The Experts below are selected from a list of 1083 Experts worldwide ranked by ideXlab platform
Mônica Lopes-ferreira - One of the best experts on this subject based on the ideXlab platform.
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Multiple functional therapeutic effects of TnP: A small stable synthetic peptide derived from Fish Venom in a mouse model of multiple sclerosis.
PloS one, 2017Co-Authors: Evilin Naname Komegae, Tais Aparecida Matozo Souza, Lidiane Zito Grund, Carla Lima, Mônica Lopes-ferreiraAbstract:The pathological condition of multiple sclerosis (MS) relies on innate and adaptive immunity. New types of agents that beneficially modify the course of MS, stopping the progression and repairing the damage appear promising. Here, we studied TnP, a small stable synthetic peptide derived from Fish Venom in the control of inflammation and demyelination in experimental autoimmune encephalomyelitis as prophylactic treatment. TnP decreased the number of the perivascular infiltrates in spinal cord, and the activity of MMP-9 by F4/80+ macrophages were decreased after different regimen treatments. TnP reduces in the central nervous system the infiltration of IFN-γ-producing Th1 and IL-17A-producing Th17 cells. Also, treatment with therapeutic TnP promotes the emergence of functional Treg in the central nervous system entirely dependent on IL-10. Therapeutic TnP treatment accelerates the remyelination process in a cuprizone model of demyelination. These findings support the beneficial effects of TnP and provides a new therapeutic opportunity for the treatment of MS.
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First report of interruption of mast cell degranulation and endothelial cells activation by anti-inflammatory drugs controlling the acute response provoked by Pseudoplatystoma fasciatum Fish Venom
Toxicon : official journal of the International Society on Toxinology, 2014Co-Authors: Mônica Lopes-ferreira, Eduardo Martins Gomes, Fernanda Miriani Bruni, Marcio Jose Ferreira, Patricia Charvet, Carla LimaAbstract:This is the first report describing in mice the enVenoming that possible to occur in humans provoked by Pseudoplatystomafasciatum and evaluated the different class of mediators involved in the inflammatory injury, identifying important targets for drugs intervention. First we demonstrate that P. fasciatum Venom induces an acute inflammatory response characterized by the recruitment of immune cells into peripheral tissues choreographed by chemoattractants including lipid mediators (LTB4 and PGE2), cytokines (IL-1β and TNF-α), and chemokines (KC and MCP-1). Intravital microscopy studies showed that only high dose (60 μg) of Venom promoted hemodynamic changes inducing an abundant number of thrombi of varying sizes in venules leading to transient venular stasis with reduced blood flow. We found that serotonin, leukotrine and prostaglandin are involved in edematogenic and nociceptive responses, since a selective COX-2 inhibitor, a non-specific inhibitor for cytokines and COX-2, and a non-selective 5-HT receptor antagonist were able to reduce both symptoms. In conclusion, our data show that the main symptoms of acute inflammation as pain provoked by P. fasciatum Fish Venom could be well managed by available drugs as COX-2 inhibitors as well dexamethasone or non-selective 5-HT receptor antagonists.
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Thalassophryne nattereri Fish Venom: from the enVenoming to the understanding of the immune system
Journal of Venomous Animals and Toxins including Tropical Diseases, 2014Co-Authors: Mônica Lopes-ferreira, Lidiane Zito Grund, Carla LimaAbstract:Thalassophryne nattereri (niquim) is a Venomous Fish found off North and Northeast coast of Brazil, where it is known by the severity of the accidents involving humans. This review article is divided into four topics. The first one provides a brief description of the animal biology and its distribution off Brazilian coastal waters, the Venom apparatus, signs and symptoms observed in enVenomated humans and also describes enVenomation in mice. The second topic describes the use of modern genetic approach and mass spectrometry for identification of highly expressed genes in its Venom glands and the sequence of major toxins. The third chapter offers a detailed study of tissue injury induced by the Venom and reveals the role of toxins that impair inflammation reduction. Finally, the fourth section expands the understanding of many extrinsic and intrinsic essential factors in maintaining survival of memory B cell compartment. Our results demonstrate the wide possibilities for research in the area of toxinology, also the necessity of interconnection among biochemistry, pharmacology and immunology areas for the expansion of knowledge and for generation of innovation.
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Anti-inflammatory effect of Natterins, the major toxins from the Thalassophryne nattereri Fish Venom is dependent on TLR4/MyD88/PI3K signaling pathway
Toxicon, 2014Co-Authors: Marcio Jose Ferreira, Carla Lima, Mônica Lopes-ferreiraAbstract:Here we evaluated whether Natterins affect the leukocyte-endothelial cell interaction, hampering leukocyte mobilization and extravasation. Leukocyte-endothelial cell interactions were evaluated in venules of mouse cremaster muscle using intravital microscopy. We reported that low doses of Natterins interfere with the cell capturing, inhibiting the interaction of blood neutrophils with the post-capillary venules induced by the TLR4 agonist LPS, or the chemokine KC. Using endotoxemic mice challenged with LPS, we confirmed that Natterins reduce neutrophil accumulation in the peritoneum exudates. The rolling of leukocytes induced by KC or LPS was not impaired in Natterins-treated TLR2, MyD88 deficient or TLR4 mutant mice, indicating that TLR2- or TLR4-MyD88-mediated signals are required for the anti-inflammatory effect of Natterins. The inhibitory effect was not influenced by endogenous regulators of inflammation such as IL-10, corticosteroids, the HO-1 or the antagonist of the receptor of IL-1, nor by the disruption of their proteolytic activity. However, it was completely dependent on the activation of serine/threonine phosphatases and the PI3K signaling pathway, but independent on increased proteasome activity. This work started asking how the main toxins in the T nattereri Venom contributes for the deficient influx of inflammatory leukocytes, which consequently drive to the delayed inflammatory reaction finalization in injured tissue; and finished demonstrating that Natterins can control the leukocyte-endothelial wall interactions in a mechanism dependent on negative signals derived from TLR2-TLR4/Myd88 signaling cascade. Interestingly, we confirmed that the antagonist effect of Natterins is mediated by the activation of serine/threonine phosphatases and by the key signaling PI3K molecule.
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Local inflammatory response induced by scorpionFish Scorpaena plumieri Venom in mice.
Toxicon : official journal of the International Society on Toxinology, 2012Co-Authors: Thiago N. Menezes, Helena L. Gomes, Mônica Lopes-ferreira, Filipe Andrich, Juliana B.t. Carnielli, Fausto Edmundo Lima Pereira, Elenice Moreira Lemos, Nazaré Souza Bissoli, Suely G. FigueiredoAbstract:The Scorpaena plumieri Fish Venom induces a severe pain and edema, observed both clinically and experimentally. In order to understand more about the enVenomation syndrome, the present study characterized experimentally the local acute inflammatory response induced by S. plumieri Venom (SpV) in a mouse model of tissue injury. Our results demonstrated that the local inflammatory response provoked after 2 h of SpV injection in footpad of mice is characterized by release of pivotal pro-inflammatory mediators (TNF, IL-6 and MCP-1). These mediators could be associated with histopathological changes observed into paw tissue, characterized by cellular infiltration, mainly neutrophils. Additionally, an investigation of edema formation pathways involved in inflammatory response was performed. SpV-induced edema was reduced significantly by previous administration of aprotinin or icatibant (HOE-140). However, the pre-treatment with diclofenac sodium and promethazine had less effect on this response. These results demonstrate that the kallikrein-kinin system (KKS) plays a major role in the edema formation. Despite the whole Venom hydrolyzed the kallikrein synthetic substrate S-2302 (Pro-Phe-Arg-pNA), its main pro-inflammatory fraction was devoid of kininogenase activity. Our results demonstrate that SpV evokes a complex inflammatory reaction stimulating a secretion of TNF, IL-6, MCP-1 and leukocytes recruitment at the site of Venom injection. In addition provide clear evidence of the involvement of the KKS in inflammatory response induced by S. plumieri Venom.
Venugopal P. Menon - One of the best experts on this subject based on the ideXlab platform.
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Fish Venom pterios volitans peptide reduces tumor burden and ameliorates oxidative stress in ehrlich s ascites carcinoma xenografted mice
Bioorganic & Medicinal Chemistry Letters, 2006Co-Authors: Sri M Balasubashini, S. Karthigayan, S. T. Somasundaram, T. Balasubramanian, V. Viswanathan, P. Raveendran, Venugopal P. MenonAbstract:The present study was carried out to assess the effect of Pterios volitans Venom (mixture of peptides) on Ehrlich’s ascites carcinoma (EAC) and its influence on antioxidant status in the liver. Among six groups of albino mice, three were treated with sublethal doses of Venom, along with the standard drug, 5-fluorouracil. In EAC-bearing mice, mean life span and antioxidants were significantly decreased, whereas, body weight, tumor volume, viable tumor cell count, lipid peroxidation and expression of proliferating cell nuclear antigen were significantly increased. These changes were brought back to near normal in treatment groups. The findings are further confirmed by histopathological observations.
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FV peptide induces apoptosis in HEp 2 and HeLa cells: An insight into the mechanism of induction
Journal of carcinogenesis, 2006Co-Authors: M. Sri Balasubashini, S. Karthigayan, S. T. Somasundaram, T. Balasubramanian, R. Rukkumani, Venugopal P. MenonAbstract:The present study is an attempt to evaluate the antiproliferative potential of peptide (7.6 kDa) from lionFish (Pterios volitans) Venom on cultured HEp2 and HeLa cells. Different dose of purified peptide (1, 2 and 4 μg/ml) at different time points (12, 24 and 36 hrs) were tested for antiproliferative index of the peptide. Among them, 2 μg/ml at 24 hrs was found to effectively inhibit cancer cell growth in vitro and did not cause any adverse effect on normal human lymphocytes. Apoptosis was examined by propidium iodide staining, confirmed by the expression of caspase-8 and caspase-3, down regulation of Bcl-2 expression and DNA fragmentation in treated cells, when compared to untreated HEp2 and HeLa cells. Thus Fish Venom peptide was found to selectively induce apoptosis in cancer cell.
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Fish Venom (Pterios volitans) peptide reduces tumor burden and ameliorates oxidative stress in Ehrlich’s ascites carcinoma xenografted mice
Bioorganic & medicinal chemistry letters, 2006Co-Authors: M. Sri Balasubashini, S. Karthigayan, S. T. Somasundaram, T. Balasubramanian, V. Viswanathan, P. Raveendran, Venugopal P. MenonAbstract:The present study was carried out to assess the effect of Pterios volitans Venom (mixture of peptides) on Ehrlich’s ascites carcinoma (EAC) and its influence on antioxidant status in the liver. Among six groups of albino mice, three were treated with sublethal doses of Venom, along with the standard drug, 5-fluorouracil. In EAC-bearing mice, mean life span and antioxidants were significantly decreased, whereas, body weight, tumor volume, viable tumor cell count, lipid peroxidation and expression of proliferating cell nuclear antigen were significantly increased. These changes were brought back to near normal in treatment groups. The findings are further confirmed by histopathological observations.
Carla Lima - One of the best experts on this subject based on the ideXlab platform.
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Multiple functional therapeutic effects of TnP: A small stable synthetic peptide derived from Fish Venom in a mouse model of multiple sclerosis.
PloS one, 2017Co-Authors: Evilin Naname Komegae, Tais Aparecida Matozo Souza, Lidiane Zito Grund, Carla Lima, Mônica Lopes-ferreiraAbstract:The pathological condition of multiple sclerosis (MS) relies on innate and adaptive immunity. New types of agents that beneficially modify the course of MS, stopping the progression and repairing the damage appear promising. Here, we studied TnP, a small stable synthetic peptide derived from Fish Venom in the control of inflammation and demyelination in experimental autoimmune encephalomyelitis as prophylactic treatment. TnP decreased the number of the perivascular infiltrates in spinal cord, and the activity of MMP-9 by F4/80+ macrophages were decreased after different regimen treatments. TnP reduces in the central nervous system the infiltration of IFN-γ-producing Th1 and IL-17A-producing Th17 cells. Also, treatment with therapeutic TnP promotes the emergence of functional Treg in the central nervous system entirely dependent on IL-10. Therapeutic TnP treatment accelerates the remyelination process in a cuprizone model of demyelination. These findings support the beneficial effects of TnP and provides a new therapeutic opportunity for the treatment of MS.
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anti inflammatory effect of natterins the major toxins from the thalassophryne nattereri Fish Venom is dependent on tlr4 myd88 pi3k signaling pathway
Toxicon, 2014Co-Authors: Marcio Jose Ferreira, Carla Lima, Monica LopesferreiraAbstract:Here we evaluated whether Natterins affect the leukocyte-endothelial cell interaction, hampering leukocyte mobilization and extravasation. Leukocyte-endothelial cell interactions were evaluated in venules of mouse cremaster muscle using intravital microscopy. We reported that low doses of Natterins interfere with the cell capturing, inhibiting the interaction of blood neutrophils with the post-capillary venules induced by the TLR4 agonist LPS, or the chemokine KC. Using endotoxemic mice challenged with LPS, we confirmed that Natterins reduce neutrophil accumulation in the peritoneum exudates. The rolling of leukocytes induced by KC or LPS was not impaired in Natterins-treated TLR2, MyD88 deficient or TLR4 mutant mice, indicating that TLR2- or TLR4-MyD88-mediated signals are required for the anti-inflammatory effect of Natterins. The inhibitory effect was not influenced by endogenous regulators of inflammation such as IL-10, corticosteroids, the HO-1 or the antagonist of the receptor of IL-1, nor by the disruption of their proteolytic activity. However, it was completely dependent on the activation of serine/threonine phosphatases and the PI3K signaling pathway, but independent on increased proteasome activity. This work started asking how the main toxins in the T nattereri Venom contributes for the deficient influx of inflammatory leukocytes, which consequently drive to the delayed inflammatory reaction finalization in injured tissue; and finished demonstrating that Natterins can control the leukocyte-endothelial wall interactions in a mechanism dependent on negative signals derived from TLR2-TLR4/Myd88 signaling cascade. Interestingly, we confirmed that the antagonist effect of Natterins is mediated by the activation of serine/threonine phosphatases and by the key signaling PI3K molecule.
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First report of interruption of mast cell degranulation and endothelial cells activation by anti-inflammatory drugs controlling the acute response provoked by Pseudoplatystoma fasciatum Fish Venom
Toxicon : official journal of the International Society on Toxinology, 2014Co-Authors: Mônica Lopes-ferreira, Eduardo Martins Gomes, Fernanda Miriani Bruni, Marcio Jose Ferreira, Patricia Charvet, Carla LimaAbstract:This is the first report describing in mice the enVenoming that possible to occur in humans provoked by Pseudoplatystomafasciatum and evaluated the different class of mediators involved in the inflammatory injury, identifying important targets for drugs intervention. First we demonstrate that P. fasciatum Venom induces an acute inflammatory response characterized by the recruitment of immune cells into peripheral tissues choreographed by chemoattractants including lipid mediators (LTB4 and PGE2), cytokines (IL-1β and TNF-α), and chemokines (KC and MCP-1). Intravital microscopy studies showed that only high dose (60 μg) of Venom promoted hemodynamic changes inducing an abundant number of thrombi of varying sizes in venules leading to transient venular stasis with reduced blood flow. We found that serotonin, leukotrine and prostaglandin are involved in edematogenic and nociceptive responses, since a selective COX-2 inhibitor, a non-specific inhibitor for cytokines and COX-2, and a non-selective 5-HT receptor antagonist were able to reduce both symptoms. In conclusion, our data show that the main symptoms of acute inflammation as pain provoked by P. fasciatum Fish Venom could be well managed by available drugs as COX-2 inhibitors as well dexamethasone or non-selective 5-HT receptor antagonists.
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Thalassophryne nattereri Fish Venom: from the enVenoming to the understanding of the immune system
Journal of Venomous Animals and Toxins including Tropical Diseases, 2014Co-Authors: Mônica Lopes-ferreira, Lidiane Zito Grund, Carla LimaAbstract:Thalassophryne nattereri (niquim) is a Venomous Fish found off North and Northeast coast of Brazil, where it is known by the severity of the accidents involving humans. This review article is divided into four topics. The first one provides a brief description of the animal biology and its distribution off Brazilian coastal waters, the Venom apparatus, signs and symptoms observed in enVenomated humans and also describes enVenomation in mice. The second topic describes the use of modern genetic approach and mass spectrometry for identification of highly expressed genes in its Venom glands and the sequence of major toxins. The third chapter offers a detailed study of tissue injury induced by the Venom and reveals the role of toxins that impair inflammation reduction. Finally, the fourth section expands the understanding of many extrinsic and intrinsic essential factors in maintaining survival of memory B cell compartment. Our results demonstrate the wide possibilities for research in the area of toxinology, also the necessity of interconnection among biochemistry, pharmacology and immunology areas for the expansion of knowledge and for generation of innovation.
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Anti-inflammatory effect of Natterins, the major toxins from the Thalassophryne nattereri Fish Venom is dependent on TLR4/MyD88/PI3K signaling pathway
Toxicon, 2014Co-Authors: Marcio Jose Ferreira, Carla Lima, Mônica Lopes-ferreiraAbstract:Here we evaluated whether Natterins affect the leukocyte-endothelial cell interaction, hampering leukocyte mobilization and extravasation. Leukocyte-endothelial cell interactions were evaluated in venules of mouse cremaster muscle using intravital microscopy. We reported that low doses of Natterins interfere with the cell capturing, inhibiting the interaction of blood neutrophils with the post-capillary venules induced by the TLR4 agonist LPS, or the chemokine KC. Using endotoxemic mice challenged with LPS, we confirmed that Natterins reduce neutrophil accumulation in the peritoneum exudates. The rolling of leukocytes induced by KC or LPS was not impaired in Natterins-treated TLR2, MyD88 deficient or TLR4 mutant mice, indicating that TLR2- or TLR4-MyD88-mediated signals are required for the anti-inflammatory effect of Natterins. The inhibitory effect was not influenced by endogenous regulators of inflammation such as IL-10, corticosteroids, the HO-1 or the antagonist of the receptor of IL-1, nor by the disruption of their proteolytic activity. However, it was completely dependent on the activation of serine/threonine phosphatases and the PI3K signaling pathway, but independent on increased proteasome activity. This work started asking how the main toxins in the T nattereri Venom contributes for the deficient influx of inflammatory leukocytes, which consequently drive to the delayed inflammatory reaction finalization in injured tissue; and finished demonstrating that Natterins can control the leukocyte-endothelial wall interactions in a mechanism dependent on negative signals derived from TLR2-TLR4/Myd88 signaling cascade. Interestingly, we confirmed that the antagonist effect of Natterins is mediated by the activation of serine/threonine phosphatases and by the key signaling PI3K molecule.
Monica Lopesferreira - One of the best experts on this subject based on the ideXlab platform.
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anti inflammatory effect of natterins the major toxins from the thalassophryne nattereri Fish Venom is dependent on tlr4 myd88 pi3k signaling pathway
Toxicon, 2014Co-Authors: Marcio Jose Ferreira, Carla Lima, Monica LopesferreiraAbstract:Here we evaluated whether Natterins affect the leukocyte-endothelial cell interaction, hampering leukocyte mobilization and extravasation. Leukocyte-endothelial cell interactions were evaluated in venules of mouse cremaster muscle using intravital microscopy. We reported that low doses of Natterins interfere with the cell capturing, inhibiting the interaction of blood neutrophils with the post-capillary venules induced by the TLR4 agonist LPS, or the chemokine KC. Using endotoxemic mice challenged with LPS, we confirmed that Natterins reduce neutrophil accumulation in the peritoneum exudates. The rolling of leukocytes induced by KC or LPS was not impaired in Natterins-treated TLR2, MyD88 deficient or TLR4 mutant mice, indicating that TLR2- or TLR4-MyD88-mediated signals are required for the anti-inflammatory effect of Natterins. The inhibitory effect was not influenced by endogenous regulators of inflammation such as IL-10, corticosteroids, the HO-1 or the antagonist of the receptor of IL-1, nor by the disruption of their proteolytic activity. However, it was completely dependent on the activation of serine/threonine phosphatases and the PI3K signaling pathway, but independent on increased proteasome activity. This work started asking how the main toxins in the T nattereri Venom contributes for the deficient influx of inflammatory leukocytes, which consequently drive to the delayed inflammatory reaction finalization in injured tissue; and finished demonstrating that Natterins can control the leukocyte-endothelial wall interactions in a mechanism dependent on negative signals derived from TLR2-TLR4/Myd88 signaling cascade. Interestingly, we confirmed that the antagonist effect of Natterins is mediated by the activation of serine/threonine phosphatases and by the key signaling PI3K molecule.
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thalassophryne nattereri Fish Venom biological and biochemical characterization and serum neutralization of its toxic activities
Toxicon, 1998Co-Authors: Monica Lopesferreira, Katia C Barbaro, D F Cardoso, Ana M Mouradasilva, I. MotaAbstract:Abstract EnVenomation by Thalassophryne nattereri Fishes are an important medical problem in northeast of Brazil, causing in human victims considerable pain and edema followed by necrosis. Venom obtained from fresh captured specimens of this Fish was tested in vitro or in animal models for a better characterization of its toxic activities. Intradermal injection of the Venom in the foot pad of mice induced local edema and hemorrhage followed a few hours later by necrosis. Subcutaneous injection of the Venom induced systemic effects consisting in jerking motions, paralysis of hind limbs, erection of hair, rotational movements and violent convulsions followed by death. Dead animals showed hyperemia of the small intestine and lungs. The Venom showed distinct edematous, necrotizing and hemolytic activities, a low level of hemorrhagic, myotoxic and proteolytic activities and no detectable phospholipase A 2 activity. SDS-PAGE analysis of the crude Venom showed at least 17 components with the major band located around M w =19,000. Almost all proteins stained by amido black were also revealed by Western blotting with antibodies to T. nattereri Venom. Fractionation of the Venom by either gel filtration or cation exchange chromatography resulted in a few distinct peaks but in both situations the biological activities were located in only one of the peaks which corresponded to basic proteins with approximately M w =47,000. Heating of the Venom at 56°C for 60 min completely destroyed its biological activities. All Venom toxic activities except edema were completely neutralized after in vitro incubation with anti- T. nattereri serum.
S. Karthigayan - One of the best experts on this subject based on the ideXlab platform.
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Fish Venom pterios volitans peptide reduces tumor burden and ameliorates oxidative stress in ehrlich s ascites carcinoma xenografted mice
Bioorganic & Medicinal Chemistry Letters, 2006Co-Authors: Sri M Balasubashini, S. Karthigayan, S. T. Somasundaram, T. Balasubramanian, V. Viswanathan, P. Raveendran, Venugopal P. MenonAbstract:The present study was carried out to assess the effect of Pterios volitans Venom (mixture of peptides) on Ehrlich’s ascites carcinoma (EAC) and its influence on antioxidant status in the liver. Among six groups of albino mice, three were treated with sublethal doses of Venom, along with the standard drug, 5-fluorouracil. In EAC-bearing mice, mean life span and antioxidants were significantly decreased, whereas, body weight, tumor volume, viable tumor cell count, lipid peroxidation and expression of proliferating cell nuclear antigen were significantly increased. These changes were brought back to near normal in treatment groups. The findings are further confirmed by histopathological observations.
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FV peptide induces apoptosis in HEp 2 and HeLa cells: An insight into the mechanism of induction
Journal of carcinogenesis, 2006Co-Authors: M. Sri Balasubashini, S. Karthigayan, S. T. Somasundaram, T. Balasubramanian, R. Rukkumani, Venugopal P. MenonAbstract:The present study is an attempt to evaluate the antiproliferative potential of peptide (7.6 kDa) from lionFish (Pterios volitans) Venom on cultured HEp2 and HeLa cells. Different dose of purified peptide (1, 2 and 4 μg/ml) at different time points (12, 24 and 36 hrs) were tested for antiproliferative index of the peptide. Among them, 2 μg/ml at 24 hrs was found to effectively inhibit cancer cell growth in vitro and did not cause any adverse effect on normal human lymphocytes. Apoptosis was examined by propidium iodide staining, confirmed by the expression of caspase-8 and caspase-3, down regulation of Bcl-2 expression and DNA fragmentation in treated cells, when compared to untreated HEp2 and HeLa cells. Thus Fish Venom peptide was found to selectively induce apoptosis in cancer cell.
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Fish Venom (Pterios volitans) peptide reduces tumor burden and ameliorates oxidative stress in Ehrlich’s ascites carcinoma xenografted mice
Bioorganic & medicinal chemistry letters, 2006Co-Authors: M. Sri Balasubashini, S. Karthigayan, S. T. Somasundaram, T. Balasubramanian, V. Viswanathan, P. Raveendran, Venugopal P. MenonAbstract:The present study was carried out to assess the effect of Pterios volitans Venom (mixture of peptides) on Ehrlich’s ascites carcinoma (EAC) and its influence on antioxidant status in the liver. Among six groups of albino mice, three were treated with sublethal doses of Venom, along with the standard drug, 5-fluorouracil. In EAC-bearing mice, mean life span and antioxidants were significantly decreased, whereas, body weight, tumor volume, viable tumor cell count, lipid peroxidation and expression of proliferating cell nuclear antigen were significantly increased. These changes were brought back to near normal in treatment groups. The findings are further confirmed by histopathological observations.