Effects of caffeine on sister chromatid exchange (SCE) after exposure to UV light or triaziquone studied with a fluorescence plus Giemsa (FPG) technique

1978 ◽  
Vol 40 (2) ◽  
pp. 193-198 ◽  
Author(s):  
W. Vogel ◽  
Th. Bauknecht
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Uv Light

scholarly journals Unique DNA repair properties of a xeroderma pigmentosum revertant.

1987 ◽  
Vol 7 (9) ◽  
pp. 3353-3357 ◽  
Author(s):  
J E Cleaver ◽  
F Cortés ◽  
L H Lutze ◽  
W F Morgan ◽  
A N Player ◽  
...  
Keyword(s):  
Dna Repair ◽  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Xeroderma Pigmentosum ◽  
Uv Light ◽  
Shuttle Vector ◽  
Chemical Mutagenesis ◽  
Pyrimidine Dimers ◽  
Group A ◽  
Normal Sensitivity

A group A xeroderma pigmentosum revertant with normal sensitivity was created by chemical mutagenesis. It repaired (6-4) photoproducts normally but not pyrimidine dimers and had near normal levels of repair replication, sister chromatid exchange, and mutagenesis from UV light. The rate of UV-induced mutation in a shuttle vector, however, was as high as the rate in the parental xeroderma pigmentosum cell line.

Unique DNA repair properties of a xeroderma pigmentosum revertant

1987 ◽  
Vol 7 (9) ◽  
pp. 3353-3357
Author(s):  
J E Cleaver ◽  
F Cortés ◽  
L H Lutze ◽  
W F Morgan ◽  
A N Player ◽  
...  
Keyword(s):  
Dna Repair ◽  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Xeroderma Pigmentosum ◽  
Uv Light ◽  
Shuttle Vector ◽  
Chemical Mutagenesis ◽  
Pyrimidine Dimers ◽  
Group A ◽  
Normal Sensitivity

A group A xeroderma pigmentosum revertant with normal sensitivity was created by chemical mutagenesis. It repaired (6-4) photoproducts normally but not pyrimidine dimers and had near normal levels of repair replication, sister chromatid exchange, and mutagenesis from UV light. The rate of UV-induced mutation in a shuttle vector, however, was as high as the rate in the parental xeroderma pigmentosum cell line.

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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