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Hydroxyl Radicals Assayed by Aromatic Hydroxylation and Deoxyribose Degradation
Published in Robert A. Greenwald, CRC Handbook of Methods for Oxygen Radical Research, 2018
Barry Halliwell, John M. C. Gutteridge
The residue is dissolved in 0.25 mℓ cold double-distilled water and the following reagents added in the order stated: (a) 0.125 mℓ 10% (w/v) trichloroacetic acid dissolved in 0.5 M HCl; (b) 0.25 mℓ 10% (w/v) sodium tungstate (in water); and (c) 0.25 mℓ 0.5% (w/v) NaNO2 (fresh every day).
Free Radicals and Ethanol Toxicity
Published in Victor R. Preedy, Ronald R. Watson, Alcohol and the Gastrointestinal Tract, 2017
Experiments performed with cultured gastric mucosal cells have confirmed that superoxide anion is actually produced following the addition of ethanol and that O-2 generation increases with the amount of ethanol used.80 Cellular damage also increases concomitantly with the formation of superoxide anion. The addition of the iron chelator desferoxamine, or of superoxide dismutase, catalase, and hydroxyl radical scavengers to cultured gastric mucosal cells prevents cell death,80 suggesting that the intracellular production of reactive oxygen species might be responsible for the ethanol-induced damage of gastric mucosal cells. Ethanol is actively metabolized by gastric mucosa,81 thus the stimulation in O-2 production observed in the presence of ethanol could be caused by an increased acetaldehyde oxidation within the mucosal cells by xanthine oxidase or aldehyde oxidase. In support of this possibility, the pretreatment of rats with allopurinol or oxypurinol to block xanthine oxidase protects against the appearance of hemorrhagic lesions due to alcohol administration.76,77'82 Shaw and co-workers have observed that acute ethanol dosage of rats affects the gastric uptake of vitamin B12 by the intrinsic factor and in parallel lowers GSH content of the mucosa.83 Oxidative damage might be implicated in these effects of alcohol, since the same authors have also reported that in gastric homogenates the formation of oxygen radicals by xanthine oxidase and acetaldehyde also impairs the binding efficiency of the intrinsic factor.83 Moreover, feeding sodium tungstate to rats (which decreases xanthine oxidase activity) markedly attenuates the effects of ethanol on both intrinsic factor activity and GSH levels.83
Comparative outcomes of exposing human liver and kidney cell lines to tungstate and molybdate
Published in Toxicology Mechanisms and Methods, 2021
Sherry Sachdeva, Wolfgang Maret
Sodium tungstate induces oxidative stress in various tissues/organs. Intraperitoneal injection of 20 mg (41 mg/kg/d) was more toxic than oral gavage of 119 mg (238 mg/kg/d) given for two weeks (Sachdeva et al. 2013). Remarkably, the administration of antioxidants such as N-acetylcysteine and some flavonoids ameliorated the oxidative stress induced by sodium tungstate (Sachdeva and Flora 2014). N-acetylcysteine also reversed some of the oxidative stress-dependent neurotoxicity of tungstate (Sachdeva et al. 2015). Administration of tungstate in drinking water increased its concentrations in the blood and in tissues and elicited hematological changes, histological changes in the liver, kidneys and spleen, and oxidative stress-triggered apoptosis (Sachdeva et al. 2020). However, mechanistic insights into the health risk of tungsten remain elusive (Datta et al. 2017).
MiADMSA abrogates sodium tungstate-induced oxidative stress in rats
Published in Drug and Chemical Toxicology, 2022
Sherry Sachdeva, Ankita Sharma, S. J. S. Flora
Tungsten is a unique transition metal of group VI in the periodic table with an array of enviable attributes which include flexibility, great strength, good conductance, and a high melting point. These properties have led to an increase in the usage of tungsten commercially in a broad spectrum of industrial goods, ammunition, electronics, X-ray equipment, and implanted medical devices which has led to high levels of exposure to tungsten (Keith et al. 2007). However, there is a lacuna in the information regarding the potential human health risks of increased tungsten exposure which has led Environmental Protection Agency and the National Toxicology Program to identify tungsten as an emerging toxicant (Leffler and Kazantzis 2015, Bolt and Mann 2016, Steenstra et al. 2020). Sodium tungstate is the sodium salt of tungstic acid used as a source of tungsten for chemical synthesis. Sodium tungstate is a thermodynamically stable form showing chemical resistance in several oxidation states (0, +2, +3, +4, +5, and +6) (Bostick et al. 2018). Human exposure to tungsten can be either from natural sources or anthropogenic sources. The main source of occupational exposure of tungsten is via inhalation route which occurs during mining from its ore and also preparation of tungsten carbide products (Wasel and Freeman 2018). The oral route remains the primary route of exposure to tungsten, and soluble tungsten compounds. Pharmacokinetic studies have shown the rapid absorption of tungstate through the oral route, followed by metabolic reactions and rapid elimination via urine in both humans and laboratory animals (ATSDR 2005, Guandalini et al. 2011). Trace amounts of tungsten are also present in human serum and feces, with elimination approximately balancing intake of the metal (Leffler and Kazantzis 2015). Sodium tungstate, the oxidized naturally occurring water-soluble form released by weathering of rocks and soils, fertilizers, and sewage sludge escalates the risk of environmental tungstate exposure (Lemus and Venezia 2015, Liu et al. 2020). Sub-chronic exposure to sodium tungstate has been associated with renal dysfunction at the higher doses of 125 and 250 mg (McCain et al., 2007, 2008). Sodium tungstate exposure has also been found to induce mitochondrial dysfunction leading to the increased formation of ROS, TBARS generation, and loss of mitochondrial membrane potential (Witten et al. 2012, Cheraghi et al. 2019). In-vitro studies have also shown the cell cycle arrest and apoptosis-inducing properties of sodium tungstate in human peripheral blood lymphocytes (Osterburg et al. 2010).