Assessment of Genetic Damage Induced by Gadolinium-Based Radiocontrast Agents

Author(s):  
Hayal Cobanoglu
2021 ◽  
Vol 22 (12) ◽  
pp. 6320
Author(s):  
Monia Lenzi ◽  
Veronica Cocchi ◽  
Sofia Gasperini ◽  
Raffaella Arfè ◽  
Matteo Marti ◽  
...  

Mexedrone, α-PVP and α-PHP are synthetic cathinones. They can be considered amphetamine-like substances with a stimulating effect. Actually, studies showing their impact on DNA are totally absent. Therefore, in order to fill this gap, aim of the present work was to evaluate their mutagenicity on TK6 cells. On the basis of cytotoxicity and cytostasis results, we selected the concentrations (35–100 µM) to be used in the further analysis. We used the micronucleus (MN) as indicator of genetic damage and analyzed the MNi frequency fold increase by flow cytometry. Mexedrone demonstrated its mutagenic potential contrary to the other two compounds; we then proceeded by repeating the analyzes in the presence of extrinsic metabolic activation in order to check if it was possible to totally exclude the mutagenic capacity for α-PVP and α-PHP. The results demonstrated instead the mutagenicity of their metabolites. We then evaluated reactive oxygen species (ROS) induction as a possible mechanism at the basis of the highlighted effects but the results did not show a statistically significant increase in ROS levels for any of the tested substances. Anyway, our outcomes emphasize the importance of mutagenicity evaluation for a complete assessment of the risk associated with synthetic cathinones exposure.


Author(s):  
Ana C. Quevedo ◽  
Iseult Lynch ◽  
Eugenia Valsami-Jones

The dynamic interplay between toxicity pathways (oxidative stress, calcium disturbances, genetic damage) caused by nanoparticles and the repair mechanisms of inhibition of cell division and induction of cell death is explored in zebrafish embryo cells.


1986 ◽  
Vol 47 (1) ◽  
pp. 77-80 ◽  
Author(s):  
B. O. Bengtsson

SummaryRecombination is hard to understand in darwinian terms when the process is identified with the production of crossover chromosomes. As an alternative explanation I propose instead that biased conversion is the primary function of meiotic recombination. In particular I show that a conversion process directed against the most common type of genetic damage can substantially reduce the mutational load, even if the conversion force is weak and if the conversion process occasionally creates new mutations.


JAMA ◽  
2013 ◽  
Vol 310 (11) ◽  
pp. 1113
Author(s):  
M. J. Friedrich
Keyword(s):  

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