Regular ArticleSulfur Mustard-Induced Increase in Intracellular Free Calcium Level and Arachidonic Acid Release from Cell Membrane
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Dermal toxicity of sulfur mustard
2020, Handbook of Toxicology of Chemical Warfare AgentsTemozolomide has anti-tumor effects through the phosphorylation of cPLA<inf>2</inf> on glioblastoma cells
2019, Brain ResearchCitation Excerpt :Cytosolic phospholipase A₂ (cPLA₂) hydrolyzes the acyl bond at the sn-2 position of phospholipids, generating arachidonic acid (Bonventre, 1992). The alkylating agent, sulfur mustard suppresses cell growth in the murine neuroblastoma-rat glioma hybrid NG108 cell line via activation of cPLA₂ and arachidonate release (Ray et al., 1995). Moreover, arachidonic acid suppresses cell growth and promotes apoptosis in breast cancer (Comba et al., 2016).
Mustard Lung: Diagnosis and Treatment of Respiratory Disorders in Sulfur-Mustard Injured Patients
2016, Mustard Lung: Diagnosis and Treatment of Respiratory Disorders in Sulfur-Mustard Injured PatientsSulfur mustard-stimulated proteases and their inhibitors in a cultured normal human epidermal keratinocytes model: A potential approach for anti-vesicant drug development
2016, Toxicology ReportsCitation Excerpt :Since NAD is also required as a cofactor for cellular energy metabolism, its depletion causes hexose monophosphate shunt metabolic pathway stimulation and consequently protease activation and release. Another possible mechanism of SM-induced protease stimulation has been proposed to be related to an increase in intracellular free calcium ion concentration due to SM [13], which may activate calcium-dependent enzymes like phospholipases and/or proteases [26]. The major target of SM in the skin are the replicating basal epidermal keratinocytes, which remain attached to the sub epithelial layer (dermis) via some attachment proteins e.g., laminin-5, integrin etc.
A guanine-ethylthioethyl-glutathione adduct as a major DNA lesion in the skin and in organs of mice exposed to sulfur mustard
2015, Toxicology LettersCitation Excerpt :It can occur either spontaneously or be mediated by glutathione-S-transferases (Kinsey and Grant, 1947; Davison et al., 1961; Black et al., 1992a,b; Abel et al., 2011). The reactivity of SM toward GSH is so large that a phenomenon of GSH depletion was observed both in in vitro (Ray et al., 1995; Gross et al., 1997; Amir et al., 1998) and in vivo models exposed to SM (Gautam and Vijayaraghavan, 2007; Jafari, 2007; Vijayaraghavan et al., 2008; Pohanka et al., 2013). This depletion is followed by a strong oxidative stress associated with damage to proteins (Pohanka et al., 2011), lipids (Kumar et al., 2001; Jafari, 2007) and DNA (Pal et al., 2009; Tewari-Singh et al., 2012).
Dermal Toxicity of Sulfur Mustard
2015, Handbook of Toxicology of Chemical Warfare Agents: Second Edition