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Interconnection between PHA and Stress Robustness of Bacteria
Published in Martin Koller, The Handbook of Polyhydroxyalkanoates, 2020
Stanislav Obruca, Petr Sedlacek, Iva Pernicova, Adriana Kovalcik, Ivana Novackova, Eva Slaninova, Ivana Marova
Generally, microorganisms surviving in extreme conditions are called extremophiles. In the literature, the term for ultraviolet radiation-resistant (UVR) microorganisms which are known for the production of various metabolites such as pigments, mycosporine-like amino acids, melanin, pannarin and sphaerophorin, can be found [75,76]. Another group of UVR microorganisms possesses the capability to repair already-changed DNA due to their specific enzymes, e.g. photolyases, which directly break covalent bonding between pyrimidine dimers to form original pyrimidine monomers. This process is known as photoreactivation and it requires light in the near U/blue light (300–500 nm) region as an energy source [72,77]. Another enzymatic DNA repair pathway includes the DNA glycosylase base excision repair (BER) where the glycosyl bond between damaged base and deoxyribose is hydrolyzed. Next, DNA repair mode is based on the repair enzyme called UV-damage endonuclease (UVDE) which can recognize the photoproducts and cut them out immediately. The last of the most frequently used DNA repair pathways which was identified is the nucleotide excision repair (NER) which belongs to the main defensive strategies against UV radiation. This strategy consists of the removal of a damaged oligonucleotide [72,77,78].
UV Light Microbial Inactivation in Foods
Published in Tatiana Koutchma, Ultraviolet Light in Food Technology, 2019
As shown in Figure 4.2, nucleic acid absorbs UV light from 200 to 300 nm. UV light inactivates microorganisms by disrupting their DNA or RNA structures by inducing six types of damages. The primary mechanism of inactivation by UV is the creation of pyrimidine dimers (Figure 4.1), which are bonds formed between adjacent pairs of thymine or cytosine pyrimidines on the same DNA or RNA strand. Dimers prevent microorganisms from replicating, thereby rendering them inactive and unable to cause infection. Figure 4.2 shows the relationship between the ability of UV light to destroy bacterial cells and the ability of this cell’s nucleic acid to absorb UV light. The germicidal lamp emitting UV at 254nm is operating very close to the optimized wavelength for maximum absorption by nucleic acids at around of 260 nm.
Polar Macroalgae
Published in Donat-P. Häder, Kunshan Gao, Aquatic Ecosystems in a Changing Climate, 2018
An important molecular target of UV radiation is the DNA resulting in single- or double-strand breaks, inter- or intra-strand crosslinks and the formation of cyclobutane pyrimidine dimers (CPD) and pyrimidine (6-4)-pyrimidone photoproducts which—if not repaired efficiently—can lead to errors in replication, mutations, and mortality (Karentz et al. 1991, Lois and Buchanan 1994). Different life stages of polar macroalgae show different susceptibility to UV-B damage of their DNA. Zoospores of the kelps Alaria esculenta, Laminaria digitata, and Saccorhiza dermatodea were found to be more susceptible to UV-B radiation than young sporophytes (Roleda et al. 2005, Roleda et al. 2006b, Roleda et al. 2006c, Roleda et al. 2006d). Low doses of UV-B < 72 J/m2) were found to promote the growth of Chondrus ocellatus while higher doses inhibited it (Ju et al. 2015). Application of blue light promoted DNA photorepair while red light inhibited it. But both blue and red light reduced the synthesis of MAAs. Other major targets of solar UV radiation are proteins. The photosystem II (PS II) D1 protein and the Rubisco enzyme in the Calvin cycle are of significant importance (Bischof 2000, Bischof et al. 2000).
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Following exposure to the individual components of ultraviolet radiation, i.e. UVA, UVB or UVC, there is an overlapping profile of DNA damage, in particular for cyclobutane-pyrimidine dimers. However, the proportion of different base-pair changes shows variation depending on the radiation wavelength and the cell type or species used. The mechanisms leading to the formation of these photoproducts may also be different. Cyclobutane-pyrimidine dimers at cytosine-containing DNA sequences are formed following exposure to both UVA and UVB individually in human skin ex vivo. Human cells have repair systems that eliminate DNA photoproducts: the absence of these enzymes, as seen in Xeroderma Pigmentosum (XP) patients, leads to an increased risk of developing squamous cell carcinomas and melanomas, which supports a major role of DNA photoproducts in photo-carcinogenesis. Mutations have been detected in human cells exposed to UVA, UVB and UVC’ (IARC 2012d, 89-90).
Dose estimation methodology for the UV inactivation of bioaerosols in a Continuous-Flow reactor
Published in Aerosol Science and Technology, 2019
Maria E. Martínez Retamar, Claudio Passalía, Rodolfo J. Brandi, Marisol D. Labas
It is a well-known fact that UV rays have a lethal effect on microorganisms. The vulnerability of microorganism to UV light is basically due to the absorption of radiation by the DNA molecule. At a wavelength of 253.7 nm the DNA molecule has its maximum absorption. As a result of the radiation absorption by the nucleic acid, pyrimidine dimers are formed and the double helix structure of DNA is altered; this affects the cellular replication and can lead to the cellular death.