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Bioremediation of Cr(VI)-Contaminated Soil using Bacteria
Published in Maulin P. Shah, Removal of Refractory Pollutants from Wastewater Treatment Plants, 2021
Browning and Wise (2017) discovered the mechanism of carcinogenesis in lung carcinoma, which is induced by particulate Cr(VI). A stable, heritable structural change in chromosome resulted in the formation of lung carcinoma. Cr(VI) has been found to interrupt the normal pathway of homologous recombination (HR) repair of DNA double-strand breaks by changing the subcellular localization of protein RAD51, an essential protein for the HR repair mechanism. An organism may encounter Cr(VI) from contaminated food or food supplements, water, or air. The mean daily dietary intake of Cr is estimated to be <0.2–0.4, 2.0, and 60 mg from the air, water, and food, respectively (ATSDR). Cr inhalation can cause nasal perforation, thus increasing the risk of respiratory tract diseases. Though most reports are based on the toxic effects of Cr(VI), Cr(III), though less toxic, is also reported to cause damage to lymphocyte DNA.
Pro-inflammatory and toxic effects of silver nanoparticles
Published in Ana Rute Neves, Salette Reis, Nanoparticles in Life Sciences and Biomedicine, 2018
Marisa Freitas, Daniela Ribeiro, Paula Silva, Jose L. F. C. Lima, Felix Carvalho, Eduarda Fernandes
It is known that RS constitutes one of the major sources of spontaneous damage to DNA. Among RS, a hydroxyl radical is one of the most harmful, as it can cause DNA damage to generate 8-hydroxyguanine, leading to a decrease in the stability of repetitive sequences and single- and double-strand breaks. Subsequently DNA damage will culminate in cell cycle arrest, and once the damage is too extensive, cells may irreversibly undergo into apoptosis [62]. The genotoxic effects of AgNPs have already been discussed by Kim and Ryu [68]. The authors reported that many biochemical and molecular changes related to genotoxicity are promoted by AgNPs in cultured cells, as AgNPs induce DNA breakage. For example, Eom and Choi [39] reported that in Jurkat T cells, AgNPs induced ROS production, subsequently resulting in DNA strand breaks, cell cycle arrest at the G2/M phase, and cell viability decline in AgNP-treated cells, via p38 MAPK and Nrf-2 signaling pathways [39]. Moreover, it is known that AgNPs possess a strong tendency to interact with the thiol groups of enzymes, and the phosphate group of DNA bases, impairing their activity. It was also described that AgNPs increased the expression of a DNA damage repair protein, Rad51, precluding safe DNA repair damage [68]. The formation of bulky DNA adducts induced by AgNPs were reverted by the use of antioxidants, proving the important role of RS in the induction of DNA damage [68]. Furthermore, as has been mentioned above, the interaction of AgNPs with mitochondria results in the release of caspase-3, an effector protein, which has also the ability to induce the cleavage of DNA [69].
Risk of Low-Level Exposure to Radiation-Biological Basis
Published in Lawrence T. Dauer, Bae P. Chu, Pat B. Zanzonico, Dose, Benefit, and Risk in Medical Imaging, 2018
Tatjana Paunesku, Gayle E. Woloschak
In human hepatic cell line exposure to 10 mGy led to histone deacetylation of the micro-RNA miR-193b-3p promoter. Change in expression of this miRNA was first found in spleen and liver of mice exposed to 10mGy whole-body irradiation. Suppression of miR-193b-3p leads to a subsequent increase in expression of the DNA double-strand break repair gene Rad51 [74].
The expression of Phase II drug-metabolizing enzymes in human B-lymphoblastoid TK6 cells
Published in Journal of Environmental Science and Health, Part C, 2022
Xilin Li, Yuxi Li, Kylie G. Ning, Si Chen, Lei Guo, Jessica A. Bonzo, Nan Mei
SAT1 is the rate-limiting enzyme for polyamine catabolism. The level of polyamines often increases in tumor cells, stimulating their growth and proliferation. Recent studies have demonstrated that a reduced level of polyamines may increase the susceptibility of cells in response to many double-strand break (DSB)-inducing agents, including ionizing radiation, ultraviolet, and etoposide.35 The underlying mechanism has been associated with the role of polyamine in stimulating homologous recombination mediated DSB repair by enhancing the DNA strand exchange activity of RAD51. SAT1 governs the transportation of polyamines in cells. The overexpression of SAT1 leads to excessive export of polyamines, which may further impair homologous recombination and sensitize cells to genotoxic stresses. Although TK6 cells expressed SAT1 mRNA, the level was significantly lower than that in HepG2 cells or PHHs (Table 1). The impact of this difference on sensitivity of cells to various DNA DSB-inducing agents warrants further investigation.