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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].
Licochalcone A, a licorice flavonoid: antioxidant, cytotoxic, genotoxic, and chemopreventive potential
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Karoline Soares de Freitas, Iara Silva Squarisi, Nathália Oliveira Acésio, Heloiza Diniz Nicolella, Saulo Duarte Ozelin, Matheus Reis Santos de Melo, Ana Paula Prado Guissone, Gabriela Fernandes, Lívia Mara Silva, Ademar Alves da Silva Filho, Denise Crispim Tavares
The results obtained by the in vitro MN test also showed that LicoA diminished the damage initiated by MMS. This SN2 alkylating agent exhibits high affinity for nitrogen in purines, resulting in N-alkylation. The methylation process mediated by MMS leads to formation of adducts such as N7- and N3-methyladenine, which induce double-strand breaks or inhibit DNA replication. If not repaired, these events are responsible for mutagenic consequences (Kaina 2004; Wyatt and Pittman 2006). DNA damage mediated by these agents is mainly repaired by base excision repair, with the participation of glycosylases. The N7- and N3-methyladenine adducts are repaired by DNA glycosylase (Baute and Depicker 2008; Sedgwick 2004). LicoA exhibited antimutagenic activity against the direct-acting alkylating agent N-methyl-N-nitrosourea as demonstrated by the Ames test (Inami et al. 2017).
Risk management of free radicals involved in air travel syndromes by antioxidants
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Most of the above-described risk factors promote the generation of free radicals, which subsequently induce adverse outcomes. The molecular mechanisms underlying ionizing radiation-induced diseases, including cancer of lung, thyroid, leukemia and skin, as well as birth defects, have been extensively investigated in both in vitro and in vivo (Nie et al. 2016; Iglesias et al. 2017; Huang et al. 2017b; Lecomte-Pradines et al. 2017). Once exposed to radiation, free radicals, such as ROS or RNS are generated and damage biomolecules, including DNA, protein and lipids (Matsumoto et al. 2001; Wang and Zhang 2017; Yakovlev 2015) (Figure 2 and Table 2). Radiation directly damages biomolecules to induce oxidative DNA damage including (1) single- or double-strand breakage, cross-linking, and elevated 8-hydroxy deoxyguanosine (8-OHdG) levels (Fardid et al. 2017; Huang et al. 2017a, 2017b; Ji et al. 2016), (2) alters carbonyl contents in proteins (Fernando et al. 2016), and (3) yields lipid peroxidation products, such as malonedialdehyde (MDA), croton aldehyde, and 4-hydroxy nonenal (Dubey et al. 2017; Nirwane, Sridhar, and Majumdar 2016) that lead to mutations and cancer. Oxidative damage may also underlie other adverse effects, such as inflammation, cardiovascular diseases, developmental disorders, and reproductive abnormalities (Jia et al. 2017; Sarma, Blais, and Chan 2017). ROS and RNS induce apoptosis either through the apoptosis-inducing factor (AIF) and endonuclease G protein (endo G) or cytochrome C and caspase cascade pathway (Lee et al. 2017b; Pereira, Porto, and Abdalla 2014; Salah et al. 2017), although cellular damage may also induce necrosis (Joubert et al. 2008; Li, Luo, and Wang 2001). A study of early thyroid cancer cases in children exposed to radiation noted an increased prevalence of gene rearrangement between the rearranged during transfection (RET) gene and papillary thyroid carcinoma (PTC) gene (RET/PTC rearrangement) (Fugazzola et al. 1995). As previously noted, circadian rhythms regulate physical, mental, and behavioral changes over a 24-hr cycle (Duffy and Wright 2005; Wilking et al. 2013). Although ROS/RNS-induced DNA damage is generally repaired by the nucleotide excision repair (NER) or base excision repair (BER) pathway, the observed damage may also be controlled by the circadian clock (Kang et al. 2009; Sancar et al. 2010). It is known that 8-oxoguanine (8-oxoG), a type of oxidative DNA damage, is repaired primarily by 8-oxoguanine DNA glycosylase (OGG1). In 15 healthy volunteers, the levels of 8-oxoG and activity of OGG1 were respectively lower and higher in the morning. However, the opposite results were detected in the evening (Manzella et al. 2015). Altered OGG1 expression was also observed in shift workers experiencing a dysregulation of circadian clock genes, compared to controls.