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Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
The active form of cyanide is HCN. When salts of cyanide are ingested, they react with the acid containing HCl or with water to release the toxic HCN. So, people having achlorhydria, are immune to cyanide poisoning. Cyanide also inhibits various enzymes like glutathione dehydrogenase, superoxide dismutase, carbonic anhydrase, catalase, superoxide dismutase etc. Apart from acting on the electron transport chain, it also acts as a corrosive on the mucosa. Cyanide metabolites are excreted primarily in the urine, and small parts through the lungs. Fatal dose of cyanide salts (of sodium, potassium, or calcium) is 100–200 mg. 20 ppm is maximum safe period for prolonged exposure.6
Toxicology Studies of Semiconductor Nanomaterials: Environmental Applications
Published in Suresh C. Pillai, Yvonne Lang, Toxicity of Nanomaterials, 2019
T. P. Nisha, Meera Sathyan, M. K. Kavitha, Honey John
Several engineered photocatalyst nanoparticles such as TiO2, ZnO, SiO2, CuO, graphene, and CNTs cause oxidative stress by the generation of ROS. ROS generation mainly depends on type and concentration of nanoparticles as well as light irradiation intensity wavelength and duration. The concentration and type of ROS generated is strongly related to the particle size and band edge structure of the photocatalyst (Jiang et al., 2009, Karlsson et al., 2009). Oxidative stress induced by ROS is quantitatively related to the antibacterial activity of the nanoparticles. This can be examined by the viability of E. coli cells in aqueous suspension of nanoparticles (Carré et al., 2014, Leung et al., 2016, Li et al., 2012b). Carré et al. (2014) demonstrated two-dimensional electrophoresis proteomic analysis as the first study to gain insight into the antimicrobial effect of a TiO2 photocatalyst is to identify potential protein targets modified during the cytotoxic treatment in dark and in the presence of UV-A irradiation. This proteomics method can provide quantitative evidence for toxicity by detecting changes in protein expression as a reaction of exposure of bacteria to the nanomaterial. In the dark, TiO2 shows no cytotoxic effect while UV-A photocatalytic treatment results in lipid peroxidation from the reaction with the superoxide radical ROS. Leung et al. studied the toxicity of TiO2 and ZnO nanoparticles using E. coli as a model organism and examined cell count, ROS generation, and proteomics investigations. Toxicity of these nanoparticles can be mainly due to the interaction with liposaccharide molecules in the cell membrane and ROS-induced oxidative stress under illumination. Both TiO2 and ZnO are good photocatalysts, which can inactivate microorganisms. It is found that ZnO shows less anti-bacterial activity compared to TiO2. However, ZnO-treated bacterial cells show significant up-regulation of ROS-related proteins (glutathione reductase and glutathione dehydrogenase). For TiO2, ROS-related protein bacterial response is not significant, but the outer membrane protein expression is observed (Leung et al., 2016).
Molecular mechanisms of ethanol biotransformation: enzymes of oxidative and nonoxidative metabolic pathways in human
Published in Xenobiotica, 2020
Grażyna Kubiak-Tomaszewska, Piotr Tomaszewski, Jan Pachecka, Marta Struga, Wioletta Olejarz, Magdalena Mielczarek-Puta, Grażyna Nowicka
Low Michaelis constant value for all class I ADH forms (Km: 0.2–2.0 mM) indicates a relatively high affinity of all forms of ADH of this class to ethanol (Lieber, 1997; Ramchandani, 2013). Class II ADH, accompanying the previously mentioned isoenzyme in hepatocyte cytosol, has a much smaller share in liver biotransformation of ethanol under conditions of low consumption, because its affinity to ethanol is much lower (Km = 30.0–34.0 mM) than that of class I ADH. The share of this isoenzyme in ethanol metabolism increases under conditions of intoxicating the body with large doses of alcohol. The contribution of class III ADH to the metabolism of ethanol in the liver can be neglected due to the extremely low affinity of this isoenzyme to ethanol (Km>1000 mM), so that in practice it is not possible to obtain a sufficiently high concentration of ethanol even in heavy drinkers. Under physiological conditions, this isoenzyme participates in the oxidation of long-chain primary alcohols and S-hydroxymethylglutathione, and the reaction of formaldehyde with glutathione. Therefore, class III ADH is sometimes referred to as glutathione-dependent ALDH, glutathione-dependent formaldehyde dehydrogenase (FALDH, GSH-FDH, EC 1.1.1.-) or S-(hydroxymethyl)glutathione dehydrogenase (EC 1.1.1.284) (Orywal & Szmitkowski, 2017; UniProt Knowledgebase, 2020). Other ADH isoenzymes (class IV and V) are present in the liver in an extremely small number of copies due to low expression of their genes in hepatocytes. The Km value for class IV ADH is Km = 30 mM and the Km value for the class V isoenzyme has not yet been determined (ExPasy, 2020; Lieber, 1997; Ramchandani, 2013) (Table 2).
Preclinical renal chemo-protective potential of Prunus amygdalus Batsch seed coat via alteration of multiple molecular pathways
Published in Archives of Physiology and Biochemistry, 2018
Preeti Pandey, Prakash Chandra Bhatt, Mahfoozur Rahman, Dinesh Kumar Patel, Firoz Anwar, Fahad Al-Abbasi, Amita Verma, Vikas Kumar
Fe-NTA treatment altered the activity of anti-oxidant enzymes viz., catalase, superoxide dismutase, glutathione dehydrogenase, glutathione reductase and phase II metabolising enzymes viz., QR and GST, which were restored by the GA treatment in a dose-dependent manner. Fe-NTA treatment significantly diminishes the renal GSH content and its metabolising enzymes (Khan et al. 2004, Iqbal et al. 2007, 2009). Quinone reductase and glutathione-S-transferase are Phase-II enzymes, which are involved in the elimination, conjugation, and detoxification of carcinogens either in the form of sulphates, glucuronides, or glutathione conjugates. QR alters the activation of cytochrome P-450 to toxic semiquinone to soluble hydroquinones. On the other hand, GST used as an indicator of anti-carcinogenesis agent which catalyses the reduced GSH with electrophilic conjugation (Kaur et al. 2007). Alterations of QR and GST are the measures of strong correlation with the chemo-protective effect of the drug (Khan and Sultana 2005). GSH is consider as a natural endogenous cellular anti-oxidant and its reduce level is associated with enhanced activity of oxidative stress and tissue injury. It scavenges the toxic hydroxyl and singlet oxygen radicals. Decreased level of NADPH and increased absorption of GSH (utilisation to remove the free radical) is responsible for reduce level of GSH. The redox system is maintained by endogenous process of GSH where GSSG is oxidised to GR to uphold the reduced GSH, whereas GPx used to reduce the renal GSH along with down-regulation of GPx, GR, GST, and QR during the Fe-NTA treatment (Jahangir et al. 2006, Ahmad et al. 2011). Dose-dependent treatment of GA extract significantly (p < .001) recovers the altered GSH, GR, GST, and GPx. Free radicals such as NO, •OH, H2O2, and O2 boost the ROS and RNS. The boosted level of ROS, RNS, and free radical interacts with the other toxic product and induce the structural and functional damage on all cellular molecules. The results suggest that the GA extract significantly inhibits the generation of free radicals and inhibits the interaction of toxic product with these radicals. Carcinogens like Fe-NTA increased the iron content, which increase the oxidative stress level and initiate the damage to DNA and lipids, both are considered as the indicators of early stage of toxicity and tissue damage. Various well documented proofs are available, which suggest that 4-hydroxynonenal, lipid peroxidation (LPO), and DNA bases have close relation with the DNA and lipids destruction. LPO and coupled membrane damage are concerned as primary factors in pathophysiology of various diseases and renal dysfunction is one of them (Iqbal et al. 1998, Kaur et al. 2009, Rehman et al. 2013). Fe-NTA induced toxicity enhances the level of malonaldehyde (MDA) (a LPO indicator) and suggest the tissue toxicity, which was altered in dose-dependent manner when treatment was initiated by GA extract suggesting the renal protective effect of GA.