Reduced (3H) thymidine incorporation into human lymphocytes exposed in vitro to ultrasound may be due to DNA damage

1981 ◽  
Vol 69 (S1) ◽  
pp. S26-S27
Author(s):  
Michael H. Repacholi
2002 ◽  
Vol 49 (1) ◽  
pp. 145-155 ◽  
Author(s):  
Janusz Błasiak ◽  
Ewa Gloc ◽  
Mariusz Warszawski

Idarubicin is an anthracycline antibiotic used in cancer therapy. Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity. Using the alkaline comet assaywe showed that the drugs at 0.01-10 microM induced DNA damage in normal human lymphocytes. The effect induced by idarubicin was more pronounced than by mitoxantrone (P < 0.001). The cells treated with mitoxantrone at 1 microM were able to repair damage to their DNA within a 30-min incubation, whereas the lymphocytes exposed to idarubicin needed 180 min. Since anthracyclines are known to produce free radicals, we checked whether reactive oxygen species might be involved in the observed DNA damage. Catalase, an enzyme inactivating hydrogen peroxide, decreased the extent of DNA damage induced by idarubicin, but did not affect the extent evoked by mitoxantrone. Lymphocytes exposed to the drugs and treated with endonuclease III or formamidopyrimidine-DNA glycosylase (Fpg), enzymes recognizing and nicking oxidized bases, displayed a higher level of DNA damage than the untreated ones. 3-Methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing and nicking mainly methylated bases in DNA, increased the extent of DNA damage caused by idarubicin, but not that induced by mitoxantrone. Our results indicate that the induction of secondary malignancies should be taken into account as side effects of the two drugs. Direct strand breaks, oxidation and methylation of the DNA bases can underlie the DNA-damaging effect of idarubicin, whereas mitoxantrone can induce strand breaks and modification of the bases, including oxidation. The observed in normal lymphocytes much lesser genotoxicity of mitoxantrone compared to idarubicin should be taken into account in planning chemotherapeutic strategies.


1995 ◽  
Vol 16 (3) ◽  
pp. 507-512 ◽  
Author(s):  
P.A.E.L. Schilderman ◽  
E. Rhijnsburger ◽  
I. Zwingmann ◽  
J.C.S. Kleinjans

Author(s):  
Emiliano Basso ◽  
Giulia Regazzo ◽  
Mario Fiore ◽  
Valentina Palma ◽  
Gianandrea Traversi ◽  
...  

2015 ◽  
Vol 29 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Ninoslav Djelić ◽  
Milena Radaković ◽  
Biljana Spremo-Potparević ◽  
Lada Živković ◽  
Vladan Bajić ◽  
...  
Keyword(s):  

2006 ◽  
Vol 164 ◽  
pp. S261 ◽  
Author(s):  
Faith M. Williams ◽  
Kathryn M. Atherton ◽  
Samantha Jamieson ◽  
Elaine Mutch

Homeopathy ◽  
2016 ◽  
Vol 105 (03) ◽  
pp. 265-269 ◽  
Author(s):  
Henrique Fonseca Sousa do Nascimento ◽  
Plínio Cerqueira dos Santos Cardoso ◽  
Helem Ferreira Ribeiro ◽  
Tatiane Cristina Mota ◽  
Lorena Monteiro Gomes ◽  
...  

Background: CANOVA® (CA) is a homeopathic immunomodulator. It contains several homeopathic medicines prepares according to the Brazilian Pharmacopoeia. CA is indicated in clinical conditions in which the immune system is impaired and against tumors. N-methyl-N-nitrosourea (NMU) is an N-nitroso compound, with genotoxic/mutagenic properties. Although several studies have shown promising results in the use of CA, there are no studies reporting possible antigenotoxic effects. Method: This study evaluated the in vitro antigenotoxic and anticytotoxic effects of CA in human lymphocytes exposed to NMU. Samples of human lymphocytes that were subjected to different concentrations of a mixture containing CA and NMU were used. The genotoxicity/antigenotoxicity of CA was evaluated by the comet assay, anticytotoxicity was assessed by quantification of apoptosis and necrosis using acridine orange/ethidium bromide. Results: CA significantly reduced DNA damage induced by NMU and reduced significantly the frequency of NMU-induced apoptosis after 24 h of treatment. Conclusion: CA has an important cytoprotective effect significantly reducing the DNA damage and apoptosis induced by the carcinogen NMU.


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