China
Africa
Explore chapters and articles related to this topic
Cobalt Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Muhammad Umar, Ayyaz Sultan, Noman Jahangir, Zobia Saeed
Cobalt metal and salts are genotoxic in mammalian in vitro test systems. Mainly it is caused by oxidative DNA damage by reactive oxygen species, along with inhibition of DNA repair.32 Although evidence of carcinogenicity of cobalt is considered sufficient in experimental animals but is deemed to be inadequate in humans. However, cobalt, in combination with tungsten carbide, has been found to have carcinogenic potential.69 International Agency for Research on Cancer (IARC) classified the mixture of cobalt and tungsten carbide (Co/WA) as “probably carcinogenic to humans.”70 In an occupational exposure setting, cobalt-containing dust has been considered as a risk for lung cancer.
Microbial Removal of Toxic Chromium for Wastewater Treatment
Published in Maulin P. Shah, Removal of Refractory Pollutants from Wastewater Treatment Plants, 2021
Joorie Bhattacharya, Rahul Nitnavare, Thomas J Webster, Sougata Ghosh
In spite of being an essential trace element, even the slightest increase in Cr(VI) level is enough to render it toxic. The mutagenicity and carcinogenicity of chromium to biological systems are greatly attributed to the high oxidizing potential of Cr(VI). Moreover, Cr(VI) is not able to directly interact with the cellular DNA. Thus, its toxicity is believed to be due to the intracellular reduction of Cr(VI) to Cr(III). Additionally, the intracellular reduction of Cr(VI) forms intermediate chromium species, essentially Cr(V) and Cr(IV). This also leads to an increase in the concentration of reactive oxygen species (ROS) which causes oxidative DNA damage (Dhal et al. 2013).
Cytotoxicity and genotoxicity of light emitted by incandescent, halogen, and LED bulbs on ARPE-19 and BEAS-2B cell lines
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Marta Gea, Tiziana Schilirò, Paola Iacomussi, Raffaella Degan, Sara Bonetta, Giorgio Gilli
The formamidopyrimidine glycosylase (Fpg)-modified Comet assay was used to evaluate oxidative DNA damage. The test was carried out as described above with the exception that, after lysis, the slides were washed three times for 5 min with Fpg Buffer (40 mM HEPES, 0.1 M KCl, 0.5 mM EDTA disodium salt dihydrate, 0.2 mg/ml bovine serum albumin, pH 8). Then, the slides were incubated with 0.5 unit of Fpg enzyme (Escherichia coli Fpg enzyme and Buffer- Trevigen) at 37°C for 30 min. Control slides were incubated with buffer only. A hundred randomly selected cells per sample (2 spots) were analyzed using an image analysis system (Comet Assay IV) (Perceptive Instruments Ltd). For each experimental point, the mean % tail DNA in enzyme-untreated cells (direct DNA damage) and mean % tail DNA in Fpg-enzyme-treated cells (direct and indirect DNA damage) were calculated.
Risk management of free radicals involved in air travel syndromes by antioxidants
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Air travelers and crews may have impaired antioxidant/oxidant status and immune system due to oxidative stress like ceramic workers (Anlar et al. 2017). To reduce radiation-induced oxidative DNA damage and genomic instability, supplementation with antioxidant vitamins C and E, lipoic acid, antioxidant herbs or plants might be effective against genotoxicity produced by free radicals (Acésio et al. 2017; Fagundes et al. 2017; Velauthapillai et al. 2017). Other radioprotective agents include N-acetyl cysteine (NAC), resveratrol, polyphenols, lactoferrin, melatonin, and fruit juice (Jia et al. 2010; Mohammad et al. 2014; Nishimura et al. 2014; Ortiz et al. 2015; Zhang et al. 2017).
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Arsenicals do not react directly with DNA. The major underlying carcinogenic mechanisms observed at low concentrations are rapid induction of oxidative DNA damage and inhibition of DNA repair. Some forms of arsenic induce chromosomal aberrations in vitro, but this is significant only at toxic doses. Chronic low-dose exposure in animal models produces genomic instability and leads to chromosomal aberrations and micronucleus formation. AsIII interferes with spindle function during mitosis. Increased mutagenesis is observed as a consequence of enhanced genomic instability.