No evidence of chromosome damage in children and adolescents with differentiated thyroid carcinoma after receiving 131I radiometabolic therapy, as evaluated by micronucleus assay and microarray analysis

Federico, Giovanni; Boni, Giuseppe; Fabiani, Barbara; Fiore, Lisa B.; Lazzeri, Patrizia; Massart, Francesco; Traino, Claudio; Verola, Carmela; Saggese, Giuseppe; Mariani, Giuliano; Scarpato, Roberto

doi:10.1007/s00259-008-0867-1

Cited by 17 publications

(14 citation statements)

References 46 publications

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“…Dose-dependent results were also found by Gutiérrez et al (1997) MN, which is a small nuclear mass that is surrounded by membrane and separated from the main nucleus, can be derived from chromatid or chromosome breaks (Fenech, 2000); although Saffi and Henriques (2003) argue that chromatid/chromosome breaks are the main type of radiation-induced DNA damage, MN may also result from single-strand breaks, double-strand breaks, base and sugar damage, and oxidative damage to bases between protein-DNA and DNA-DNA interchange bridges. Federico et al (2008) reported negative results for the MN test using blood from 11 patients who received an average of 94,594.59 ± 10,000 μCi [ 131 I] for ablation of thyroidal remnants. According to the authors, this may be due to an early activation of cellular repair machinery that maintains the integrity of the genome and may prevent double-strand DNA breaks from progressing to chromosomal mutations by either repairing the lesions or by eliminating the damaged cells via apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic and mutagenic effects of iodine-131 and radioprotection of acerola (Malpighia glabra L.) and beta-carotene in vitro

Almeida

Düsman²,

Heck³

et al. 2013

Genet. Mol. Res.

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Section: Discussionmentioning

confidence: 99%

Cytotoxic and mutagenic effects of iodine-131 and radioprotection of acerola (Malpighia glabra L.) and beta-carotene in vitro

Almeida

Düsman²,

Heck³

et al. 2013

Genet. Mol. Res.

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“…However, it should be stressed that the maximum mean MN value obtained by us (2.45Ϯ0.22‰) falls into the expected range for healthy children and adolescents. In fact, several studies have reported baseline frequencies of underage subjects as generally oscillating from 1.6 to 8.3‰ (33,(37)(38)(39)(40). It probably depends on the experimental procedure used, which may vary from laboratory to laboratory (different modality of cell culturing, harvesting, and staining, different scoring criteria, variation in the numbers of readers, etc.…”

Section: Discussionmentioning

confidence: 99%

Nuclear damage in peripheral lymphocytes of obese and overweight Italian children as evaluated by the γ‐H2AX focus assay and micronucleus test

et al. 2010

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Childhood obesity, often characterized by a chronic low-grade inflammation, has been associated with an increased risk of developing some types of cancer later in life. Nuclear γ-H2AX foci represent the first detectable response of cells to DNA tumorigenesis lesions, such as the double-strand breaks (DSBs). An excess of micronucleated peripheral lymphocytes was found in subjects with cancer or inflammation-based diseases. We set out to investigate the expression of genome damage, from DNA lesions to chromosome mutations (micronuclei), in overweight and obese children. Using the γ-H2AX focus assay and micronucleus (MN) test, we analyzed peripheral lymphocytes from 119 Italian children classified as normal weight (n=38), overweight (n=20), or obese (n=61). Cultures treated with bleomycin (BLM) were also set up for each child in both assays to check functioning of the apparatus that ensures DNA integrity. We measured serum TNF-α, IL-6, and C-reactive protein (CRP) as markers of inflammation. Overweight and obese children had significantly higher levels of H2AX phosphorylation (0.0191±0.0039 and 0.0274±0.0029 γ-H2AXF/n) and increased MN frequencies (2.30±0.25 and 2.45±0.22‰) than normal-weight children (0.0034±0.0006 γ-H2AXF/n, and 0.92±0.12‰ MN), while all subjects responded to BLM induction, irrespective of their weight status. The fold increase of spontaneous MN frequencies in overweight and obese subjects was 2.5 and 2.7, respectively, well below the corresponding increase in the γ-H2AX foci (5.6- and 8.0-fold, respectively). IL-6 and CRP mean values were significantly higher in obese and overweight children than in controls. Here, we demonstrated that peripheral cells of overweight and obese children showed increased levels of DSBs, which were not completely repaired as part of them has been converted into micronuclei. Characterization of childhood obesity inflammation could be implemented using molecular markers of genome damage.

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“…However, some studies have demonstrated that patients who received 131 I did not exhibit chromosomal damage from radiometabolic therapy (Gil et al 2000b;Federico et al 2008).…”

Section: Discussionmentioning

confidence: 98%

“…The chromosomal damage induced by radioiodine exposure predisposes individuals to a future risk of developing cancer (Federico et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Mutagenicity of diagnostic and therapeutical doses of radiopharmaceutical iodine-131 in Wistar rats

Düsman

Berti

Mariucci

et al. 2011

Radiat Environ Biophys

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Iodine-131 ((131)I) is a radioisotope used for the diagnosis and treatment of thyroidal disorders such as hyperthyroidism and cancer. During its decay, (131)I emits beta particles and gamma rays; its physical half-life is 8 days, and it is accumulated preferentially in the thyroid tissue. This study aimed to evaluate the cytotoxicity and mutagenicity of diagnostic and therapeutic doses of (131)I using bone marrow cells of rats treated in vivo in a test system with a single dose by gavage. Concentrations of 5, 25, 50 and 250 μCi in 1 ml of water were used, and after 24 h, the animals were killed. Also, a concentration of 25 μCi/ml of water was used, and the animals were killed after 5 days. The results showed that no concentration of (131)I was cytotoxic and that all concentrations were mutagenic. As a result, there was no statistically significant difference detected by the χ(2) test in the induction of chromosomal aberrations between the different doses. Thus, the present study demonstrated a significant increase in chromosomal aberration in bone marrow cells exposed to (131)I regardless of the dose or the treatment time.

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No evidence of chromosome damage in children and adolescents with differentiated thyroid carcinoma after receiving 131I radiometabolic therapy, as evaluated by micronucleus assay and microarray analysis

Cited by 17 publications

References 46 publications

Cytotoxic and mutagenic effects of iodine-131 and radioprotection of acerola (Malpighia glabra L.) and beta-carotene in vitro

Cytotoxic and mutagenic effects of iodine-131 and radioprotection of acerola (Malpighia glabra L.) and beta-carotene in vitro

Nuclear damage in peripheral lymphocytes of obese and overweight Italian children as evaluated by the γ‐H2AX focus assay and micronucleus test

Mutagenicity of diagnostic and therapeutical doses of radiopharmaceutical iodine-131 in Wistar rats

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