Riboflavin and UV-Light Based Pathogen Reduction: Extent and Consequence of DNA Damage at the Molecular Level

2004 ◽  
Vol 80 (1) ◽  
pp. 15 ◽  
Author(s):  
Vijay Kumar ◽  
Owen Lockerbie ◽  
Shawn D. Keil ◽  
Patrick H. Ruane ◽  
Matthew S. Platz ◽  
...  
Keyword(s):  
Dna Damage ◽  
Molecular Level ◽  
Uv Light ◽  
Pathogen Reduction

Riboflavin and UV-Light Based Pathogen Reduction: Extent and Consequence of DNA Damage at the Molecular Level

2007 ◽  
Vol 80 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Vijay Kumar ◽  
Owen Lockerble ◽  
Shawn D. Kell ◽  
Patrick H. Ruane ◽  
Matthew S. Platz ◽  
...  
Keyword(s):  
Dna Damage ◽  
Molecular Level ◽  
Uv Light ◽  
Pathogen Reduction

scholarly journals Pterygium—The Good, the Bad, and the Ugly

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1567
Author(s):  
Sara I. Van Acker ◽  
Bert Van den Bogerd ◽  
Michel Haagdorens ◽  
Vasiliki Siozopoulou ◽  
Sorcha Ní Dhubhghaill ◽  
...  
Keyword(s):  
Dna Damage ◽  
Molecular Level ◽  
The Self ◽  
Grading System ◽  
Ocular Surface Squamous Neoplasia ◽  
True Nature ◽  
Intervention Point ◽  
Pathological Evaluation ◽  
Repair Mechanisms ◽  
Life Threatening

Pterygium is a multifaceted pathology that displays apparent conflicting characteristics: benign (e.g., self-limiting and superficial), bad (e.g., proliferative and potentially recurrent) and ugly (e.g., signs of preneoplastic transformation). The natural successive question is: why are we lacking reports showing that pterygium lesions become life-threatening through metastasis, especially since pterygium has considerable similarities with UV-related malignancies on the molecular level? In this review, we consider how our pathophysiological understanding of the benign pterygium pathology overlaps with ocular surface squamous neoplasia and skin cancer. The three UV-related disorders share the same initial insult (i.e., UV radiation) and responsive repair mechanisms to the ensuing (in)direct DNA damage. Their downstream apoptotic regulators and other cellular adaptations are remarkably alike. However, a complicating factor in understanding the fine line between the self-limiting nature of pterygium and the malignant transformation in other UV-related diseases is the prominent ambiguity in the pathological evaluation of pterygium biopsies. Features of preneoplastic transformation (i.e., dysplasia) are used to define normal cellular reactions (i.e., atypia and metaplasia) and vice versa. A uniform grading system could help in unraveling the true nature of this ancient disease and potentially help in identifying the earliest intervention point possible regarding the cellular switch that drives a cell’s fate towards cancer.

scholarly journals Cellular response to DNA damage is enhanced by the pR plasmid in mouse cells and in Escherichia coli.

1986 ◽  
Vol 6 (2) ◽  
pp. 586-592 ◽  
Author(s):  
L Marcucci ◽  
F Gigliani ◽  
P A Battaglia ◽  
R Bosi ◽  
E Sporeno ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Statistical Analysis ◽  
Cellular Response ◽  
Regulatory Mechanism ◽  
Uv Light ◽  
Transformed Cells ◽  
Insertion Mutagenesis ◽  
Mouse Cells ◽  
Inducible Repair

The pR plasmid, which enhances the survival of Escherichia coli C600 exposed to UV light by induction of the SOS regulatory mechanism, showed the same effect when it transformed mouse LTA cells (tk-, aprt-). With Tn5 insertion mutagenesis which inactivates UV functions in the pR plasmid, we recognized two different regions of the plasmid, uvp1 and uvp2. These pR UVR- mutants exhibited the same effect in LTA transformed cells, demonstrating that resistance to UV light, carried by the pR plasmid, was really due to the expression of these two regions, which were also in the mouse cells. Statistical analysis showed that the expression of the uvp1 and uvp2 regions significantly increased (P less than 0.01) the survival upon exposure to UV light in mouse cells and bacteria. These results might suggest the presence of an inducible repair response to DNA damage in mouse LTA cells.

scholarly journals Smart covalent organic networks (CONs) with “on-off-on” light-switchable pores for molecular separation

2020 ◽  
Vol 6 (34) ◽  
pp. eabb3188 ◽  
Author(s):  
Jiangtao Liu ◽  
Shaofei Wang ◽  
Tiefan Huang ◽  
Priyanka Manchanda ◽  
Edy Abou-Hamad ◽  
...  
Keyword(s):  
Visible Light ◽  
Molecular Level ◽  
Uv Light ◽  
Building Blocks ◽  
Membrane Selectivity ◽  
Molecular Separation ◽  
Stimuli Response ◽  
Dye Rejection ◽  
New Generation ◽  
Azobenzene Derivatives

Development of the new-generation membranes for tunable molecular separation requires materials with abilities beyond strict separation. Stimuli response could remotely adjust the membrane selectivity. Azobenzene derivatives can be photo-switched between trans and cis isomers under ultraviolet or visible light. Here, the azobenzenes were implanted as light switches to bridge the flexible cyclen building blocks. The smart covalent organic network membranes fold and unfold as origami that can be photo-switched between on-state (large) and off-state (small) pores. The cis membranes with off state under ultraviolet (UV) light have higher dye rejection than trans membranes with on-state channels. By controlling the trans-to-cis azobenzene isomerization via UV/Vis light, the pore size can be remotely controlled at the molecular level and the solvent permeance and dye rejection can be dynamically tuned.

scholarly journals The Dark Side of UV-Induced DNA Lesion Repair

Genes ◽  
2020 ◽  
Vol 11 (12) ◽  
pp. 1450
Author(s):  
Wojciech Strzałka ◽  
Piotr Zgłobicki ◽  
Ewa Kowalska ◽  
Aneta Bażant ◽  
Dariusz Dziga ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Uv Light ◽  
Genetic Material ◽  
Dna Lesions ◽  
Dark Side ◽  
Repair System ◽  
Strand Breaks ◽  
Dna Lesion ◽  
Pyrimidine Dimers

In their life cycle, plants are exposed to various unfavorable environmental factors including ultraviolet (UV) radiation emitted by the Sun. UV-A and UV-B, which are partially absorbed by the ozone layer, reach the surface of the Earth causing harmful effects among the others on plant genetic material. The energy of UV light is sufficient to induce mutations in DNA. Some examples of DNA damage induced by UV are pyrimidine dimers, oxidized nucleotides as well as single and double-strand breaks. When exposed to light, plants can repair major UV-induced DNA lesions, i.e., pyrimidine dimers using photoreactivation. However, this highly efficient light-dependent DNA repair system is ineffective in dim light or at night. Moreover, it is helpless when it comes to the repair of DNA lesions other than pyrimidine dimers. In this review, we have focused on how plants cope with deleterious DNA damage that cannot be repaired by photoreactivation. The current understanding of light-independent mechanisms, classified as dark DNA repair, indispensable for the maintenance of plant genetic material integrity has been presented.

scholarly journals Databases and Bioinformatics Tools for the Study of DNA Repair

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Kaja Milanowska ◽  
Kristian Rother ◽  
Janusz M. Bujnicki
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Excision Repair ◽  
Uv Light ◽  
Dna Lesions ◽  
Environmental Chemicals ◽  
Nonhomologous End Joining ◽  
End Joining ◽  
Repair Mechanisms ◽  
Base Excision

DNA is continuously exposed to many different damaging agents such as environmental chemicals, UV light, ionizing radiation, and reactive cellular metabolites. DNA lesions can result in different phenotypical consequences ranging from a number of diseases, including cancer, to cellular malfunction, cell death, or aging. To counteract the deleterious effects of DNA damage, cells have developed various repair systems, including biochemical pathways responsible for the removal of single-strand lesions such as base excision repair (BER) and nucleotide excision repair (NER) or specialized polymerases temporarily taking over lesion-arrested DNA polymerases during the S phase in translesion synthesis (TLS). There are also other mechanisms of DNA repair such as homologous recombination repair (HRR), nonhomologous end-joining repair (NHEJ), or DNA damage response system (DDR). This paper reviews bioinformatics resources specialized in disseminating information about DNA repair pathways, proteins involved in repair mechanisms, damaging agents, and DNA lesions.

scholarly journals The ATPase Domain but Not the Acidic Region of Cockayne Syndrome Group B Gene Product Is Essential for DNA Repair

1999 ◽  
Vol 10 (11) ◽  
pp. 3583-3594 ◽  
Author(s):  
Robert M. Brosh ◽  
Adayabalam S. Balajee ◽  
Rebecca R. Selzer ◽  
Morten Sunesen ◽  
Luca Proietti De Santis ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Excision Repair ◽  
Uv Light ◽  
Genetic Disorder ◽  
Cockayne Syndrome ◽  
Premature Aging ◽  
Atpase Domain ◽  
Acidic Region

Cockayne syndrome (CS) is a human genetic disorder characterized by UV sensitivity, developmental abnormalities, and premature aging. Two of the genes involved, CSA andCSB, are required for transcription-coupled repair (TCR), a subpathway of nucleotide excision repair that removes certain lesions rapidly and efficiently from the transcribed strand of active genes. CS proteins have also been implicated in the recovery of transcription after certain types of DNA damage such as those lesions induced by UV light. In this study, site-directed mutations have been introduced to the human CSB gene to investigate the functional significance of the conserved ATPase domain and of a highly acidic region of the protein. The CSB mutant alleles were tested for genetic complementation of UV-sensitive phenotypes in the human CS-B homologue of hamster UV61. In addition, theCSB mutant alleles were tested for their ability to complement the sensitivity of UV61 cells to the carcinogen 4-nitroquinoline-1-oxide (4-NQO), which introduces bulky DNA adducts repaired by global genome repair. Point mutation of a highly conserved glutamic acid residue in ATPase motif II abolished the ability of CSB protein to complement the UV-sensitive phenotypes of survival, RNA synthesis recovery, and gene-specific repair. These data indicate that the integrity of the ATPase domain is critical for CSB function in vivo. Likewise, the CSB ATPase point mutant failed to confer cellular resistance to 4-NQO, suggesting that ATP hydrolysis is required for CSB function in a TCR-independent pathway. On the contrary, a large deletion of the acidic region of CSB protein did not impair the genetic function in the processing of either UV- or 4-NQO-induced DNA damage. Thus the acidic region of CSB is likely to be dispensable for DNA repair, whereas the ATPase domain is essential for CSB function in both TCR-dependent and -independent pathways.

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