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Impact of Cadmium Toxicity on Environment and Its Remedy
Published in Vineet Kumar, Vinod Kumar Garg, Sunil Kumar, Jayanta Kumar Biswas, Omics for Environmental Engineering and Microbiology Systems, 2023
Pushpa Ruwali, Niharika Pandey, Tanuj Kumar Ambwani, Rahul Vikram Singh
Cadmium has adverse effects on DNA repair mechanisms (Figure 19.2). In the context of base excision repair (BER) mechanism, the exposure of human cells to sublethal concentrations of Cd leads to a decrease in hOGGO1, which is responsible for initiating the BER of 8-oxoguanine, a mutant form of oxidized guanine (Bravard et al. 2009). In the ‘nucleotide excision repair’ (NER) mechanism, the repair of thymine dimers that are formed by UV irradiation gets difficult, as cadmium blocks the repair pathway at the first step itself by inhibiting the enzyme involved (Fatur et al. 2003). Cadmium intoxication leads to the inhibition of mismatch repair in human extracts, which then propagates cellular errors. Cadmium inhibits the adenosine triphosphate binding and the hydrolysis of MSH2-MSH6 protein complex of ‘mismatch repair’ (MMR), which are encoded by MSH2 and MSH6 genes, respectively (Jin et al. 2003).
Regulatory Aspects of Nanotechnology for Food Industry
Published in Lohith Kumar Dasarahally-Huligowda, Megh R. Goyal, Hafiz Ansar Rasul Suleria, Nanotechnology Applications in Dairy Science, 2019
C. Ramkumar, Angadi Vishwanatha, Rahul Saini
The direct attack of ROS on the nucleotide bases in DNA strand modifies the base. The modified base such as 8-oxo- 7,8-dihydroguanine (8-oxoG) can cause the cancer and mutation in the cells. The presence of 8-oxoG can reflect the DNA damage due to oxidative stress after nanomaterials exposure, which is analyzed by FPG-modified comet assay. ROS will enhance the level of 8-oxoguanine DNA glycosylase (OGG1), which ultimately affects base excision repair mechanism of 8-oxoG.C60 fullerene. The geno-toxicity induced by nanomaterials can be inhibited by pre-treatment with the free radical scavenger N-acetyll- cysteine (NAC). Based on these studies we can easily understand the nanomaterials induced ROS and its effects on cellular perturbation along with DNA damage and apoptosis. The induction of inflammatory responses by oxidative stress induced by nanomaterials can lead to cancer. The main factor which makes the nanomaterials high reactive is the electron presence on their boundary. Nanomaterials are responsible for the trigger cytokine release when they interact with protein or enzyme, therefore mediate inflammatory reactions and thereby initiate series of toxic reactions.6
Asbestos, the Carcinogen, and Its Bioremediation
Published in Tanmoy Chakraborty, Lalita Ledwani, Research Methodology in Chemical Sciences, 2017
Shabori Bhattacharya, Lalita Ledwani, P. J. John
ROS/RNS-caused DNA damage studies showed that lesions such as 8-oxodeoxyguanosine or 8-oxoguanine were formed in the DNA of asbestos-exposed various human and animal cell lines.135–137 A correlation was established between concentration of 8-oxoguanine in DNA of white blood cells to time of asbestos exposure in a asbestos cohort study.138 Oxidative stress in chrysotile-exposed asbestos workers resulted in increased levels of DNA double-strand breaks.139 With respect to oxidative damage to DNA, recent research indicates that this may also probably be due to modification or oxidation of cytosine base.140 The observation that myeloperoxidase activity was found in lungs of rodents exposed to asbestos141 has been attributed as a probable secondary mechanism responsible for altered epigenetic methylation profiles as seen in human malignant pleural mesothelioma.142
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.