Iron and genome stability: An update

Prá, Daniel; Franke, Silvia Isabel Rech; Henriques, João Antônio Pêgas; Fenech, Michael

doi:10.1016/j.mrfmmm.2012.02.001

Cited by 74 publications

(51 citation statements)

References 117 publications

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“…Collectively, these observations suggest that a side effect of β-TM treatment is ALL occurrence, which adversely affects the patient's prognosis. Iron overload resulting from prolonged transfusions has been considered to be carcinogenic, as it has the ability to damage biomolecules, leading to the production of hydroxyl radicals and other reactive oxygen species that induce a wide array of DNA lesions, from base modifications to strand breaks and adducts (13). Additionally, iron accumulation has been shown to induce DNA hypermethylation.…”

Section: Discussionmentioning

confidence: 99%

A strategy for the clinical remission of acute lymphoblastic leukemia elicited by treatment of β‑thalassemia major: A case report

et al. 2017

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Abstract. Acute lymphoblastic leukemia (ALL) has been suggested as a long-term complication in patients with β-thalassemia major (β-TM). A 12-months-old male patient was diagnosed with β-TM. The patient required a blood transfusion weekly for 2 years. At the age of 4 years, a splenectomy was performed due to massive splenomegaly and frequent transfusion requirements. The histopathological analysis of the spleen revealed extensive hemosiderosis. ALL-L1 with the T immunophenotype and without central nervous system (CNS) involvement was diagnosed when the patient was 5 years old, and treated with anti-leukemic combination chemotherapy and CNS radiotherapy. The patient completed 24 months of treatment and has been in complete remission for 7 years, without long-term adverse events.

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Section: Discussionmentioning

confidence: 99%

A strategy for the clinical remission of acute lymphoblastic leukemia elicited by treatment of β‑thalassemia major: A case report

et al. 2017

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“…Iron catalyses the Fenton reaction by generating the 8-hydroxy-guanine adduct, one of the most common DNA oxidative damages [13], found also in telomeres [17]. Iron overload induces DNA hypermethylation and can shorten telomere length [122], although the relationship between iron status and telomere dynamics is not totally clear. Shortened telomeres were found in patients with primary hematochromatosis and in patients taking supplements containing iron [123].…”

Section: What Can Be Done To Help Maintain Telomere Length?mentioning

confidence: 99%

Telomere Length and Its Relation to Human Health

Kahl¹,

Silva²

2016

Telomere - A Complex End of a Chromosome

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Telomeres are complex nucleotide sequences that cap the end of chromosomes from degradation, unwanted recombination-fusion, inappropriate activation of DNA damage response and play a critical role in cell division and chromosome stability. There is growing evidence that telomere stability can be affected by occupational and environmental exposure, as some of these factors have been correlated with increase in inflammation, oxidative stress, DNA damage, chromosome aberration, and epigenetic alterations. Both extremely short and long telomeres have been associated with neurodegenerative, cardiovascular diseases (CVD) and cancer risk. Occupational and environmental exposure to several synthetic and natural chemicals has been found to be associated with changes in telomere length, although the molecular mechanism is not fully understood. Telomeric DNA is relatively less capable of repair, resulting in accelerated shortening during the cell cycle and replicative senescence. It is recognized that diet plays an important role in telomere maintenance. Prevention of exposure to environmental and occupational hazards as well as psychological stressors can reduce the risk of telomere instability. This review provides a broad evaluation of the associated mechanism between human health and environmental and occupational exposure with telomere length, including recent findings and future perspectives.

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“…In general, impacts on DNA include DNA base modifications, sugar lesions, single-and double-DNA strand breaks, DNAeprotein crosslinks, DNAeDNA crosslinks, and abasic sites. For instance, the genotoxic effects of iron are mainly derived from hydroxyl radical production by Fenton and Haber-Weiss chemistry, leading to base oxidation (as 8-hydroxy-2 0 -deoxyguanosine), DNA strand breaks and micronuclei, which are then mutagenic [59]. Somatic mutations can lead to a sustained proliferative signaling or evasion to antiproliferative signaling, two of the capabilities that enable tumor growth and metastatic dissemination [8,9].…”

Section: Pm-awmentioning

confidence: 99%