Trisomy 18p caused by a supernumerary marker with a chromosome 13/21 centromere: A possible recurrent chromosome aberration

2013 ◽  
Vol 161 (9) ◽  
pp. 2363-2368 ◽  
Author(s):  
Alberto Plaja ◽  
Elisabet Lloveras ◽  
Cristina Martinez-Bouzas ◽  
Beatriz Barreña ◽  
Miguel Del Campo ◽  
...  
Keyword(s):  
Chromosome Aberration ◽  
Chromosome 13 ◽  
Trisomy 18P

In Vitro Genotoxicity and Molecular Docking Study of Ellagic Acid

2020 ◽  
Vol 16 (7) ◽  
pp. 1072-1082
Author(s):  
Tuba C. Dördü ◽  
Rüştü Hatipoğlu ◽  
Mehmet Topaktaş ◽  
Erman S. İstifli
Keyword(s):  
Dna Damage ◽  
Molecular Docking ◽  
Comet Assay ◽  
Treatment Period ◽  
Chromosome Aberration ◽  
Human Lymphocyte ◽  
Sister Chromatid ◽  
Ellagic Acid ◽  
Sister Chromatid Exchange ◽  
Nuclear Division

Background: Ellagic Acid (EA) is a polyphenolic compound that is classified in the natural antioxidants group. Polyphenolic compounds that exert antioxidant activity possess particular importance for scientists, food producers and consumers due to their positive effects on human health. However, despite considerable evidence that EA shows antigenotoxic activity by binding to DNA, there is no systematic genotoxicity study of this substance, which can covalently bind to DNA. This study aims to reveal the possible genotoxic activity of EA using widely accepted assays for the assessment of DNA clastogenic activity: sister chromatid exchange, chromosome aberration, micronucleus and comet assays as well as to predict the interactions among EA and DNA through molecular docking. Methods: Different assays were carried out to identify the clastogenic activity of EA on human lymphocyte DNA using Sister Chromatid Exchange (SCE), Chromosome Aberration (CA), Micronucleus (MN) and single-cell gel electrophoresis (SCGE/comet) assays. For this aim, human peripheral blood lymphocytes were treated with EA (60, 80 and 100 μg/ml) for 24 and 48 hrs in the SCE, CA and MN assays and for 1 hr in the comet assay. Furthermore, molecular docking experiments were also performed to calculate the binding energy of EA on human B-DNA structure (B-DNA dodecamer) as well as to predict noncovalent interactions among these macromolecules. Results: At the concentrations and treatment times (24- or 48-hr) tested, EA did not induce either SCE or Chromosome Aberrations (CAs) as compared to the negative and solvent controls. Although EA slightly increased the percentage of Micronucleated Binuclear (%MNBN) cells as well as the percentage of Micronucleus (%MN) in 24 or 48-hr treatment periods at all concentrations, this increase was not statistically significant as compared to both controls. The effect of EA on DNA replication (nuclear division) was determined by the Proliferation Index (PI), the Nuclear Division Index (NDI) and the Mitotic Index (MI). No statistically significant differences were observed in the PI or NDI in 24- or 48-hr treatment periods in human lymphocyte cultures treated with EA at various concentrations. EA generally had no significant effect on the MI, as observed with the PI and NDI. Discussion: Although the concentrations of 60 and 80 μg/mL at a 24-hr treatment period and the concentrations of 60 μg/mL and 100 μg/mL at 48-hr treatment period generally decreased the MI, those decreases were not statistically significant when compared to negative and solvent controls. Moreover, none of the concentrations of EA tested in this study were able to increase DNA damage determined by the tail DNA length, %DNA in tail and tail moment parameters in the comet assay. Although the amount of DNA damage in the comet assay decreased with increasing concentrations of EA, this decrease was not statistically significant as compared to both controls. However, molecular docking experiments interestingly showed that the binding free energy of EA with B-DNA was -7.84 kcal/mol-1, indicating a strong interaction between the two molecules. Conclusion : Although the findings of our study show that EA does not have genotoxic potential in human chromosomes, molecular docking experiments revealed strong hydrogen bonding between EA and B-DNA molecules. Therefore, it has been proposed that the prevailing information suggesting that the molecules that bind to DNA cause genotoxic effects should be reconsidered from a wider perspective.

Evaluation of genotoxicity of pan masala employing chromosomal aberration and micronucleus assay in bone marrow cells of the mice

2009 ◽  
Vol 25 (7) ◽  
pp. 467-471 ◽  
Author(s):  
BN Mojidra ◽  
K. Archana ◽  
AK Gautam ◽  
Y. Verma ◽  
BC Lakkad ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chromosome Aberration ◽  
Chromosomal Aberration ◽  
Bone Marrow Cells ◽  
Micronucleus Assay ◽  
Control Group ◽  
Genotoxic Potential ◽  
Polychromatic Erythrocytes ◽  
Significant Difference ◽  
Marrow Cells

Pan masala is commonly consumed in south-east Asian and other oriental countries as an alternate of tobacco chewing and smoking. Genotoxic potential of pan masala (pan masala plain and pan masala with tobacco known as gutkha) was evaluated employing chromosome aberration (CA) and micronucleus (MN) assay in vivo. Animals were exposed to three different doses (0.5%, 1.5% and 3%) of pan masala plain (PMP) and gutkha (PMT) through feed for a period of 6 months and micronucleus and chromosomal aberrations were studied in the bone marrow cells. Induction of mean micronuclei in polychromatic erythrocytes (MNPCE) and normochromatic erythrocyte (MNNCE) was higher in both types of pan masala treated groups with respect to control group. Both pan masala plain and gutkha treatment significantly induced the frequency of MNPCE and MNNCE in the bone marrow cells, indicating the genotoxic potential. Furthermore, slight decline in the ratio of polychromatic erythrocytes to normochromatic erythrocytes was also noticed, suggesting the cytotoxic potential even though the ratio was statistically non significant. A dose-dependent, significant increase in chromosome aberration was observed in both types of pan masala treated mice with respect to control. However, no significant difference in micronucleus and chromosomal aberration induction was noticed between two types of pan masala exposed (PMP and PMT) groups. Results suggest that both types of pan masala, i.e. plain and gutkha, have genotoxic potential.

scholarly journals Prenatal diagnosis of recurrent mosaic ring chromosome 13 of maternal origin

2021 ◽  
Vol 60 (4) ◽  
pp. 771-774
Author(s):  
Chih-Ping Chen ◽  
Chen-Yu Chen ◽  
Schu-Rern Chern ◽  
Shin-Wen Chen ◽  
Fang-Tzu Wu ◽  
...  
Keyword(s):  
Prenatal Diagnosis ◽  
Ring Chromosome ◽  
Maternal Origin ◽  
Chromosome 13

scholarly journals Localization of the Ceruloplasmin (CP) Gene to the q32-q33 Bands of Chromosome 13 in Pigs by in Situ Hybridization

Hereditas ◽  
2004 ◽  
Vol 119 (1) ◽  
pp. 7-10 ◽  
Author(s):  
Renuka Chaudhary ◽  
Bhanu P. Chowdhary ◽  
Ingrid Harbitz ◽  
Ingemar Gustavsson
Keyword(s):  
In Situ Hybridization ◽  
Chromosome 13 ◽  
Cp Gene

scholarly journals Partial Trisomies and Deletions of Chromosome 13

1978 ◽  
Vol 12 (10) ◽  
pp. 1029-1029 ◽  
Author(s):  
Roberto Coco ◽  
Graciela M Del Rey
Keyword(s):  
Chromosome 13

Relevance of chromosome 13 aberrations in canine tumours

2012 ◽  
Vol 40 (04) ◽  
pp. 267-270 ◽  
Author(s):  
H. Escobar ◽  
I. Nolte ◽  
N. Reimann-Berg
Keyword(s):  
Chromosome Aberrations ◽  
Human Chromosomes ◽  
High Homology ◽  
Chromosome 13 ◽  
Human Tumours ◽  
Cytogenetic Studies ◽  
Canine Chromosome ◽  
Chromosomal Changes

SummaryFor human tumours there are many reports documenting the correlation between chromosome aberrations and tumour entities. Due to the complex canine karyotypic pattern (78 chromosomes), cytogenetic studies of tumours of the dog are rare. However, the reports in the literature show, that canine chromosome 13 (CFA 13) is predominantly involved in chromosomal changes. Interestingly, CFA 13 shows high homology to regions on the human chromosomes 4 (HSA 4) and 8 (HSA 8), which harbour the proto-oncogenes c-KIT and c-MYC. Both of these genes are involved in the development and progression of some human and canine tumour diseases.

Genotoxicity Studies on Sel-Plex®, a Standardized, Registered High-Selenium Yeast

2006 ◽  
Vol 25 (6) ◽  
pp. 477-485 ◽  
Author(s):  
James C. Griffiths ◽  
Ray A. Matulka ◽  
Ronan Power
Keyword(s):  
Chromosome Aberration ◽  
Micronucleus Test ◽  
Mutagenic Activity ◽  
Human Lymphocytes ◽  
Selenium Yeast ◽  
Yeast Saccharomyces Cerevisiae ◽  
Reverse Mutation ◽  
High Selenium ◽  
Chromosome Aberration Test

Selenium, recognized as an essential nutrient for human health, is a component of proteins and enzymes required for various biological functions and is currently being used as a feed supplement for livestock in geographical areas that are naturally low in selenium. Selenium is structurally similar to sulfur, replacing the sulfur atom in stoichiometric amounts and thus functions through an association with proteins, termed selenoproteins. In geographic areas low in selenium, there is the potential for animals (including humans) to become selenium deficient and this potential deficiency can be remedied by consumption of exogenous selenium, including selenium-enriched yeast ( Saccharomyces cerevisiae) that contains high levels of organic selenium (e.g., selenized yeast). A unique, standardized, registered high selenium food-grade baker’s yeast ( S. cerevisiae; Sel-Plex®), was tested in the following battery of Genotoxicity assays; (1) a bacterial reverse mutation test (Ames test); (2) an in vitro mammalian chromosome aberration test; and (3) a mouse micronucleus test. Under the conditions of this assay, Sel-Plex® showed no evidence of mutagenic activity in Salmonella typhimurium, in the bacterial reverse mutation test. Sel-Plex® did not induce significant chromosomal aberrations in cultured human lymphocytes in the in vitro mammalian chromosome aberration test. Sel-Plex® did not statistically increase the frequency or proportion of micronucleated immature erythrocytes in the mouse micronucleus test. Thus, from the studies presented here, the authors conclude that Sel-Plex® is nongenotoxic.

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