Table 3.

Molecular mechanisms involved in nettle vesicant CX (A), mustard vesicant SM (B), and arsenical vesicant LEW (C) induced toxicity.

CX	SM	LEW
p53 phosphorylation (Ser15) and accumulation, DNA damage Apoptosis Inflammation (Mast cell degranulation, increased MPO activity, increased COX-2, and TNF-α expression) Necrosis	H2A.X phosphorylation (Ser139), p53 phosphorylation (Ser15) and accumulation, DNA damage Apoptosis Inflammation [MAP kinases, NF-κB activation, increased COX-2 expression, and cytokine release (IL- 1α/β, IL-6, IL-8, and TNF-α)] Oxidative and nitrosative stress Proteolytic activation (Matrix- metalloproteases or MMPs and serine proteases) Ca imbalance (ER stress) PARP activation Necrosis	Apoptosis Inflammation (NF-κB activation, increased COX-2 expression, and cytokine release (IL-1β, IL-6, IL-8, and IFN-α) Oxidative stress Proteolytic activation (Matrix- metalloproteases or MMPs) Activation of UPR signaling pathway

Sources: (Ghabili et al., 2011; Gordon et al., 2010; Kehe et al., 2009; Kohnavard, 2016; Laskin et al., 2010; Li et al., 2016b; Nguon et al., 2014; Paromov et al., 2007; Shakarjian et al., 2010; Srivastava et al., 2013; Srivastava et al., 2016; Tewari-Singh et al., 2017).