, 2011). Mastoparans present several biological activities such as degranulation of mast cells, release of histamine, activation of GTP-binding proteins, bactericidal potential and haemolytic activity (Čeřovský et al., 2008), besides being able to inhibit, in vitro, the transport of Golgi vesicles ( Weidman and Winter, 1994). Venoms of Neotropical vespids have polycationic peptides, such as polybines, which seem to be related with the occurrence of inflammation, including the initial process of the cell membrane lysis (Ribeiro et al., 2004). According to a study performed by Pembrolizumab de Paula et al. (2006),

the venom of P. paulista causes acute ERK inhibitor libraries inflammation, but according to Ferguson and Laing (2010), this event can lead to a series of adverse effects, including an increase in the rates of somatic mutation. Furthermore, during the inflammatory process there is the formation of reactive oxygen species (ROS), which are highly

reactive molecules and able to interact and cause damages in the genetic material of the cells ( Azad et al., 2008). At low concentrations, the venom of P. paulista is not able to induce, by itself, damages in the genetic material, but when a substance with genotoxic and mutagenic potential is administered together with the venom, the substances present in the venom (phospholipase, hyaluronidase and mastoparans) seem to help in the entrance of the aggressor agent, since they can disrupt the cell membrane and, consequently, allow the entrance of xenobiotics into the cell. Although several substances, such as Polybia-MPI present anti-tumour activity ( Wang et al., 2008 and Wang et al., 2009), caution is needed when administering substances derived from the venom of P. paulista in the treatment of cancer, since it was observed in this study that very low concentrations of the wasp venom do not present cytotoxic potential but can induce genotoxicity and mutagenicity. The authors would like to thank CAPES (Coordination for the Improvement of

Higher Education Personnel) and the Covenant-REPLAN: 1100.0067969.11.4 for the Meloxicam financial support. “
“Every year, 2.5 million people are bitten by snakes in South America with approximately 100,000 deaths as a result. Administration of specific antivenoms has been the most efficient treatment for snake envenoming. The effectiveness of anti-bothropic horse antivenom for the neutralization of the toxic and pharmacological effects of Bothrops jararacussu venom has been investigated by many groups ( dos Santos et al., 1992, de Roodt et al., 1998, de Roodt et al., 1999, Oshima-Franco et al., 2001, Zamunér et al., 2004 and Beghini et al., 2007), yet an understanding of the mechanism has not been elucidated.

Jim began his independent academic career

in 1970 as an Assistant Professor in the Department of Chemistry at the Rensselaer Polytechnic Institute. In 1974, he moved to the University of Michigan as an Associate Professor, and a few years later became a Full Professor in the Department of Biological Chemistry, School of Medicine, PLX4032 solubility dmso University of Michigan. Never one to be easily categorized, Jim left the University in 1985, to become the Director of the NIH Stable Isotope Resource at the Los Alamos National Laboratory, and a Section Leader in Biological Chemistry. Jim was a glider pilot, and the appeal of the wide-open air space and updrafts of the Southwest surely influenced his decision to move to New Mexico. He also maintained an appointment as an Adjunct Professor of Biochemistry at the University of New Mexico Medical School, 1989–1993. In 1993 Jim moved to the University of California, San Diego, as a Research Scientist, where he remained until 2001, at which point he moved to the Scripps Research Institute as a Professor of Research. The move to California allowed Jim to develop another passion, sailing. During the course of his career, Jim made fundamental contributions to our understanding of redox metalloproteins, and his scientific achievements are reflected

in more than 150 publications. Jim was well funded, attesting to the vitality of his research program and the high esteem of his peers. He also provided service to the science community by serving on NIH study sections and the editorial boards of journals. Jim gave many research talks at conferences and universities, selleck screening library both within the US and abroad and was Rucaparib datasheet a regular participant in the Metals in Biology Gordon Conference, serving as a Vice-Chair (1976–78) and Chair (1979–1980). Jim’s honors include the Harry J. Duell Award from the University of Southern California and a National Science Foundation Fellowship at the University of Göteborg, Sweden. He was a member of the American Association for the Advancement of Science, American Chemical Society, and American Society

for Biochemistry and Molecular Biology. Jim’s early work focused on biophysical studies of the newly discovered copper–zinc and then the manganese, and iron superoxide dismutases (SOD), key enzymes in defense against oxidative stress. His studies of enzymatic mechanisms and of structure–function relationships created the foundation for our current understanding of the biophysical and functional properties of these important enzymes. He also played an important role in the development of our understanding of biological oxidative stress, challenging investigators to discover the exact identities of toxic reactive oxygen species and the chemical nature of their toxic reactions. In the 1980s, Jim jumped into the study of large, membrane-bound metalloproteins, and more specifically, the respiratory proteins of thermophilic bacteria, in particular, Thermus thermophilus.