2 edition of role of DNA repair and genotoxic stress responses in xenobiotic-initiated teratogenesis. found in the catalog.
role of DNA repair and genotoxic stress responses in xenobiotic-initiated teratogenesis.
Rebecca Rachelle Laposa
Written in English
|The Physical Object|
|Number of Pages||248|
DNA repair is critical for genotoxic susceptibility and cancer development. Forty-seven patients with head and neck squamous cell carcinoma (HNSCC) and 38 healthy controls were enrolled in this study. Among the patients, 16 subjects had metastasis of HNSCC. The extent of DNA damage, including oxidative lesions, and efficiency of repair after genotoxic . The association of increased levels of DNA damage with both structural and functional deficits suggests that xenobiotic-initiated oxidative stress is causing oxidatively damaged DNA, particularly the 8-oxodGuo lesion, which if not repaired, can initiate changes in gene expression resulting in a number of developmental pathologies.
All species require DNA repair pathways to maintain the integrity of their genomes. Bacterial damage repair mechanisms have broader roles encompassing responses to stress, long-term colonization, as well as virulence. The SOS response regulates DNA repair and damage tolerance genes in many bacterial species. W.J. Rogers, in Sterilisation of Biomaterials and Medical Devices, Genotoxicity – ISO –3. Genotoxicity testing evaluates gene mutations, changes in chromosomes or DNA and gene toxicities caused by by-products or compounds over an extended period of time. The International Organization for Standardization (ISO) standard –3 outlines tests for .
IL-1α is a DNA damage sensor linking genotoxic stress signaling differences related to their role in disease, tissue repair and immune upregulated during several stress responses . Further, ATM phosphorylated PTEN on threonine , and a PTEN mutant that cannot be phosphorylated at this position (PTEN TA) resist nuclear exclusion following genotoxic stress. Judging by various readouts of the DNA damage response, cells lacking nuclear PTEN are hypersensitive to DNA damage and display impaired homologous recombination.
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DNA repair pathways that are activated in response to genotoxic stress in plants have implications in plant growth, development, diversity and productivity. The DNA repair process varies significantly in efficiency between different regions of the genome.
In general, plants contain more multiple gene copies than by: As for the role of genes involved in pathways of DNA metabolism under salt stress conditions, informations are still limited.
DNA repair genes that are induced in response to salt stress. In order to combat these attacks on the genome, the cell has evolved a response system that induces cell cycle arrest to allow sufficient time to repair the incurred damage. The genotoxic stress response system also activates the appropriate DNA repair pathway, or, in the case of irreparable damage, induces apoptosis.
Lans, H. et al. Involvement of global genome repair, transcription coupled repair, and chromatin remodeling in UV DNA damage response changes during development.
PLOS Genet. 6, e ().Cited by: in vivo testing. The purpose for in vivo testing is to determine the potential of DNA damage that can affect chromosomal structure or disturb the mitotic apparatus that changes chromosome number; the factors that could influence the genotoxicity are ADME and DNA repair.
It can also detect genotoxic agents missed in in vitro tests. The positive result of induced chromosomal. Yokoi M, Masutani C, Maekawa T, Sugasawa K, Ohkuma Y, Hanaoka F () The Xeroderma Role of DNA repair in the protection against genotoxic stress pigmentosumgroup C protein complex XPC-HR23B plays an important role in the recruitment of transcription factor IIH to damaged DNA.
The response to genotoxic stresses and the repair mechanisms involved in plants has only recently begun to be investigated. Herein, we present a comprehensive account of the types of DNA damage, the DNA damage response, and the repair pathways with reference to the recent insights gained from the plants.
Genotoxic stress-triggered p53 activation. p53 is a sequence-specific transcription factor that plays a major role in the regulation of DNA repair, apoptosis and cell cycle progression. p53 becomes activated on DNA replication arrest and DSB induced by chemical genotoxins and irradiation via the ATM/ATR pathway (Figure 1 B).Thus, following DSB formation, ATM.
Suggestive of an indispensable role of DNA‐PK in modulating pre‐mRNA splicing in the genotoxic stress response, we found that DNA‐PK inactivation, by both a small molecule inhibitor and RNA interference, affects splicing of a set of pre‐mRNAs in DSB‐inducer MTX‐treated A cells.
DNA repair has been well reviewed elsewhere (Hoeijmakers,Riches et al., ). Hence, it is likely that DNA repair will impact directly on the linearity of genotoxic dose–responses by removing DNA damage, particularly at low doses. At higher doses DNA repair may be saturated and hence not be able to remove newly damaged DNA bases.
The cell response to oxidative stress includes several DNA repair pathways, which are activated to remove the damaged bases and other lesions. Information concerning DNA repair in plants is still limited, although results from gene profiling and mutant analysis suggest possible differences in repair mechanisms between plants and other eukaryotes.
Genotoxic stress and activation of novel DNA repair enzymes in human endothelial cells and in the retinas and kidneys of streptozotocin diabetic rats Chunyan Wang Department of Pathology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
More recently, an examination of RPA phosphorylation in response to DNA damage and replication stress revealed a complex coordination of RPA phosphorylation via ATM, ATR and DNA-PK to initiate replication arrest and recovery after cisplatin induced DNA damage.
42 These data are consistent with earlier studies suggesting that activation of ATR. Cells lacking nuclear PTEN were hypersensitive to DNA damage, whereas PTEN-deficient cells were susceptible to killing by a combination of genotoxic stress and a small-molecule PI3K inhibitor both in vitro and in vivo.
Our findings may have implications for individualized therapy for patients with PTEN-deficient tumors. DNA damage response genes play vital roles in the maintenance of a healthy genome.
Defects in cell cycle checkpoint and DNA repair genes, especially mutation or aberrant downregulation, are associated with a wide spectrum of human disease, including a predisposition to the development of neurodegenerative conditions and cancer. Introduction. Human DNA is continuously exposed to a variety of endogenous and exogenous chemicals.
Some of these chemicals are DNA reactive, thereby inducing DNA damage such as base modifications, abasic sites, single- or double-strand breaks in gh all cells possess defense systems against DNA damage, some damage escapes from the DNA repair mechanisms and induces mutations upon DNA.
The cell response to oxidative stress includes several DNA repair pathways, which are activated to remove the damaged bases and other lesions. that play a key role in DNA repair. DNA repair and genotoxic stress response genes have been previously shown to exhibit differing basal levels of expression in the whole which may play a role in VPA-initiated teratogenesis.
View. This sub-group’s broad research interest is to understand the role of various DNA repair enzymes in protection against the adverse consequences of DNA damage. More specifically, the subgroup is interested in the role of DNA polymerase β (pol β) in base excision repair (BER) of damaged DNA bases, and in the requirement of other repair.
If the DNA repair machinery fails to fix the damaged site during a temporary cell-cycle arrest, or if massive genotoxic stress overwhelmed the repair capacity, cellular failsafe programs such as apoptosis or senescence will be triggered to limit aberrant propagation of these damaged and potentially harmful cells.
This is the first evidence that G6PD is a developmentally critical cytoprotective enzyme for both endogenous and xenobiotic‐initiated embryopathic oxidative stress and DNA damage.
G6PD deficiencies accordingly may have a broader biological relevance as important determinants of infertility, in utero and postnatal death, and teratogenesis.If the DNA repair machinery fails to fix the damaged site during a temporary cell-cycle arrest, or if massive genotoxic stress overwhelmed the repair capacity, cellular failsafe programs such as apoptosis or senescence will be triggered to limit aberrant propagation of these damaged and potentially harmful cells.This is the first evidence that G6PD is a developmentally critical cytoprotective enzyme for both endogenous and xenobiotic-initiated embryopathic oxidative stress and DNA damage.
G6PD deficiencies accordingly may have a broader biological relevance as important determinants of infertility, in utero and postnatal death, and teratogenesis.