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Biological Effects of Millimeter and Submillimeter Waves
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Stanislav I. Alekseev, Marvin C. Ziskin
Sergeeva et al. (2016) studied the effect of 2.3 THz irradiation on bacteria Salmonella (S) typhimurium and E. coli cells. The samples were exposed to 1.4 W/cm2 for 5, 10, and 15 min. For the genotoxicity test, the authors measured SOS induction in E. coli PQ37. SOS response is a global response to DNA damage. No significant differences were found between exposed and control cells indicating that THz radiation did not produce a genotoxic effect. Nevertheless, a small increase in total number of S. typhimurium after 15 min exposure and an increase in several enzyme activities in E. coli PQ37 were indications that THz radiation affected cell metabolism.
Hexavalent chromium bioremediation with insight into molecular aspect: an overview
Published in Bioremediation Journal, 2021
Sreejita Ghosh, Amrita Jasu, Rina Rani Ray
Another defense mechanism of bacteria against Cr (VI) contamination is the presence of DNA repair enzymes that help in repairing damaged DNA caused because of Cr (VI) toxicity. Once Cr (VI) finds its way into the bacterial cells, it is actively reduced to Cr (III) by various means which is either enzymatic or non-enzymatic and in this process ROS get generated causing some adverse or deleterious effects on the bacterial proteins and subsequently bacterial DNA. The damages caused by ROS to the bacterial DNA include base substitutions or modifications, single strand nicks or double strand nicks. These DNA alterations caused by ROS can be restored by an advanced DNA repair process called the SOS response mechanism that consists of enzymes like RecA, RecG and RuvB (Thatoi et al. 2014). This SOS system prevents oxidative DNA damage due to ROS production. On the other hand enzymes like DNA helicases, RecG and RuvB along with the combination of constituents of DNA repair system has been known to take part in response to DNA damage caused by Cr (VI). Cellular reduction of Cr (VI) activates the redox-active intermediates Cr (V/IV) and produces stable Cr (III) leading to the formation of Cr-DNA adducts which is the most common reason of DNA damage causing gene mutation and chromosomal breaks (Thatoi et al. 2014).
Multiple inhibitory effects of succinic acid on Microcystis aeruginosa: morphology, metabolomics, and gene expression
Published in Environmental Technology, 2022
Yi-dong Chen, Chu Zhao, Xiao-yu Zhu, Yuan Zhu, Ru-nan Tian
The recA gene encodes a highly conserved and multifunctional RecA protein, which plays a key role in DNA repair and initiates the SOS response to DNA damage [41]. Studies have shown that the expression of recA will be up-regulated when the environmental stress is not serious but down-regulated under severe environmental stress [42, 43]. In this study, the recA transcription decreased significantly after treatment with 60 mg L−1 SA for 3 h, and then returned to the control level at 24 h. It is possible that the Microcystis cells sensed the SA stress in a short period of time, which caused the expression to decrease. With extended exposure time, the cells became adapted to this stress, and the expression returned to the control level.
Whole-cell bioreporters for evaluating petroleum hydrocarbon contamination
Published in Critical Reviews in Environmental Science and Technology, 2021
Bo Jiang, Yizhi Song, Zengjun Liu, Wei E. Huang, Guanghe Li, Songqiang Deng, Yi Xing, Dayi Zhang
Different from acute toxicity, the WCBs for genotoxicity are ‘light-on’ ones (Figure 1b). Bacterial SOS response is a global response to DNA damage in which the cell cycle is arrested, and DNA repair and mutagenesis are induced (Little & Mount, 1982; Radman & Prakash, 1973). Designing WCBs for genotoxicity relies on the mechanisms of SOS response that the DNA-damage response genes are upregulated postexposure to DNA-damaging reagents, e.g., mitomycin C or PAHs, consequently enhancing the signals produced by the reporter gene encoding enzymes. E. coli is the most commonly used host strain for genotoxicity WCBs owing to its well-established SOS response mechanisms (Bernhardt, 2006). These genotoxicity WCBs were developed with the promoters involved in DNA-damage response, such as umuC (Oda, Nakamura, Oki, Kato, & Shinagawa, 1985), recA (Min et al., 1999), recN (van der Lelie et al., 1997), sfiA (Quillardet et al., 1982) and cda (Norman, Hansen, & Sorensen, 2006). For example, Mersch-Sundermann et al. investigated the genotoxic effects of 32 PAHs on E. coli PQ37 using the SOS chromotest (sfiA), demonstrating the high genotoxicity of benzo[ghi]fluoranthene, benzo[j]fluoranthene, benzo[a]pyrene, chrysene, dibenzo[a,l]pyrene, fluoranthene and triphenylene (Mersch-Sundermann, Mochayedi, & Kevekordes, 1992). Another study using the SOS chromotest assay evaluated the PAHs genotoxicity in a complex mixture and indicated their synergistic or antagonistic effects (White, 2002). Of all the DNA damage inducible promoters, the highly conserved recA promoter attracts most attentions. For instance, a recA-based E. coli bioluminescent genotoxicity WCB was applied to distinguish the toxicity mechanisms of different DNA-damaging reagents (Min et al., 1999), categorizing them into direct DNA-damaging reagents (benzo[a]pyrene and naphthalene) and indirect DNA-damaging reagents (bisphenol A) from the response kinetics and dose-response correlation of WCBs. In addition to E. coli WCBs, genotoxicity WCB based on soil microorganism Acinetobacter baylyi ADP1 serves as an alternative and successfully evaluates the toxicity of PAHs in groundwater (Song et al., 2009), soils (Song et al., 2014) and marine water (Blanco-Ameijeiras, Cabanes, & Hassler, 2019; Jiang et al., 2017; Zhang et al., 2013). WCBs for acute toxicity and genotoxicity serve as a promising tool for the rapid screening of potential ecological risks of petroleum hydrocarbons. Though not as precise and selective as chemical analysis, WCB assay requires less pretreatment and shorter time of operation to acquire their bioavailability and toxicity information.