[13C2]- Acetaldehyde Promotes Unequivocal Formation of 1,N2-Propano-2′-deoxyguanosine in Human Cells

Cc, Garcia; Jp, Angeli; Fp, Freitas; Of, Gomes; Oliveira, Tiago Franco de; Loureiro, Ana Paula de Melo; Mascio, Paolo Di; Medeiros, Marisa H. G.

doi:10.1021/ja2004686

Cited by 64 publications

(54 citation statements)

References 35 publications

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“…Indeed, higher aldehyde concentrations seem to interact directly with lipid peroxidation of the cell and induce DNA damage (Garcia et al 2011). Ethanol exposure can also lead to acetaldehyde accumulation, causing bone marrow dysfunction in FA patients (Ghosh et al 2014).…”

Section: Discussionmentioning

confidence: 99%

The Salivary Microbiome and Oral Cancer Risk: A Pilot Study in Fanconi Anemia

et al. 2016

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Fanconi anemia (FA) is a rare genetic disease characterized by chromosomal instability and impaired DNA damage repair. FA patients develop oral squamous cell carcinoma (OSCC) earlier and more frequently than the general population, especially after hematopoietic stem cell transplantation (HSCT). Although evidence of an etiological role of the local microbiome and carcinogenesis has been mounting, no information exists regarding the oral microbiome of FA patients. The aim of this study was to explore the salivary microbiome of 61 FA patients regarding their oral health status and OSCC risk factors. After answering a questionnaire and receiving clinical examination, saliva samples were collected and analyzed using 16S rRNA sequencing of the V3-V4 hypervariable region. The microbial profiles associated with medical and clinical parameters were analyzed using general linear models. Patients were young (mean age, 22 y) and most had received HSCT (n = 53). The most abundant phyla were Firmicutes [mean relative abundance (SD), 42.1% (10.1%)] and Bacteroidetes [(25.4% (11.4%)]. A history of graft-versus-host disease (GVHD) (n = 27) was associated with higher proportions of Firmicutes (43.8% × 38.5%, P = 0.05). High levels of gingival bleeding were associated with the genera Prevotella (22.25% × 20%), Streptococcus (19.83% × 17.61%), Porphyromonas (3.63% × 1.42%, P = 0.03), Treponema (1.02% × 0.28%, P = 0.009), Parvimonas (0.28% × 0.07%, P = 0.02) and Dialister (0.27% × 0.10%, P = 0.04). Finally, participants transplanted over 11 y ago showed the highest levels of Streptococcus (18.4%), Haemophilus (12.7%) and Neisseria (6.8%). In conclusion, FA patients that showed poor oral hygiene harbored higher proportions of the genera of bacteria compatible with gingival disease. Specific microbial differences were associated with a history of oral GVHD and a history of oral mucositis.

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Section: Discussionmentioning

confidence: 99%

The Salivary Microbiome and Oral Cancer Risk: A Pilot Study in Fanconi Anemia

et al. 2016

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“…They are also highly reactive, being able to form DNA adducts in vitro and in vivo. 63,64 Moreover, FA-deficient cells have been shown to be hypersensitive to both of these compounds and to accumulate double-strand breaks and chromosomal aberrations. [65][66][67][68] Finally, acetaldehyde treatment induces the activation of the FA pathway in wild-type cells.…”

Section: What Is the Cause Of Dna Damage In Hscs?mentioning

confidence: 99%

Why does the bone marrow fail in Fanconi anemia?

Garaycoechea

Patel

2014

Blood

141

121

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The inherited bone marrow failure (BMF) syndromes are a rare and diverse group of genetic disorders that ultimately result in the loss of blood production. The molecular defects underlying many of these conditions have been elucidated, and great progress has been made toward understanding the normal function of these gene products. This review will focus on perhaps the most well-known and genetically heterogeneous BMF syndrome: Fanconi anemia. More specifically, this account will review the current state of our knowledge on why the bone marrow fails in this illness and what this might tell us about the maintenance of bone marrow function and hematopoiesis.

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“…It is possible that some process during development increases the likelihood of exposing cells to a source of aldehyde-mediated DNA damage. Acetaldehyde can cause many forms of DNA damage, including base damage, inter-and intrastrand crosslinks and protein adducts [138][139][140][141]. It will be critical to our understanding of FA to show which of these DNA lesions is repaired by the FA pathway.…”

Section: Fanconi Anaemia and Endogenous Dna Damagementioning

confidence: 99%

The Fanconi anaemia pathway orchestrates incisions at sites of crosslinked DNA

Crossan

Patel

2011

The Journal of Pathology

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Fanconi anaemia (FA) is a rare, autosomal recessive, genetically complex, DNA repair deficiency syndrome in man. Patients with FA exhibit a heterogeneous spectrum of clinical features. The most significant and consistent phenotypic characteristics are stem cell loss, causing progressive bone marrow failure and sterility, diverse developmental abnormalities and a profound predisposition to neoplasia. To date, 15 genes have been indentified, biallelic disruption of any one of which results in this clinically defined syndrome. It is now apparent that all 15 gene products act in a common process to maintain genome stability. At the molecular level, a fundamental defect in DNA repair underlies this complex phenotype. Cells derived from FA patients spontaneously accumulate broken chromosomes and exhibit a marked sensitivity to DNA-damaging chemotherapeutic agents. Despite complementation analysis defining many components of the FA DNA repair pathway, no direct link to DNA metabolism was established until recently. First, it is now evident that the FA pathway is required to make incisions at the site of damaged DNA. Second, a specific component of the FA pathway has been identified that regulates nucleases previously implicated in DNA interstrand crosslink repair. Taken together, these data provide genetic and biochemical evidence that the FA pathway is a bona fide DNA repair pathway that directly mediates DNA repair transactions, thereby elucidating the specific molecular defect in human Fanconi anaemia.

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[¹³C₂]- Acetaldehyde Promotes Unequivocal Formation of 1,N²-Propano-2′-deoxyguanosine in Human Cells

Cited by 64 publications

References 35 publications

The Salivary Microbiome and Oral Cancer Risk: A Pilot Study in Fanconi Anemia

The Salivary Microbiome and Oral Cancer Risk: A Pilot Study in Fanconi Anemia

Why does the bone marrow fail in Fanconi anemia?

The Fanconi anaemia pathway orchestrates incisions at sites of crosslinked DNA

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