A growing body of evidence suggests that ribosome-inactivating proteins (RIPs) remove adenine moieties not only from rRNA, but also from DNA--an effect leading to DNA damage in cultured cells. We herein report that two distinct RIPs of bacterial (shiga toxin 1, Stx1) and plant (ricin) origin, inhibit the repair of the DNA lesions generated by hydrogen peroxide in cultured human cells. This effect is unrelated either to inhibition of protein synthesis or to depletion of cellular antioxidant defenses and is likely to derive from direct interactions with cellular DNA repair machinery. Therefore, the genotoxicity of these toxins on mammalian cells seems to be a complex phenomenon resulting from the balance between direct (DNA damaging activity), indirect (DNA repair inhibition) effects and the eventual presence of other DNA damaging species. In particular, with regard to Stx1, it could be hypothesized that Stx-producing bacteria increase the risk of transformation of surrounding, inflamed tissues in the course of human infections.

Shiga toxin 1 and ricin inhibit thr repair of H2O2-induced DNA single strand breks in cultured mammalian cells / Sestili, P.; Alfieri, Roberta; Carnicelli, D.; Martinelli, C.; Barbieri, L.; Stirpe, F.; Bonelli, Mara; Petronini, Pier Giorgio; Brigotti, M.. - In: DNA REPAIR. - ISSN 1568-7864. - 4:(2005), pp. 271-277. [10.1016/j.dnarep.2004.09.007]

Shiga toxin 1 and ricin inhibit thr repair of H2O2-induced DNA single strand breks in cultured mammalian cells

ALFIERI, Roberta;BONELLI, Mara;PETRONINI, Pier Giorgio;
2005-01-01

Abstract

A growing body of evidence suggests that ribosome-inactivating proteins (RIPs) remove adenine moieties not only from rRNA, but also from DNA--an effect leading to DNA damage in cultured cells. We herein report that two distinct RIPs of bacterial (shiga toxin 1, Stx1) and plant (ricin) origin, inhibit the repair of the DNA lesions generated by hydrogen peroxide in cultured human cells. This effect is unrelated either to inhibition of protein synthesis or to depletion of cellular antioxidant defenses and is likely to derive from direct interactions with cellular DNA repair machinery. Therefore, the genotoxicity of these toxins on mammalian cells seems to be a complex phenomenon resulting from the balance between direct (DNA damaging activity), indirect (DNA repair inhibition) effects and the eventual presence of other DNA damaging species. In particular, with regard to Stx1, it could be hypothesized that Stx-producing bacteria increase the risk of transformation of surrounding, inflamed tissues in the course of human infections.
2005
Shiga toxin 1 and ricin inhibit thr repair of H2O2-induced DNA single strand breks in cultured mammalian cells / Sestili, P.; Alfieri, Roberta; Carnicelli, D.; Martinelli, C.; Barbieri, L.; Stirpe, F.; Bonelli, Mara; Petronini, Pier Giorgio; Brigotti, M.. - In: DNA REPAIR. - ISSN 1568-7864. - 4:(2005), pp. 271-277. [10.1016/j.dnarep.2004.09.007]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/1445406
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