Olfactory toxicity of diethyldithiocarbamate (DDTC) and disulfiram and the protective effect of DDTC against the olfactory toxicity of dichlobenil
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Toxic exposures and the senses of taste and smell
2019, Handbook of Clinical NeurologyCitation Excerpt :Systemically administered compounds can also cause damage to the olfactory system and sense of smell; for example, some orally-administered antihyperthyroid drugs such as methimazole and carbimazole have been shown to be capable of causing olfactory dysfunction (Schiffman, 1983; Carpenter et al., 2007); both methimazole and carbimazole were subsequently shown to cause olfactory epithelial degeneration and olfactory dysfunction in rodents (Genter et al., 1995; Genter, 1998). Bioactivation by metabolic enzymes present in the olfactory mucosa of some parent compounds generates toxic intermediate metabolites in rodents, which leads to olfactory mucosal degeneration (e.g., Deamer and Genter, 1995; Genter et al., 1998; Wetmore et al., 1999; Genter, 2006). Given that metabolic enzyme expression is similar in human and rodent olfactory mucosa (Gu et al., 2000), olfactory damage in response to drugs or other chemicals in humans may also occur by bioactivation to toxic metabolites.
Olfactory mucosal necrosis in rats following acute intraperitoneal administration of 1,2-diethylbenzene, 1,2-diacetylbenzene and 2,5-hexanedione
2014, NeuroToxicologyCitation Excerpt :Results from these experiments suggest that CYP2E1 and/or CYP2F4 may strongly contribute to the formation of 1,2-DAB, as 5-phenyl-1-pentyne effectively prevented 1,2-DEB from inducing nasal lesions. We did not attempt to determine which of these isozymes was responsible for 1,2-DEB metabolism as diethyldithiocarbamate, a relatively selective inhibitor of CYP2E1, has been reported to cause degeneration of the olfactory mucosa in rat (Deamer and Genter, 1995). However, it is worth noting that IDPN, known to cause proximal neurofilamentous axonopathy in rats (Chou and Hartmann, 1964; Robinson et al., 2003), also causes olfactory toxicity (Genter et al., 1992) that appears to depend on bioactivation by cytochrome P450 2E1 (Genter et al., 1994).
Transcriptional impact of organophosphate and metal mixtures on olfaction: Copper dominates the chlorpyrifos-induced response in adult zebrafish
2011, Aquatic ToxicologyCitation Excerpt :Exposure to several classes of chemicals has been linked to impaired chemosensory function and loss of olfaction in vertebrates (Deamer and Genter, 1995; Sandahl et al., 2007; Tierney et al., 2007b, 2008, 2010).
Status of antioxidant defense system and expression of toxicant responsive genes in striatum of maneb- and paraquat-induced Parkinson's disease phenotype in mouse: Mechanism of neurodegeneration
2006, Brain ResearchCitation Excerpt :The central nervous system is extensively susceptible to free radical damage due to its high metabolic rate and high levels of unsaturated lipids (Singh et al., 2004). The involvement of cytochrome P4502E1 and glutathione S-transferases A4-4 enzymes in the detoxification of several pesticides viz. atrazine, fenamirol, methoxychlor, mancozeb, organophosphorous insecticide parathion, diethyl dithiocarbamate and paraquat has been known (Di Ilio et al., 1995; O'Shaughnessy and Sultatos, 1995; Siddiqui et al., 1993; Oropeza-Hernandez et al., 2003; Mutch et al., 1999; Deamer and Genter, 1995; Hanioka et al., 1998; Eaton, 2000). CYP2E1 plays a role in the detoxification of several environmental neurotoxins and oxidative stress due to the formation of reactive oxygen species from P450 enzymes results in neurodegeneration (Tindberg and Ingelman-Sundberg, 1996; Watts et al., 1998).
Regulation of cytochrome P450 gene expression in the olfactory mucosa
2004, Chemico-Biological InteractionsCitation Excerpt :Collectively, the microsomal CYPs expressed in the OM metabolize numerous endogenous as well as xenobiotic compounds. In animals, the presence of relatively high levels and unique forms of CYP enzymes in this tissue leads to very high activity for target tissue metabolic activation, and presumably tissue-selective toxicity, of many nasal toxicants, such as 2,6-dichlorobenzonitrile (DCBN) [7,8], 2,6-dichlorophenyl methylsulphone [9], coumarin [10], N-nitrosopiperidine [11], and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone [12]. There is no report on CYP activities in human OM to date, although CYP-mediated metabolism of several compounds has been demonstrated with microsomes of human nasal respiratory mucosa [13].
Antioxidant status of the rat nasal cavity
2003, Free Radical Biology and Medicine