Radiation sensitivity of leukocytes from healthy individuals and breast cancer patients as measured by the alkaline and neutral comet assay

Shahidi, Maryam; Mozdarani, Hossein; Bryant, Peter E.

doi:10.1016/j.canlet.2007.08.002

Cited by 31 publications

(29 citation statements)

References 48 publications

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“…Since the OTM values at pH [ 13 were 5.1-15.3 times higher than those at pH 12.1, we deduce that compared with the DNA strand breaks, ALS was the main type of DNA damage produced by monocrotophos exposure. As the neutral comet assay was reported to be more specific for the detection of DSB (Shahidi et al 2007;Cortés-Gutiér-rez et al 2012;Ribas-Maynou et al 2012) and the OTM values at pH 12.1 were 4.9-31.5 times higher than those at pH 8.2-8.5, it was predominantly SSB with much fewer DSB detected by the pH 12.1 comet assay in this study. Consistently, Tice et al (2000) suggested that almost all genotoxic agents induce SSB orders of magnitude more than DSB.…”

Section: Discussionmentioning

confidence: 51%

Induction of DNA base damage and strand breaks in peripheral erythrocytes and the underlying mechanism in goldfish (Carassius auratus) exposed to monocrotophos

Zhao

Wei

Zhang

et al. 2015

Fish Physiol Biochem

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Using goldfish (Carassius auratus) as the model animal, the present study revealed the types of the DNA damage induced by monocrotophos, a highly toxic organophosphorus pesticide, and explored the mechanism underlying the DNA-damaging effect of this pesticide. Results of the alkaline comet assay showed that global DNA damage (including single- and double-strand breaks and alkali-labile sites) in peripheral erythrocytes of goldfish, measured as olive tail moment, was significantly increased by exposure to 0.01, 0.10, and 1.00 mg/L monocrotophos for 24, 48, 96, and 168 h. In particular, alkali-labile sites rather than single- or double-strand breaks, distinguished by the alkaline, pH 12.1, and neutral comet assays, were mainly induced by monocrotophos at 48 h. Oxidative damage in DNA bases and telomeric DNA was investigated by using the alkaline comet assay combined with endonuclease III or formamidopyrimidine DNA glycosylase and with fluorescence in situ hybridization, respectively. Further, glutathione peroxidase activity significantly decreased at 24 h but increased at 96 and 168 h, and malondialdehyde concentrations significantly increased at 48 h but gradually decreased at 96 and 168 h, which indicated an over-production of reactive oxygen species (ROS) at short exposure durations, but effective scavenging at long exposure durations in the peripheral blood tissues. Accordingly, our results suggest that DNA damage induced by monocrotophos in fish blood cells is possibly due to the inhibition of ROS scavenging and resulted accumulation of ROS.

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Section: Discussionmentioning

confidence: 51%

Induction of DNA base damage and strand breaks in peripheral erythrocytes and the underlying mechanism in goldfish (Carassius auratus) exposed to monocrotophos

Zhao

Wei

Zhang

et al. 2015

Fish Physiol Biochem

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“…9,10 In several studies, the authors did not find an association between age and DNA damage when using the comet assay. 5,28,29,35,36 In the present study, no association between levels of DNA damage and age (> 50 years or ≤ 50 years) was found.…”

Section: A U T H O R P R O O Fcontrasting

confidence: 57%

Relationship between Genotoxic Effects of Breast Cancer Treatments and Patient Basal DNA Integrity

Ceballos

Funes

Massa

et al. 2014

J Environ Pathol Toxicol Oncol

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Radiotherapy and chemotherapy cause genotoxic side effects that are highly variable among patients. In this study, we evaluated DNA integrity using the comet assay in peripheral blood lymphocytes from breast cancer patients before ("pre-treatment patients"; n = 47) and after ("post-treatment patients"; n = 24) radiotherapy and/or chemotherapy treatment and from healthy donors (n = 15). Comet evaluation was made by visual (types 0-4) and digital (percentage of DNA remaining in the comet head = % head DNA) analysis. The association between the level of DNA damage and cancer prognostic factors was assessed. The treatments caused a significant increase in DNA damage registered by both visual (p < 0.001) and digital (p < 0.001) analyses. No significant associations between the level of DNA damage in pre-treatment patients and cancer prognostic factors were found. A significant correlation between the comet results from each patient before and after treatment (r = 0.64, p = 0.001) was observed. The % head DNA in post-treatment samples from patients with a high level of DNA damage before treatment (30.3 ± 3.1%, p < 0.01) was lower than in post-treatment samples from patients with a low-to-medium level of DNA damage before therapy (49.2 ± 4.4%). These results support the usefulness of the comet assay as a sensitive technique to evaluate basal DNA status and DNA damage caused by cancer treatments. The comet assay could contribute to treatment decisions, especially by taking into account the patient's basal DNA damage before therapy.

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“…26 In the recent studies 24 hours of recovery time has been applied. 27,28 Shahidi et al 28 have reported that in healthy individuals no residual DNA damage has been observed after a 24-hour repair incubation of leukocytes exposed to radiation. In the present study, an incubation time of 24 hours was chosen to guarantee the completion of repair.…”

Section: Discussionmentioning

confidence: 99%

DNA Repair Gene Polymorphisms and Their Relation With DNA Damage, DNA Repair, and Total Antioxidant Capacity in Childhood Acute Lymphoblastic Leukemia Survivors

Dinçer¹,

Yüksel²,

Batar³

et al. 2015

Journal of Pediatric Hematology/Oncology

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Oxidative stress and defective DNA repair are major contributory factors in the initiation and progression of carcinogenesis. Chemotherapy and radiotherapy cause oxidative DNA damage, consume antioxidant capacity, and impair DNA repair activity. These effects of chemotherapy and radiotherapy may be contributory factors in the development of secondary malignancy in cancer survivors. Basal, H2O2-induced, and postrepair DNA damage; urinary 8-hydroxydeoxyguanosine level as a marker of oxidatively damaged DNA; and serum total antioxidant capacity were measured; XPD Lys751Gln, XRCC1 Arg399Gln, and XRCC1 Arg194Trp polymorphisms were analyzed in childhood acute lymphoblastic leukemia (ALL) survivors. Basal and H2O2-induced DNA damage were found to be higher in the ALL survivor group versus the control group, however, there was no significant difference between the other parameters. No association was found between the examined parameters and polymorphisms of XPD 751 and XRCC1 399 and both the groups. XRCC1 194Trp allele was found to be associated with a low level of postrepair DNA damage in the ALL survivors. In conclusion, basal DNA damage and susceptibility to oxidation are high in childhood ALL survivors. This situation which may easily lead to occurrence of a secondary cancer does not seem to be a result of deficient DNA repair.

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Radiation sensitivity of leukocytes from healthy individuals and breast cancer patients as measured by the alkaline and neutral comet assay

Cited by 31 publications

References 48 publications

Induction of DNA base damage and strand breaks in peripheral erythrocytes and the underlying mechanism in goldfish (Carassius auratus) exposed to monocrotophos

Induction of DNA base damage and strand breaks in peripheral erythrocytes and the underlying mechanism in goldfish (Carassius auratus) exposed to monocrotophos

Relationship between Genotoxic Effects of Breast Cancer Treatments and Patient Basal DNA Integrity

DNA Repair Gene Polymorphisms and Their Relation With DNA Damage, DNA Repair, and Total Antioxidant Capacity in Childhood Acute Lymphoblastic Leukemia Survivors

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