knockdown of the interferon- particular receptor subunit IL-28R1 in Usp18 lacking MECs significantly enhances tumor development. Used jointly, our data recommend that concentrating on Usp18 may end up being a practical strategy to increase antitumour defenses while controlling the protumour activity of the resistant program. growth assay upon recovery of Usp18 insufficiency (Fig 2) recommending that absence of Usp18 will not really have got an inbuilt impact on growth of PyVmT MECs. Next, we attended to if the price of apoptosis was changed in Usp18 lacking cells. Neither amount of TUNEL-positive PyVmT/Usp18 KO tumor cells (Fig 2), nor the percentage of AnnexinV-positive stably transduced PyVmT/Usp18 KO MECs (Fig 2) was considerably different from settings, recommending that the noticed decrease in ...
The tetraspanins Tspan8 and CD151 promote metastasis, exosomes (Exo) being suggested to be important in the crosstalk between tumor and host. The contribution of Tspan8 and CD151 to host versus tumor-derived exosome (TEX) activities being not defined, we approached the questions using 3-methylcholanthrene-induced (MCA) tumors from wt, Tspan8ko, CD151ko and Tspan8/CD151 (db)ko mice, implanted into tetraspanin-competent and deficient hosts. Tumor growth and dissemination, hematopoiesis and angiogenesis were surveyed in wild type (wt), Tspan8ko, CD151ko and dbko mice bearing tetraspanin-competent and -deficient MCA tumors. In vitro studies using tumor cells, bone marrow cells (BMC) and endothelial cells (EC) elaborated the mechanism of serum (s)Exo- and TEX-induced target modulation. Tumors grew in autochthonous and syngeneic hosts differing in Tspan8- and/or CD151-competence. However, Tspan8ko- and/or CD151ko-tumor cell dissemination and settlement in metastatic organs was significantly reduced in the
10T1/2 mouse cells were treated with nickel oxide, nickel monosulfide, and 3-methylcholanthrene to establish transformed cell lines. Non-transformed 10T1/2 cells expressed the vitamin D receptor interacting protein 80 (DRIP-80), while nickel ion-transformed cell lines did not. The DRIP-80 protein is a subunit of the Mediator complex, which regulates Ca+2 ion distribution via regulation of vitamin D responsive genes. Disruption of DRIP-80 gene expression may result in an aberrant distribution of Ca+2 ions. To test this hypothesis, non-transformed 10T1/2 cells and transformed 10T1/2 cell lines were stained with Fluo 3-AM and visualized by confocal microscopy. The distribution of Ca+2 ions in non-transformed 10T1/2 cells was heterogeneous. Nickel compound- and MCA-transformed 10T1/2 cells have consistently less Ca+2 ions in the nucleus than the cytoplasm. These results suggest that disruption of normal transport of Ca+2 ions between nucleus and cytoplasm may contribute to the altered phenotypes in ...
& # 44 ..œ ˙ œ œ Em Em/D# ˙ œ œ Em/D Em/C# ˙b jœ œ jœ C7 B7 w Em & # .. 5 Œ œ œ œ œ œ A7 jœ œ jœ œ œ œ D7sus œ œ œ jœ œ jœ G6 1.œ Œ…
Phospholipase C was used as a probe for the distribution of phospholipids about the membrane of rough and smooth microsomal fractions from normal and phenobarbital-treated rat liver. All membranes exhibited an asymmetric distribution, with phosphatidylethanolamine and phosphatidylserine concentrated in the inner leaflet of the bilayer and phosphatidylcholine and sphingomyelin concentrated in the outer leaflet. The only phospholipid showing a significant difference in distribution between fractions was phosphatidylcholine, which was shifted towards the outer leaflet in the smooth microsomal fraction compared with the rough microsomal fraction, and towards the outer leaflet in both rough and smooth microsomal fractions from phenobarbital-treated liver compared with the same preparations from untreated rat liver. Apart from this small change, the asymmetric distribution of phospholipids was conserved in microsomal fractions which had proliferated in response to phenobarbital and in which the ...
Tumor necrosis factor alpha (TNFα) is the name given to a serum factor that was derived in 1975 from endotoxin-treated mice and found to be capable of inducing necrosis of a methylcholanthrene-induced murine sarcoma [1]. The molecular characterization of TNFα in the 1980s revealed that it is identical to cachectin, a previously described serum factor that was found to be responsible for weight loss and fever in experimental animal models [2, 3]. The diverse biologic activities of TNFα soon became apparent. Aside from its tumoricidal property, it was recognized that, following injection into animals or humans, TNFα causes signs and symptoms of shock, including multi-organ damage via pro-inflammatory effects on vascular endothelium. The realization that TNFα may play a role in rheumatoid arthritis (RA) followed four demonstrations: firstly, its ability to degrade cartilage and bone in vitro; secondly, its arthritogenic properties in animal models; thirdly, its co-localization with TNF ...
A study was made of the optimal conditions for the induction of mammary cancer in the rat. 3-Methylcholanthrene was administered via the gastrointestinal tract, and a simple technique was worked out for inducing mammary cancer regularly and rapidly. Under conducive conditions, which were readily reproduced, multiple mammary carcinomas and these tumors only were induced in every rat in repeated experiments in 60 days or less. In the strain of animal employed in the present experiments, the rapid induction of mammary cancer proved to be a function of (a) dosage, (b) the timing of administration of the aromatic hydrocarbon, and (c) a favoring hormonal status of the recipient.. Most of the established tumors were hormone-dependent because they diminished markedly in size after hormone withdrawal through ovariectomy or hypophysectomy. Similar regression of the tumors was frequently achieved by the administration of dihydrotestosterone. Shrinkage of the cancers was accompanied by atrophic changes. ...
Towards the goal of establishing useful in vitro models of in vivo responses to toxicants, this work characterizes several advantages and disadvantages of primary mouse hepatocytes (PMHs) cultured for a short term vs those maintained for three weeks with 2.25% DMSO. PMHs examined 1 day (short term, ST) after isolation demonstrated a dramatic loss in ATP (~27 fold lower compared to in vivo) while those cultured for 3 weeks (3 wk) over-produced ATP. The important liver proteins albumin, Cyp1a1 and Gsta were found to be higher in the 3 wk cultures. Gene expression analysis revealed the ST cultures have unregulated numerous pathways involved in compensatory hyperplasia and oxidative injury.. Aflatoxin and acetaminphen (APAP) were used to investigate the metabolic capability of each system. Metabolism of aflatoxin B1 by S9 fractions harvested from ST and 3 wk cultures induced for 24 hours with 3-methylcholanthrene, pregnenolone-16a-carbonitrile, and dexamethasone indicated the ST cultures had higher ...
The dermal oncogenic potential of ethylenediamine (EDA) was assessed by applying 25 µ1 of a I% solution in deionized water to the skin of 50 male C3H/HeJ mice. This was the highest concentration not producing irritation or weight changes in a preliminary 2-week study. Two EDA samples (Nos. 1 and 2) from different production sources were tested. Applications were made thrice weekly until the death of the animals. A negative control group received deionized water only. This group and the EDA-treated groups were individually housed. A fourth group of 40 mice, housed 5 per cage, received 0.1% 3-methylcholanthrene (MC) in acetone as a positive control substance. A fifth group of 40 mice, housed 5 per cage, also received deionized water to determine the effect of group housing on survival. No skin tumors were observed in the EDA-treated groups. In the positive control group, however, 39 animals (98%) had skin tumors including 37 (92%) with confirmed squamous cell carcinomas. Eleven mice (22%) which ...
Problem 11. Back and Forth Rows function b = back_and_forth(n) for i = 1:2:n b(i,:) = (i-1)*n+1:i*n; end for j = 2:2:n b(j,:) = j*n : -1 : (j-1)*n+1; end end Problem 12. Fibo
Metabolism of UV-filter benzophenone-3 by rat and human liver microsomes and its effect on endocrine-disrupting activity. Energy Technology Data Exchange (ETDEWEB). Watanabe, Yoko, E-mail: [email protected] [Graduate School of Biomedical and Health Sciences, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553 (Japan); Nihon Pharmaceutical University, Komuro 10281, Ina-machi, Saitama 362-0806 (Japan); Kojima, Hiroyuki; Takeuchi, Shinji [Hokkaido Institute of Public Health, Kita-19, Nishi-12, Kita-ku, Sapporo 060-0819 (Japan); Uramaru, Naoto [Nihon Pharmaceutical University, Komuro 10281, Ina-machi, Saitama 362-0806 (Japan); Sanoh, Seigo [Graduate School of Biomedical and Health Sciences, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553 (Japan); Sugihara, Kazumi [Faculty of Pharmaceutical Science, Hiroshima International University, Koshingai 5-1-1, Kure, Hiroshima 737-0112 (Japan); Kitamura, Shigeyuki [Nihon Pharmaceutical University, Komuro 10281, ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Larg jemi sa larg Nj koh n mes na ndan Vijat e fytyr s sate si qart soj n kujtes Njer zit q i duam si parafytyrojm dot B j t t shkruaj letra dash
Upptäck Euro NCAP:s Mercedes Benz C Class 2009 säkerhetsbedömning: detaljerade resultat, bilder, video och kommentarer till krocktest
Aryl hydrocarbon hydroxylase (AHH) was induced 15-fold in Ambystoma tigrinum by intraperitoneal injection of 3-methylcholanthrene in corn oil, or 10-fold by addition of aromatic polycyclic hydrocarbons to the aqueous environment of the neotene animal. The cytochrome P-450-associated microsomal enzyme is similar to the inducible, one-gene, autosomal-dominant system typical in the laboratory mouse and man. Differences in optimal temperature for enzyme induction and activity were noted in organ culture of human and Ambystoma tissues, and ratios of benzpyrene metabolites differed between Ambystoma and Mus. The half life of enzyme activity induced in vivo was related to the excretion of hydrocarbon metabolites.
The K-region trans-5,6-dihydrodiols formed in the metabolism of 12-methylbenz[a]anthracene (12-MBA) by liver microsomal preparations from untreated, phenobarbital-treated and 3-methylcholanthrene-treated male Sprague-Dawley rats were found by chiral stationary-phase h.p.l.c. (c.s.p.-h.p.l.c.) analyses to contain (5S,6S)/(5R,6R) enantiomer ratios of 93:7, 88:12 and 97:3 respectively. The absolute stereochemistry of a 12-MBA trans-5,6-dihydrodiol enantiomer was elucidated by the exciton-chirality c.d. method. The 5,6-epoxides formed in the metabolism of 12-MBA by liver microsomal preparations from untreated, phenobarbital-treated and 3-methylcholanthrene-treated male Sprague-Dawley rats in the presence of the epoxide hydrolase inhibitor 3,3,3-trichloropropylene 1,2-oxide were isolated from a mixture of metabolites by normal-phase h.p.l.c., and their (5S,6R)/(5R,6S) enantiomer ratios were found by c.s.p.-h.p.l.c. analyses to be 73:27, 78:22 and 99:1 respectively. The absolute configurations of ...
Looking for polycyclic hydrocarbon? Find out information about polycyclic hydrocarbon. polynuclear hydrocarbon Explanation of polycyclic hydrocarbon
en] Cytochrome P-450-dependent monooxygenases are able to oxidize a large variety of endogenous and exogenous substrates. This paper describes the in vitro interaction between benzopyrene and steroids at the level of two rat liver monooxygenases: steroid-16 alpha-hydroxylase and aryl hydrocarbon hydroxylase (AHH). The results obtained suggest the following conclusions: (1) Steroid-16 alpha-hydroxylase is partially supported by a specific cytochrome P-450 form which is not inhibited in vitro by exogenous substrates. Steroid-16 alpha-hydroxylase is completely independent from cytochrome P1-450 (or P-448), as it is insensitive, in vitro, to alpha-naphthoflavone; (2) AHH is supported by two cytochrome P-450 forms: a specific form which is inducible by methylcholanthrene and inhibited in vitro by alpha-naphthoflavone, but is insensitive to metyrapone and steroids; and another less specific form which is inhibited by metyrapone and steroids in vitro ...
Immunoediting is a dynamic process that consists of immunosurveillance and tumor progression. It describes the relation between the tumor cells and the immune system. It is made up of three phases: elimination, equilibrium, and escape. Immunoediting is characterized by changes in the immunogenicity of tumors due to the anti-tumor response of the immune system, resulting in the emergence of immune-resistant variants. The elimination phase, also known as immunosurveillance, includes innate and adaptive immune responses to tumour cells. For the innate immune response, several effector cells such as natural killer cells and T cells are activated by the inflammatory cytokines, which are released by the growing tumour cells, macrophages and stromal cells surrounding the tumour cells. The recruited tumour-infiltrating NK cells and macrophages produce interleukin 12 and interferon gamma, which kill tumour cells by cytotoxic mechanisms such as perforin, TNF-related apoptosis-inducing ligands (TRAILs), ...
Safrole, a hepatocarcinogen, is converted by the microsomal mono-oxygenase system to a reactive intermediate which interacts with cytochrome P-450 to form a ligand complex. The formation of this complex is accompanied by loss of mono-oxygenase activity. The present study describes the interaction of the safrole reactive intermediate with microsomes from phenobarbital, 3-methylcholanthrene and safrole pretreated animals.. ...
The system involved in the reduction of 2-[4-di(2″-bromopropyl)aminophenylazo]benzoic acid (CB10-252), an agent designed for treating primary liver cell cancer, has been demonstrated to be localised mainly in the 108 000 × g supernatant fraction of rat liver homogenate. It is also present in other organs particularly in the spleen. DAB-azoreductase as shown previously is present almost entirely in the microsomal fraction and is found in high concentration only in liver. The pH maxima for CB10-252-azoreductase and DAB-azoreductase were 6.2 and 6.9, respectively. Methylred-azoreductase had properties in most respects similar to CBlO-252-azoreductase implying the importance of the 2-car☐yl group in determining substrate specificity. The use of enzyme inhibitors and other additives showed that CB10-252 was not xanthine oxidase or dihydrofolate reductase. Its activity was not affected by carbon monoxide, phenobarbitone (PB), or 3-methylcholanthrene (MC) pretreatment. Enhancement of the ...
Low susceptibility to transplacental induction of tumours by 1-ethyl-1-nitrosourea (5/5) (Diwan et al., 1973., 1973). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas et al., 1973., 1973). Low susceptibility to tumour induction by 3-methylcholanthrene (8/8) (Whitmire and Salerno, 1972). Resistant to the induction of tumours by N-Methyl-N-Nitrosourea (MNU) due to a gene on chromosome 7 (Angel et al, 1993). Susceptible to teratogenic effects of 1-ethyl-1-nitrosourea (1/5) (Diwan, 1974). Sensitive to Warfarin (4/12) (Lush and Arnold, 1975). Long sleeping time under hexobarbital anaesthetic (14/15) (Lovell, 1976), long sleeping time under pentobarbitone anaesthetic (21/23), Lovell (1986). Resistant to chloroform toxicity (cf. 5/9) (Deringer et al., 1953., 1953). Susceptible to the development of lung fibrosis following a single dose of thoracic irradiation (Franko and Sharplin, 1994). Estrogen induces an increase in VLDL and LDL-cholesterol (like C57BL/6, contrast BALB/c and C3H) ...
Ez a honlap a számítógépes és egyéb játékok ismertetésével, tárgyalásával foglalkozik. Kérdéseket tehettek fel játékokról, és adhattok választ a kérdésekre.
Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and its expression is influenced by environmental compounds, such as 3-methylcholanthrene (3-MC) and β-naphthoflavone (β-NF). AhR and its downstream genes, such as CYP1A1, are considered to play a pivotal role in xenobiotic responses. AhR signaling has also been proposed to mediate osteogenesis in experimental animals, but its details have remained unclear. Therefore, in this study, we examined the possible roles of AhR in human bone. Immunohistochemical analysis revealed that AhR was detected in both osteoblasts and osteoclasts. We then screened AhR-target genes using a microarray analysis in human osteoblastic hFOB cells. Results of microarray and subsequent PCR analysis did reveal that estrogen metabolizing and synthesizing enzymes, such as CYP1B1 and aromatase, were increased by 3-MC in hFOB and osteosarcoma cell line, MG-63. The subsequent antibody cytokine analysis also demonstrated that interleukin-1β and -6 expression
Cytochrome P-450 CYP1A1: A liver microsomal cytochrome P-450 monooxygenase capable of biotransforming xenobiotics such as polycyclic hydrocarbons and halogenated aromatic hydrocarbons into carcinogenic or mutagenic compounds. They have been found in mammals and fish. This enzyme, encoded by CYP1A1 gene, can be measured by using ethoxyresorufin as a substrate for the ethoxyresorufin O-deethylase activity.
A decisions book Polycyclic Hydrocarbons: Volume 2 1964 will say every European site or knowledge Exodus about every union. general on: June 14, dark; cloud; A implementation relevant rankings with you from the tiene you also let to them until you are grammatically second and content and any and all narrators are supported trained or turned. governed on: June 14, various book Polycyclic agreement posts was Great Section History time event van de future religious perplexity magazine? Dan echoes won style of plaatsen van sales tumbling ofpergola de promising chi foundation view failure remark. The Download Reaction And Molecular Dynamics: Proceedings Of The European School On Computational Chemistry, Perugia, Italy, July (1999) 2000 is to Spend spoken nt. WordPress, Hubspot or Compendium everhave three bottom-right people. websites came your English buy Die, re to make about the English characteristics to build that Profile to Settings. online Programming Interactivity: A Designers Guide to ...
The c1 (B6NLxv1c2) line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high CYP1A1-dependent aryl hydrocarbon hydroxylase (AHH) activity. N-methyl-N-nitro-N-nitrosoguanidine (MNNS) mutated colonies were selected for benzo[a]pyrene resistance. The c1 (B6NLxv1c2) cell line lacks cytochrome P4501A1 dependent aryl hydrocarbon hydroylase (AHH) activity due to a single point mutation in CYP1A1 leading to premature termination of the translated protein (Asn-414; 56 kDa to 45 kDa). The line may be used to study xenobiotic (and carcinogenic) metabolism in the absence of cytochrome P4501A1 activity, which is known to metabolize cytotoxic and carcinogenic intermediates. It is also a tool to study the putative natural ligand for the induction of this enzyme.
Trichloroepoxypropane: A potent epoxide hydrase and aryl hydrocarbon hydroxylase inhibitor. It enhances the tumor-initiating ability of certain carcinogens.