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      Effect of Bothrops alternatus snake venom on macrophage phagocytosis and superoxide production: participation of protein kinase C

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          Abstract

          Envenomations caused by different species of Bothrops snakes result in severe local tissue damage, hemorrhage, pain, myonecrosis, and inflammation with a significant leukocyte accumulation at the bite site. However, the activation state of leukocytes is still unclear. According to clinical cases and experimental work, the local effects observed in envenenomation by Bothrops alternatus are mainly the appearance of edema, hemorrhage, and necrosis. In this study we investigated the ability of Bothrops alternatus crude venom to induce macrophage activation. At 6 to 100 ¼g/mL, BaV is not toxic to thioglycollate-elicited macrophages; at 3 and 6 ¼g/mL, it did not interfere in macrophage adhesion or detachment. Moreover, at concentrations of 1.5, 3, and 6 ¼g/mL the venom induced an increase in phagocytosis via complement receptor one hour after incubation. Pharmacological treatment of thioglycollate-elicited macrophages with staurosporine, a protein kinase (PKC) inhibitor, abolished phagocytosis, suggesting that PKC may be involved in the increase of serum-opsonized zymosan phagocytosis induced by BaV. Moreover, BaV also induced the production of anion superoxide (O2_) by thioglycollate-elicited macrophages. This BaV stimulated superoxide production was abolished after treating the cells with staurosporine, indicating that PKC is an important signaling pathway for the production of this radical. Based on these results, we suggest that phagocytosis and reactive oxygen species are involved in the pathogenesis of local tissue damage characteristic of Bothrops spp. envenomations.

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          Most cited references84

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          NADPH oxidase: an update.

          B Babior (1999)
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            Protein kinase C and lipid signaling for sustained cellular responses.

            Since the second messenger role was proposed for the products of inositol phospholipid hydrolysis, considerable progress has been made in our understanding of the biochemical mechanism of the intracellular signaling network. It is now becoming evident that stimulation of a cell surface receptor initiates a degradation cascade of various membrane lipid constituents. Many of their metabolites have potential to induce, intensify, and prolong the activation of protein kinase C that is needed for sustained cellular responses.
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              Protein kinase C: structural and spatial regulation by phosphorylation, cofactors, and macromolecular interactions.

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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                jvatitd
                Journal of Venomous Animals and Toxins including Tropical Diseases
                J. Venom. Anim. Toxins incl. Trop. Dis
                Centro de Estudos de Venenos e Animais Peçonhentos - CEVAP, Universidade Estadual Paulista - UNESP (Botucatu )
                1678-9199
                2011
                : 17
                : 4
                : 430-441
                Affiliations
                [1 ] Fundação Oswaldo Cruz Brazil
                [2 ] Universidade Federal de Rondônia Brazil
                Article
                S1678-91992011000400010
                10.1590/S1678-91992011000400010
                e9930f67-0777-46df-b988-3e028adbb460

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=1678-9199&lng=en
                Categories
                TOXICOLOGY
                TROPICAL MEDICINE

                Toxicology,Infectious disease & Microbiology
                snake venom,Bothrops,macrophages,phagocytosis,superoxide,protein kinase C,inflammation

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