Cytotoxicity and related effects of T-2 toxin on cultured Vero cells

Bouaziz, Chayma; Abid‐Essefi, Salwa; Bouslimi, Amel; Golli, Emna El; Bacha, Hassen

doi:10.1016/j.toxicon.2006.06.004

Cited by 67 publications

(40 citation statements)

References 33 publications

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“…In the present study, we showed that satratoxin H (50 nM) increased cleavage of caspase-3, which was mediated through p38 MAPK and/or JNK. Our data were concomitant with the previous studies, in which apoptosis mediated through caspase-3 is induced by other trichothecenes, such as T-2 toxin (Bouaziz et al, 2006), 4-acetyl-12,13-epoxyl-9-trichothecene-3,15-diol (Pae et al, 2003), and satratoxin G (Nagase et al, 2002). Stratoxin G-producing S. chartarum IBT 9631, as well as satratoxin G, increased phosphorylation of p38 MAPK and activation of caspase-3 (Rakkestad et al, 2010).…”

Section: Discussionsupporting

confidence: 90%

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

et al. 2012

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-Satratoxin H is an important air-and food-borne mycotoxin, which has been implicated in human health damage. Satratoxin H is known to induce apoptosis as well as genotoxicity in PC12 cells. In the present study, we further investigated the mechanism of apoptotic effects of satratoxin H with focus on caspase-3 and poly-ADP-ribose polymerase (PARP) pathway. We also examined whether it induces DNA damage in PC12 cells. In the cells treated with satratoxin H, caspase-3 was cleaved in a time-dependent manner. Furthermore, satratoxin H induced cleavage of PARP, one of the downstream molecules of caspase-3. The cleavage was inhibited by SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor. Satratoxin H, however, had no effect on expression levels of Bax and Bcl-2. Furthermore, the micronucleus assay revealed that satratoxin H induced chromosome break. Also, satratoxin H increased the level of phosphorylation of histone H2A, indicating that it caused DNA double-stranded breaks in PC12 cells. Meanwhile, no genotoxicity was detected with any of treatments carried out in the alkaline comet assay. These results imply that satratoxin H induces genotoxicity by DNA double-stranded break. Our results suggest a considerable potential for the genotoxic risk associated with the presence of satratoxin H.

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Section: Discussionsupporting

confidence: 90%

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

et al. 2012

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“…In contrast, Segal et al [30] reported that T-2 toxin and deoxynivalenol (DON) stimulated lipid peroxidation in the livers of rats. Oxidative damage caused by T-2 toxin was considered as one of the underlying mechanisms for T-2 toxin induced cytotoxicity, DNA damage, and apoptosis [31]. Oxidative stress may occur either due to the overproduction of reactive oxygen species (ROS) or due to decrease of cellular antioxidant levels.…”

Section: Discussionmentioning

confidence: 99%

Oxidative damage and gene expression profile of antioxidant enzymes after T‐2 toxin exposure in mice

Chaudhari

Ravindran

Santhosh

et al. 2009

J Biochem & Molecular Tox

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T-2 toxin is one of the most potent trichothecenes, and on exposure causes severe human and animal diseases. We investigated the dose- and time-dependent effect of T-2 toxin on certain biochemical variables, oxidative damage in terms of antioxidant enzyme activity, and gene expression profile in mice. Mice treated intraperitoneally with either 1 LD50 or 2 LD50 dose (5.61 and 11.22 mg/kg body weight, respectively) of T-2 toxin showed significant alterations in hepatic alanine amino transferase, aspartate amino transferase, and lactate dehydrogenase. Significant changes in hepatic lipid peroxidation, depletion of glutathione (GSH), and expression of heat shock protein-70 indicated oxidative damage. We also evaluated the activity of antioxidant enzymes and compared the gene expression profile by quantitative real-time reverse transcriptase-polymerase chain reaction. Except for glutathione reductase (GR), there was a significant increase in activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase at 1 LD50 dose. At 2 LD50 dose, SOD showed decrease in activity, whereas GST, GPx, and catalase showed significant increase. In contrast, gene expression profile showed downregulation in GR, GPx, GST, and catalase at 1 LD50 dose. At 2 LD50 dose except GSH synthetase, all other genes were downregulated. The results clearly show oxidative stress as one of the mechanisms of T-2 toxin-mediated toxicity.

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“…T-2 toxin produces both in vivo and in vitro, single strand breaks in the DNA of lymphoid cells. In vitro T-2 toxin causes apoptosis in various cell types like HL60, Jurkat, U937 (Huang et al, 2007), Vero cells (Bouaziz et al, 2006) and human hepatoma cells (Bouaziz et al, 2008). Apoptosis was also reported in vivo in thymic and spleenic lymphocytes as well as other tissues of mice like bone marrow and intestinal epithelial cells (Li et al, 1997;Shinozuka et al, 1997), skin (Albarenque et al, 1999), kidney (Grizzle et al, 2004) and brain (Sehata et al, 2004).…”

Section: Introductionmentioning

confidence: 96%

Oxidative stress induction by T-2 toxin causes DNA damage and triggers apoptosis via caspase pathway in human cervical cancer cells

et al. 2009

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Cytotoxicity and related effects of T-2 toxin on cultured Vero cells

Cited by 67 publications

References 33 publications

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

Oxidative damage and gene expression profile of antioxidant enzymes after T‐2 toxin exposure in mice

Oxidative stress induction by T-2 toxin causes DNA damage and triggers apoptosis via caspase pathway in human cervical cancer cells

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