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Original Articles

Effects of trichothecene mycotoxins on eukaryotic cells: A review

Pages 369-378 | Published online: 22 Aug 2006

Figures & data

Figure 1. Inhibitory effect of (A) 20 ppm DON as compared with (B) water on wheat cv. Avalon seedling growth (48 h post-treatment).

Figure 1. Inhibitory effect of (A) 20 ppm DON as compared with (B) water on wheat cv. Avalon seedling growth (48 h post-treatment).

Table I. Examples of the cellular effects of trichothecenes on animals and plants.

Figure 2. Trichothecene-mediated signal transduction and downstream processes in mammalian cells. Protein synthesis inhibition: trichothecenes interfere with the active site of peptidyl transferase on ribosomes. Mitogen-activated protein kinase (MAPK) activation: certain trichothecenes induce ERK1/2, JNK and p38 MAPKs (Laskin et al. Citation2002). A double-stranded RNA-activated protein kinase R (PKR) mediates DON-induced phosphorylation of ERK1/2, p38 and JNK MAPKs (Zhou et al. Citation2003b). DON activation of the proinflammatory response: it induces cytokine transcription and, as a consequence of MAPK activation, induces cyclooxygenase-2 (COX-2) and increases synthesis of prostaglandin endoperoxides. DON-induced apoptosis (Shifrin and Anderson Citation1999, Yang et al. Citation2000, Poapolathep et al. Citation2002): increases linearly with inhibition of protein synthesis and the peptidyl transferase site is postulated to be a regulator of both MAPK activation and apoptosis in Jurkat T cells (Shifrin and Anderson Citation1999).

Figure 2. Trichothecene-mediated signal transduction and downstream processes in mammalian cells. Protein synthesis inhibition: trichothecenes interfere with the active site of peptidyl transferase on ribosomes. Mitogen-activated protein kinase (MAPK) activation: certain trichothecenes induce ERK1/2, JNK and p38 MAPKs (Laskin et al. Citation2002). A double-stranded RNA-activated protein kinase R (PKR) mediates DON-induced phosphorylation of ERK1/2, p38 and JNK MAPKs (Zhou et al. Citation2003b). DON activation of the proinflammatory response: it induces cytokine transcription and, as a consequence of MAPK activation, induces cyclooxygenase-2 (COX-2) and increases synthesis of prostaglandin endoperoxides. DON-induced apoptosis (Shifrin and Anderson Citation1999, Yang et al. Citation2000, Poapolathep et al. Citation2002): increases linearly with inhibition of protein synthesis and the peptidyl transferase site is postulated to be a regulator of both MAPK activation and apoptosis in Jurkat T cells (Shifrin and Anderson Citation1999).

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