The chromosome damage observed in genotoxic assays performed with animal venoms showed that these toxins may possibly be used in the development of new therapeutic strategies for cancer control. There are some interesting examples with venoms from scorpions, bees and snakes (Zargan et al., 2011; Lee selleck screening library et al., 2007; Varanda et al., 1999; Wang et al., 2000; Wang and Groopman, 1999; Lerda et al., 2005; Brugger et al., 2006; Dönmez-Altuntas et al., 2007). The obtained results suggest that different toxins could induce breakages in DNA by different ways, which is corroborated by the results

obtained with BthTX-I, BthTX-II and BatxLAAO, which resulted in permanent breakages likely to be observed in the micronucleus assay. Conversely, the high rate of DNA breakage induced by BjussuMP-II is not maintained after the action of cell repair system, as observed in the micronucleus assay. Interesting, BthTX-I is an enzymatically inactive PLA2-like enzyme and showed similar mutagenic LDK378 molecular weight effect to BthTX-II, which is

catalytically active, suggesting that the genotoxicity is not related to the catalytic activity. The mechanisms of action of snake venom genotoxicity are not yet elucidated. The production of free radicals induced by some toxins is a valuable hypothesis that should be considered, since they participate in inflammatory processes and the mediators are intimately related to the oxidative stress. However, the apoptosis induction cannot be discarded considering the high number of published works describing this effect for different classes of toxins such as LAAOs,

metalloproteases and PLA2s (Iwanaga and Suzuki, 1979; Kang et al., 2011). Corroborating this hypothesis, the induction of oxidative stress has been described for some snake venoms and isolated toxins (Zhang and Cui, 2007; Yamasaki et al., 2008). This effect can also be associated with the DNA damage induced by venom toxins, through the formation of free radicals that could induce genotoxicity and, in high levels, even mutagenicity or cellular apoptosis. The induction Methane monooxygenase of micronuclei and DNA damage of lymphocytes observed after cell exposure to different concentrations of an LAAO from B. atrox showed in the present work are an indication that substantiates the hypothesis cited above. Future experiments using anti-oxidant agents, together with the toxins could elucidate the suggested mechanism, as showed for zearalenone ( Ouanes et al., 2003). The venoms from B. brazili and B. atrox did not induce DNA damage when assayed by the comet test, however, both showed genotoxic potential when assayed by the micronucleus test.