Analysis of a BrdU-sensitive site in the cactus mouse (Peromyscus eremicus): chromosomal breakage and sister-chromatid exchange

Chromosoma ◽  
1980 ◽  
Vol 77 (3) ◽  
pp. 379-389 ◽  
Author(s):  
Nancy R. Schneider ◽  
R. S. K. Chaganti ◽  
James German
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Chromosomal Breakage ◽  
Sensitive Site ◽  
Peromyscus Eremicus

Effects of theophylline on chromosomal breakage and sister-chromatid exchange

1989 ◽  
Vol 224 (4) ◽  
pp. 409-413 ◽  
Author(s):  
P. Day ◽  
Z. Shalaby ◽  
M.M. Cohen ◽  
S.S. Wasserman ◽  
S. Schwartz
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Chromosomal Breakage

Genotype- and age-associated in vivo cytogenetic alterations following mutagenic exposures in mice

1986 ◽  
Vol 28 (2) ◽  
pp. 286-293 ◽  
Author(s):  
S. M. Singh ◽  
J. F. Toles ◽  
J. Reaume
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Bone Marrow Cells ◽  
Relative Sensitivity ◽  
Age Effect ◽  
Chromosomal Breakage ◽  
Normal Individuals ◽  
The Difference ◽  
Almost All

We studied mice from eight genetic strains at two ages (young, 10 weeks; and old, more than 80 weeks) for cytogenetic alterations (sister chromatid exchange (SCE), micronulei, and metaphase indices) following challenges by two known mutagens: N-nitrosoethyl urea (ENU, 17 mg/kg) and cyclophosphamide (CP, 4.5 mg/kg) on bone marrow cells in vivo. The data were used to evaluate the effect of age, genotype, and differential aging patterns of genotypes in relative susceptibility to chromosomal breakage and instability in otherwise normal individuals. The older animals had a higher frequency of micronuclei, reduced metaphase indices, and lower SCE/cell as compared with their younger counterparts. Treatment with both mutagens significantly increased micronuclei and SCEs/cell in almost all strains at both ages but had little effect on the frequency of cells in metaphase. Among individual differences for SCEs/cell at most treatment combinations were not significant. In general, the induced SCEs (treatment–control) are significantly higher in older animals, variable among strains, and relatively higher as a result of CP than the ENU treatment. When the age effect was evaluated as the difference of SCE/cell in old and SCE/cell in young animals of each genotype–treatment combination, an age-dependent pattern was evident. In the presence of a mutagen the pattern in aging response was highly variable and strain (genotype) dependent. This variability may be viewed as subtle inherent genetic predisposition of sensitivity to mutagens that could be evaluated only using sensitive measures (e.g., SCE and not micronuclei) following more than one mutagenic challenges. These subtle differences coud become pronounced when these parameters are evaluated at different ages on the same genotype. Although these observations suggest that even normal individuals differ in their relative sensitivity to genetic instability, it may not be easy to recognize these differences in simple experimental protocols.Key words: age effect, sister chromatid exchange, mutagenesis, micronuclei.

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.

Assessment of the genotoxic potential of tetrachlorvinphos insecticide by cytokinesis-block micronucleus and sister chromatid exchange assays

2021 ◽  
pp. 096032712110361
Author(s):  
Hayal Cobanoglu ◽  
Akin Cayir
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Chromosomal Instability ◽  
Human Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Proliferation Index ◽  
Dna Damages ◽  
Genotoxic Potential ◽  
Index Level

Tetrachlorvinphos is an organophosphate that is classified as a carcinogen in humans by several authorities. Due to very limited data regarding the genotoxic potential, we aimed to comprehensively investigate in vitro genotoxic potential of tetrachlorvinphos. We performed our study by applying the cytokinesis-block micronucleus cytome and sister chromatid exchange (SCE) assays to human peripheral blood lymphocytes. We evaluated micronucleus (MN) and SCE frequencies and cytokinesis-block proliferation index in both exposed and non-exposed lymphocytes. We also calculated the chromosomal instability level in response to exposure by combining the results of MN and SCE. We found that MN frequency did not increase with exposure to tetrachlorvinphos (0–50 µg/ml). In contrast, we observed that SCE frequencies significantly increased with exposure to ≥5 µg/ml tetrachlorvinphos. Furthermore, exposure to tetrachlorvinphos at concentrations of 50 µg/ml induced a significant increase in chromosomal instability level ( p < 0.05). Cytokinesis-block proliferation index level did not significantly decrease in response to tetrachlorvinphos exposure. Our findings reveal that tetrachlorvinphos resulted in different DNA damages that were measured by two assays. Furthermore, our findings suggested that exposure to tetrachlorvinphos increased chromosomal instability that is a hallmark of many malignancies. We conclude that although tetrachlorvinphos does not significantly increase the MN level, the significant increase of both SCE and CIN frequencies indicates the genotoxic potential of tetrachlorvinphos in human peripheral lymphocytes. Additionally, tetrachlorvinphos is not cytotoxic in the range of tested concentrations.

scholarly journals Site of unequal sister chromatid exchange contains a potential Z-DNA-forming tract.

1988 ◽  
Vol 85 (2) ◽  
pp. 529-533 ◽  
Author(s):  
A. Weinreb ◽  
D. R. Katzenberg ◽  
G. L. Gilmore ◽  
B. K. Birshtein
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Z Dna
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