WordNet

markedly subnormal in structure or function or intelligence or behavior; "defective speech"
having a defect; "I returned the appliance because it was defective" (同)faulty
a threadlike strand of DNA in the cell nucleus that carries the genes in a linear order; "humans have 22 chromosome pairs plus two sex chromosomes"

PrepTutorEJDIC

『欠点のある』,欠陥のある / 欠けている,足りない,(知能的に)標準以下の / 精神障害者,身体障害者
染色体

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1. 先天性の細胞遺伝学的異常 congenital cytogenetic abnormalities
2. 症候群をきたす免疫不全症 syndromic immunodeficiencies
3. 男性不妊症の原因 causes of male infertility
4. 慢性リンパ性白血病の病態生理および遺伝学的特徴 pathophysiology and genetic features of chronic lymphocytic leukemia
5. 骨髄異形成症候群における細胞遺伝学および分子遺伝学 cytogenetics and molecular genetics of myelodysplastic syndromes

English Journal

Evaluation of the effects of ellagic acid (EA) on 7,12-dimethylbenz(α) anthracene (DMBA) induced micronuclei in mammalian cells in vitro and in vivo.

Grossi MR, Berni A, Pepe G, Filippi S, Meschini R, Papeschi C, Natarajan AT, Palitti F.Author information Department of Ecological and Biological Sciences, Università degli Studi della Tuscia, Largo dell'Università, snc, I-01100 Viterbo, Italy.AbstractWe evaluated the protective effects of EA, a promising dietary constituent against degenerative diseases, on the clastogenic action of the model carcinogen DMBA in vitro on human hepatoma cells (HepG2) and in vivo on bone marrow of mice, using the frequencies of induced micronuclei as the end point. Pre-, post- and simultaneous treatments with EA and the carcinogen were carried out in vitro. Simultaneous treatment with EA caused a statistically significant increase of DMBA induced MN, suggesting a direct interaction between the two agents. No significant reduction in DMBA induced MN was found by pre- or post treatment with EA. Similar effects were observed in the toxicity assay. In in vivo experiments, EA pre-treatment did not affect the frequencies of MN in PCEs of bone marrow induced by DMBA. A good correlation was found between in vitro and in vivo experiments. Our results did not reveal any clear indication on the efficacy of EA on the induction of micronuclei by DMBA. EA by itself did not show any harmful effects.
Toxicology letters.Toxicol Lett.2014 Jan 13;224(2):240-5. doi: 10.1016/j.toxlet.2013.10.012. Epub 2013 Nov 1.
We evaluated the protective effects of EA, a promising dietary constituent against degenerative diseases, on the clastogenic action of the model carcinogen DMBA in vitro on human hepatoma cells (HepG2) and in vivo on bone marrow of mice, using the frequencies of induced micronuclei as the end point.
PMID 24188931

Formaldehyde induces micronuclei in mouse erythropoietic cells and suppresses the expansion of human erythroid progenitor cells.

Ji Z, Li X, Fromowitz M, Mutter-Rottmayer E, Tung J, Smith MT, Zhang L.Author information Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA 94720, USA.AbstractAlthough formaldehyde (FA) has been classified as a human leukemogen, the mechanisms of leukemogenesis remain elusive. Previously, using colony-forming assays in semi-solid media, we showed that FA exposure in vivo and in vitro was toxic to human hematopoietic stem/progenitor cells. In the present study, we have applied new liquid in vitro erythroid expansion systems to further investigate the toxic effects of FA (0-150 μM) on cultured mouse and human hematopoietic stem/progenitor cells. We determined micronucleus (MN) levels in polychromatic erythrocytes (PCEs) differentiated from mouse bone marrow. We measured cell growth, cell cycle distribution, and chromosomal instability, in erythroid progenitor cells (EPCs) expanded from human peripheral blood mononuclear cells. FA significantly induced MN in mouse PCEs and suppressed human EPC expansion in a dose-dependent manner, compared with untreated controls. In the expanded human EPCs, FA slightly increased the proportion of cells in G2/M at 100 μM and aneuploidy frequency in chromosomes 7 and 8 at 50 μM. Our findings provide further evidence of the toxicity of FA to hematopoietic stem/progenitor cells and support the biological plausibility of FA-induced leukemogenesis.
Toxicology letters.Toxicol Lett.2014 Jan 13;224(2):233-9. doi: 10.1016/j.toxlet.2013.10.028. Epub 2013 Nov 1.
Although formaldehyde (FA) has been classified as a human leukemogen, the mechanisms of leukemogenesis remain elusive. Previously, using colony-forming assays in semi-solid media, we showed that FA exposure in vivo and in vitro was toxic to human hematopoietic stem/progenitor cells. In the present s
PMID 24188930

Micronucleus induction by oxidative metabolites of trichloroethylene in cultured human peripheral blood lymphocytes: a comparative genotoxicity study.

Varshney M, Chandra A, Chauhan LK, Goel SK.Author information Petroleum Toxicology Division, Indian Institute of Toxicology Research (IITR), Council of Scientific and Industrial Research, P.O. Box No. 80, Mahatma Gandhi Marg, Lucknow, 226001, India.AbstractThe genotoxic effects of oxidative metabolites of trichloroethylene (TCE), namely chloral hydrate, trichloroacetic acid (TCA), dichloroacetic acid (DCA), and trichloroethanol (TCEOH) were examined in human peripheral blood lymphocytes. In this context, lymphocytes were exposed in vitro to 25, 50, and 100 μg/ml concentrations of these metabolites separately for a period of 48 h and examined for micronucleus (MN) induction through flow cytometer. At 50 μg/ml TCE metabolites, TCA (6.33 ± 0.56 %), DCA (5.06 ± 0.55), and TCEOH (4.70 ± 1.73) induced highly significant (p<0.001) frequency of MN in comparison to control (1.03 ± 0.40) suggestive of their genotoxic potential. However, exposure of 100 μg/ml of all the metabolites consistently declined the frequencies of MN which in some cases was equable to that of observed at 25 μg/ml. Further, cytotoxicity and cell cycle disturbances were also measured to find out the association of these endpoints with the MN induction. DNA content analysis revealed 3-4-fold elevation of S-phase at all the concentrations tested. Particularly, at 100 μg/ml, treatment elevation of S-phase was significantly (p<0.0001) higher as compared to the control. Present findings together with earlier reports indicate that TCE induces genotoxicity through its metabolites. Interaction of these metabolites with DNA, as evident by elevated S-phase, seems to be the major cause of MN induction. However, involvement of spindle disruption cannot be ruled out. This comparative study also suggests that after TCE exposure, the metabolic efficiency of human to generate oxidative metabolites determines the extent of genotoxicity.
Environmental science and pollution research international.Environ Sci Pollut Res Int.2013 Dec;20(12):8709-16. doi: 10.1007/s11356-013-1806-7. Epub 2013 May 30.
The genotoxic effects of oxidative metabolites of trichloroethylene (TCE), namely chloral hydrate, trichloroacetic acid (TCA), dichloroacetic acid (DCA), and trichloroethanol (TCEOH) were examined in human peripheral blood lymphocytes. In this context, lymphocytes were exposed in vitro to 25, 50, an
PMID 23719688