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Lab-on-a-Chip-Based Devices for Rapid and Accurate Measurement of Nanomaterial Toxicity
Published in Suresh C. Pillai, Yvonne Lang, Toxicity of Nanomaterials, 2019
Mehenur Sarwar, Amirali Nilchian, Chen-zhong Li
NPs in contact with cells can generate ROS, including peroxides, superoxides, hydroxyl radicals, singlet oxygen, and alpha oxygen. Once inside a cell, NPs can damage DNA, a common pathway of nanotoxicity. Oxidation of guanine bases of DNA can produce 8-hydroxyguanine and its nucleoside 8-hydroxy-2′-deoxyguanosine (8-OHdG). Measurement of these oxidized products gives an insight of the nanotoxicity level within the body. Conventional methods of measuring 8-OHdG include high-performance liquid chromatography (HPLC), gas chromatography-mass spectrometry (GCMS), HPLC tandem mass spectrometry, and enzyme-linked immunosorbent assay (ELISA). Unfortunately, the equipment handling requires skilled personnel, and the overall procedure is time-consuming and often extremely expensive.
Devising and Synthesis of NEMS and MEMS
Published in Sergey Edward Lyshevski, Nano- and Micro-Electromechanical Systems, 2018
As was emphasized, nucleic acids are polymers of monomers called nucleotides. Each nucleotide is itself composed of three parts (nitrogenous base is joined to a pentose that is bonded to a phosphate group). The DNA molecules consist of two polynucleotide chains (strands) that spiral around forming a double helix. These polynucleotide chains are held together by hydrogen bonds between the paired bases. DNA is a linear double-stranded polymer of four nitrogenous bases, i.e., Deoxyadenosine monophosphate or adenine (A)Deoxythymidine monophosphate or thymine (T) in DNA, and uracil (U) in RNADeoxyguanosine monophosphate or guanine (G)Deoxycytidine monophosphate or cytosine (C)
Biomolecular Processing and Molecular Electronics
Published in Sergey Edward Lyshevski, Molecular Electronics, Circuits, and Processing Platforms, 2018
Nucleic acids are polymers of monomers called nucleotides. Each nucleotide is itself composed of three parts, and a nitrogenous base is joined to a pentose that is bonded to a phosphate group. The DNA molecules consist of two polynucleotide chains (strands) that spiral around forming a double helix, which was discovered by Rosalind Franklin in 1952 through x-ray crystallography. These polynucleotide chains are held together by hydrogen bonds between the paired nitrogenous bases. DNA is a linear double-stranded polymer of the following four nucleotides (bases): Deoxyadenosine monophosphate or adenine (A)Deoxythymidine monophosphate or thymine (T) in DNA, and uracil (U) in RNADeoxyguanosine monophosphate or guanine (G)Deoxycytidine monophosphate or cytosine (C)
Plant responses to per- and polyfluoroalkyl substances (PFAS): a molecular perspective
Published in International Journal of Phytoremediation, 2023
Ayesha Karamat, Rouzbeh Tehrani, Gregory D. Foster, Benoit Van Aken
A few reports indicated that PFAS may induce DNA damage in exposed plants, which is consistent with the consequences of oxidative stress and ROS. In their metabolomic study on lettuce exposed to PFOA and PFOS, Li et al. (2020a) observed an increase of 8-hydroxy-deoxyguanosine (8-OHdG), which suggests DNA damage and subsequent activation of DNA repair mechanisms. In their study on water spinach exposed to F53B and chromium, Tang et al. (2020) detected overexpression of the metallothionein gene LaMT2 in exposed plants, which may indicate DNA damage, although chromium may be the major toxicant causing this effect. Finally, exposure of the alga C. pyrenoidosa to PFBS and FBSA was found to result in the downregulation of DNA polymerase α (POLA2 and POLA1), which may indicate a negative effect on DNA replication (Liu et al. 2022).
In vivo effects of 1,4-dioxane on genotoxic parameters and behavioral alterations in Drosophila melanogaster
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Contamination of water sources (especially drinking water) and foods to this chemical constitutes a human health issue because of potential carcinogenic effects. Stickney et al. (2003) showed that DXN exposure via drinking water induced hepatic tumors in exposed mice and rats; however, the mode of action (MOA) of this carcinogenic effect still remains unknown. Gi et al. (2018) examined mutagenicity following DXN treatment at 5000 ppm concentration for 16 weeks in F344 rats and data indicated that mutation frequency, transitions, and transversions of DNA repair enzyme were significantly increased. These results demonstrated that DXN is a genotoxic hepatocarcinogen via a mutagenic MOA. In addition, Totsuka et al. (2020) found that after DXN exposure to 0, 20, 200, or 5,000 ppm DNA adduct formation was significantly elevated in rat livers compared to the control indicating DXN-mediated genotoxicity. In addition, different three different adducts were identified including thymine or cytidine/uracil moieties and 8-oxo-2’-deoxyguanosine (8-oxo-dG). Thus, Totsuka et al. (2020) proposed that oxidative stress parameters may partially be involved in the mechanisms leading to elevated mutations in rats exposed DXN. Similarly, in the current study, mutagenic effects associated with DXN were observed only at the highest concentration (%1) exposure in the SMART assay. It is noteworthy that recombinogenic effects attributed to DXN were detected at various nontoxic concentrations (0.1, 0.25, and 0.5%) with SMART.
Antigenotoxic effects of (-)-epigallocatechin-3-gallate (EGCG) and its relationship with the endogenous antioxidant system, 8-hydroxydeoxyguanosine adduct repair (8-OHdG), and apoptosis in mice exposed to chromium(VI)
Published in Journal of Toxicology and Environmental Health, Part A, 2021
María Del Carmen García-Rodríguez, Gabriela Serrano-Reyes, Lourdes Montserrat Hernández-Cortés, Mario Altamirano-Lozano
Previously García-Rodríguez, Montaño-Rodríguez, and Altamirano-Lozano (2016) administered 10 mg/kg orally EGCG prior to 20 mg/kg CrO3 and reported a reduction in MN-PCE frequency accompanied by rise in apoptotic cell number, suggesting that this process might be involved in elimination of cells with Cr(VI)-induced DNA damage. It is of interest that these doses of EGCG also elevated quantities of apoptotic cells when administered alone. Several investigators observed that EGCG was capable of regulating cell signaling pathways related to proliferation and apoptosis (Curti et al. 2017; Gao et al. 2013). The rise in number of apoptotic cells might be related to possible pro-oxidant actions of EGCG through generation of ROS via auto-oxidation. Our results showed that EGCG treatment increased 8-OHdG levels almost twofold higher than controls. The C8-OH-adduct radical of deoxyguanosine is formed during catalysis of •OH in the reaction of 2-deoxyguanosine with molecular oxygen and considered a form of oxidative DNA damage. Therefore, by activating repair mechanisms, this adduct might be removed as 8-OHdG, which is then measured in fluids such as blood, urine, and saliva. 8-OHdG is a well-established biomarker that represents oxidative DNA damage in short-term studies (Fenga et al. 2017).