Vipera Lebetina Research Articles

The snake fauna of Khabr National Park, southeast of Iran

Khabr National Park and Ruchun Wildlife Refuge are situated in the southeast of Iran, Kerman Province. Although snakes are an important group in the studied area, little is known regarding their diversity. The present study was carried out from March 2009 to late summer 2010. In this study, 74 specimens were collected (or observed) and identified, belonging to four families, 14 genera, and 17 species, including Typhlopidae: Typhlops vermicularis; Colubridae: Boiga trigonatum melanocephala, Hemorrhois ravergieri, Lytorhynchus diadema gaddi, Lytorhynchus ridgewayi, Platyceps rhodorachis ladacensis, Platyceps ventromaculatus ventromaculatus, Psammophis schokari, Pseudocyclophis persicus, Spalerosophis diadema cliffordii, Spalerosophis microlepis, Telescopus rhinopoma, Eirenis punctatolineatus; Viperidae: Echis carinatus sochureki, Macrovipera lebetina cernovi, Pseudocerastes persicus; Elapidae: Walterinnesia morgani. The records of Spalerosophis microlepis, Lytorhynchus diadema gaddi, Pseudocyclophis persicus and Walterinnesia morgani are reported for the first time from southeast of Iran.

Interactions of PLA2-s from Vipera lebetina, Vipera berus berus and Naja naja oxiana Venom with Platelets, Bacterial and Cancer Cells

Secretory phospholipasesA2 (sPLA2s) form a large family of structurally related enzymes widespread in nature. Herein, we studied the inhibitory effects of sPLA2s from Vipera lebetina (VLPLA2), Vipera berus berus (VBBPLA2), and Naja naja oxiana (NNOPLA2) venoms on (i) human platelets, (ii) four different bacterial strains (gram-negative Escherichia coli and Vibrio fischeri; gram-positive Staphylococcus aureus and Bacillus subtilis) and (iii) five types of cancer cells (PC-3, LNCaP, MCF-7, K-562 and B16-F10) in vitro. sPLA2s inhibited collagen-induced platelet aggregation: VBBPLA2 IC50 = 0.054, VLPLA2 IC50 = 0.072, NNOPLA2 IC50 = 0.814 μM. p-Bromophenacylbromide-inhibited sPLA2 had no inhibitory action on platelets. 36.17 μM VBBPLA2 completely inhibited the growth of gram-positive Bacillus subtilis whereas no growth inhibition was observed towards gram-negative Escherichia coli. The inhibitory action of sPLA2s (~0.7 μM and ~7 μM) towards cancer cells depended on both venom and cell type. VBBPLA2 (7.2 μM) inhibited significantly the viability of K-562 cells and the cell death appeared apoptotic. The sPLA2s exhibited no inhibitory effect towards LNCaP cells and some effect (8%–20%) towards other cells. Thus, already sub-μM concentrations of sPLA2s inhibited collagen-induced platelet aggregation and from the current suite of studied svPLA2s and test cells, VBBPLA2 was the most growth inhibitory towards Bacillus subtilis and K-562 cells.

Microscopic study on characterization of peripheral blood cells of Levantine viper (Macrovipera lebetina obtusa) from southwestern Iran

The present study was carried out on the microscopic characterization of peripheral blood cells (erythrocytes, leucocytes, and thrombocytes) of Levantine viper (Macrovipera lebetina obtusa) from southwestern Iran. Ten snakes were used in this study. Two blood smears for each snake were prepared immediately by syringes, air-dried, and then stained with Wright and Giemsa method. Slides were examined by light microscope. The erythrocytes of the Levantine viper were homogenous in size, shape, and color. They were typically ellipsoid or round cells, with an ellipsoid to irregularly round nuclei that contained dense chromatins. In addition, overall, five types of the leucocytes including heterophils, eosinophils, basophils, lymphocytes, and monocytes were observed in the peripheral blood smears. Our findings provide important baseline information on the reference description and morphologic classification of blood cells in the Levantine viper species and are useful for the scientists involved in snake conservation around the world.

Behavior of Proteolipid GUVs formed in Macrovipera Lebetina Obtusa Venom Solution

Introduction: Macrovipera lebetina obtusa belongs to sister clade of the Middle East complex within the monophyletic Eurasian Vipera genus. This snake is responsible for a number of bites in western Asia every year, and should be considered as dangerous. Proteolipids are a type of lipoproteins in which lipid material forms more than half of the molecule solubilized in organic solvents (chloroform/methanol/water mixtures) and have the solubility characteristics of lipids. GUVs are ideal for studying protein/lipid and lipid/lipid interactions due to their size (similar to that of cells) and to their ease of observation by optical microscopy.Method: Proteolipid fraction was separated from the bovine brain by the Folch method. Proteolipid GUVs (mean diameter 30 μm) are formed with the electroformation method as developed by Angelova and Dimitrov. GUVs have a minimum curvature and mimic cell membranes in this respect. We formed proteolipid GUVs in the solution of Macrovipera lebetina obtusa (MLO) venom (final concentration 3∗10−5M). Images were collected on an epi-fluorescent microscope FM320-5M (AmScope, USA). The GUVs were visualized with ANS fluorescent probe.Results: While GUVs filled with proteins are more stable and there are little increases in size, the GUVs filled with fewer proteins are deformed, not stable. They diminish during 25 seconds, and eventually pull in and dissolve (instead of the usual vesicles formed from phospholipids). The same effect is seen, when MLO was added after GUVs formation.

PIVL, a new serine protease inhibitor from Macrovipera lebetina transmediterranea venom, impairs motility of human glioblastoma cells

A novel Kunitz-type serine proteinase inhibitor, termed PIVL, was purified to homogeneity from the venom of the Tunisian snake Macrovipera lebetina transmediterranea. It is a monomeric polypeptide chain cross-linked by three disulfide linkages with an isotope-averaged molecular mass of 7691.7Da. The 67-residue full-length PIVL sequence was deduced from a venom gland cDNA clone. Structurally, PIVL is built by a single Kunitz/BPTI-like domain. Functionally, it is able to specifically inhibit trypsin activity. Interestingly, PIVL exhibits an anti-tumor effect and displays integrin inhibitory activity without being cytotoxic. Here we show that PIVL is able to dose-dependently inhibit the adhesion, migration and invasion of human glioblastoma U87 cells. Our results also show that PIVL impairs the function of αvβ3 and to a lesser extent, the activity of αvβ6, αvβ5, α1β1 and α5β1 integrins. Interestingly, we demonstrate that the 41RGN43 motif of PIVL is likely responsible for its anti-cancer effect. By using time lapse videomicroscopy, we found that PIVL significantly reduced U87 cells motility and affected cell directionality persistence by 68%. These findings reveal novel pharmacological effects for a Kunitz-type serine proteinase inhibitor.

Pharmaco-Modulations of Induced Edema and Vascular Permeability Changes by Vipera lebetina Venom: Inflammatory Mechanisms

The inflammatory response induced by Vipera lebetina venom (VLV) in the mice hind paw was evaluated by paw edema value and vascular permeability changes. The edema was produced in a dose- and time-dependent manner. This response was maximal within 2h and disappeared after 24h The minimum edema-forming dose was estimated at 0.8μg/20g body weight. Microscopic examination confirmed that VLV also induces skin structure alterations with collagen fiber dissociation and polynuclear infiltration, which is characteristic of edema formation. The induced edema with VLV (1μg/paw) could be due to the release of pharmacological active substances at the site of injection. Histamine, serotonine, and arachidonate metabolites may play important roles in the vasoactive and edematic effect of VLV since pretreatment of mice with cromoglycate, cyproheptadine, ibuprofen, loratidine, and indomethacin significantly reduced the edema formation (77, 63, 57, 45, and 43%, respectively). The obtained results demonstrate that the induced edema and vasodilatation by this venom may be triggered and maintained by different pharmacological mechanisms, since cromoglycate and cyproheptadine were the most active inhibitors of the edema. The relationships between histamine and serotonin release from mast cells and arachidonate metabolites activation could be the main step in edema-forming and the induced vasodilatation by the venom.

Expression of a functional recombinant C-type lectin-like protein lebecetin in the human embryonic kidney cells

Lebecetin is an anticoagulant C-type lectin-like protein that was previously isolated from Macrovipera lebetina venom and described to consist of two subunits (alpha and beta). It was reported to potently prevent platelet aggregation by binding to glycoprotein Ib and to exhibit a broad spectrum of inhibitory activities on various integrin-mediated functions of tumor cells, including adhesion, proliferation, and cell migration. This study aimed to investigate the structure-function of lebecetin. Accordingly, the cDNA of each subunit was cloned and separately or jointly expressed in the human embryonic kidney cells using two vectors with different selectable tags. The immunofluorescence analysis of transfected cells revealed significant expression levels and co-localization of the two lebecetin subunits. The recombinant proteins were efficiently secreted and purified using metal-chelating affinity chromatography. We found that the Lebecetin alpha and beta subunits were produced as a mixture of homodimers and heterodimers and that the heterodimerization represents a prerequisite for functioning.

Snake venom toxin from Vipera lebetina turanica sensitizes cancer cells to TRAIL through ROS- and JNK-mediated upregulation of death receptors and downregulation of survival proteins

We investigated whether snake venom toxin (SVT) from Vipera lebetina turanica enhances the apoptosis ability of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in cancer cells. TRAIL inhibited HCT116 cell growth in a dose-dependent manner; however, this reduction did not occur in TRAIL resistant HT-29, A549 and HepG2 cells with an even higher dose of TRAIL. SVT, but not TRAIL enhanced expression of cell death receptor (DR) in TRAIL resistant cancer cells in a dose-dependent manner. A combination of SVT with TRAIL significantly inhibited cell growth of TRAIL resistant HT-29, A549 and HepG2 cells. Consistent with cell growth inhibition, the expression of TRAIL receptors; DR4 and DR5 was significantly increased as well as apoptosis related proteins such as cleaved caspase-3, -8, -9 and Bax. However, the expression of survival proteins (e.g., cFLIP, survivin, XIAP and Bcl2) was suppressed by the combination treatment of SVT and TRAIL. Depletion of DR4 or DR5 by small interfering RNA significantly reversed the cell growth inhibitory and apoptosis blocking effects of SVT in HCT116 and HT-29 cells. Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects. The collective results suggest that SVT facilitates TRAIL-induced apoptosis in cancer cells through up-regulation of the TRAIL receptors; DR4 and DR5 via ROS/JNK pathway signals.

Snake venom toxin from Vipera lebetina turanica induces apoptosis of colon cancer cells via upregulation of ROS- and JNK-mediated death receptor expression.

BackgroundAbundant research suggested that the cancer cells avoid destruction by the immune system through down-regulation or mutation of death receptors. Therefore, it is very important that finding the agents that increase the death receptors of cancer cells. In this study, we demonstrated that the snake venom toxin from Vipera lebetina turanica induce the apoptosis of colon cancer cells through reactive oxygen species (ROS) and c-Jun N-terminal kinases (JNK) dependent death receptor (DR4 and DR5) expression.MethodsWe used cell viability assays, DAPI/TUNEL assays, as well as western blot for detection of apoptosis related proteins and DRs to demonstrate that snake venom toxin-induced apoptosis is DR4 and DR5 dependent. We carried out transient siRNA knockdowns of DR4 and DR5 in colon cancer cells.ResultsWe showed that snake venom toxin inhibited growth of colon cancer cells through induction of apoptosis. We also showed that the expression of DR4 and DR5 was increased by treatment of snake venom toxin. Moreover, knockdown of DR4 or DR5 reversed the effect of snake venom toxin. Snake venom toxin also induced JNK phosphorylation and ROS generation, however, pretreatment of JNK inhibitor and ROS scavenger reversed the inhibitory effect of snake venom toxin on cancer cell proliferation, and reduced the snake venom toxin-induced upregulation of DR4 and DR5 expression.ConclusionsOur results indicated that snake venom toxin could inhibit human colon cancer cell growth, and these effects may be related to ROS and JNK mediated activation of death receptor (DR4 and DR5) signals.

Lipid bilayer condition abnormalities following Macrovipera lebetina obtusa snake envenomation

Viper bites is an endemic public health problem in Armenia, even in the cities. Human envenomation is often characterized by clotting disorders, hypofibrinogenemia, and local tissue necrosis. In this original study, we assess some changes of cell membranes plastic properties (namely, its microviscosity, thickness, permeability) in a rat envenomation model using the biophysical approaches. We describe the interaction of Macrovipera lebetina obtusa (MLO) venom with giant unilamellar vesicles (GUVs) composed of the native phospholipid mixtures visualized through fluorescent microscopy. GUVs with a mean diameter of 30 μm have a minimum curvature and mimic cell membranes in this respect.The membrane fluorescence probe, ANS and pyrene, were used to assess the state of membrane and specifically mark the phospholipid domains. Independent of their lipid composition, GUVs were enlarged in size as venom-dependent lipid hydrolysis proceeded. Except of the visible morphological changes, ANS and pyrene also allows us to quantify the fluidity changes in the membrane by measuring of the fluorescence intensity. The presence of viper venom in GUVs media reveals a noticeable decreasing of membrane fluidity compare the control, while the binding of fluorophores with GUVs modified by venom lead to appearance of channel activity. These studies also emphasize the importance of a membrane surface curvature for its interaction with enzymatic components of venom.

Cell growth inhibition and induction of apoptosis by snake venom toxin in ovarian cancer cell via inactivation of nuclear factor κB and signal transducer and activator of transcription 3

Snake venom toxin from Vipera lebetina turanica induces apoptosis in many cancer cell lines, but there is no study about the apoptotic effect of snake venom toxin on human ovarian cancer cells. In this study, we investigated the apoptotic effect of snake venom toxin in human ovarian cancer PA-1 and SK-OV3 cells. Snake venom toxin dose dependently (0∼10 μg/mL) inhibited ovarian cancer cell growth with IC(50) values 4.5 μg/mL in PA-1 cells, and 6.5 μg/mL in SK-OV3 cells. Our results also showed that apoptotic cell death increased by snake venom toxin in a dose dependent manner (0∼10 μg/mL). Consistent with increased cell death, snake venom toxin increased the expression of pro-apoptotic protein Bax and caspase-3, but down-regulated anti-apoptotic protein Bcl-2. Untreated ovarian cancer cells showed a high DNA binding activity of nuclear factor B (NF-κB), but it was inhibited by snake venom toxin accompanied by inhibition of p50 and p65 translocation into the nucleus as well as phosphorylation of inhibitory κB. Snake venom toxin also inhibited DNA binding activity of the signal transducer and activator of transcription 3 (STAT3). Moreover, the combination treatment of NF-κB (salicylic acid, 1 or 5 μM) and STAT3 (stattic, 1 μM) with snake venom toxin (1 μg/mL) further enhanced cell growth inhibitory effects of snake venom toxin. These results showed that snake venom toxin from Vipera lebetina turanica caused apoptotic cell death of ovarian cancer cells through the inhibition of NF-κB and STAT3 signal, and suggested that snake venom toxin may be applicable as an anticancer agent for ovarian cancer.

Effect of HUVEC apoptosis inducing proteinase from Vipera lebetina venom (VLAIP) on viability of cancer cells and on platelet aggregation

Three cancer cell lines, the human androgen independent prostate cancer PC-3, androgen dependent LNCaP prostate cancer and human chronic myeloid leukaemia cell line K-562, were treated with Sephadex G-100 sf fractions of Vipera lebetina venom and with HUVEC apoptosis inducing heterodimeric metalloproteinase (VLAIP) from the same venom. The venom was separated into nine fractions using size-exclusion chromatography on Sephadex G-100 sf. The effect of V. lebetina venom gel filtration fractions on the viability of studied cancer cells was different: high molecular mass fractions were the most effective on PC-3 cells. The viability of LNCaP cells was inhibited most strongly by the third fraction. The first and the second fractions contain different metalloproteinases including VLAIP that also most effectively reduced the viability of PC-3 cells. VLAIP decreased PC-3 cell viability in a concentration- and time-dependent manner but did not induce apoptosis as shown by DNA fragmentation assay. VLAIP induced changes in cell shape, rounding up and detachment. VLAIP inhibited the PC-3 cell adhesion to extracellular matrix proteins collagen I, fibronectin and vitronectin but not to fibrinogen. VLAIP had no significant effect on the viability of LNCaP and K-562 cells.VLAIP was also capable to inhibit ADP- and collagen-induced platelet aggregation dose-dependently. IC50 was determined to be 1.89 μM and 0.94 μM, respectively.

Molecular events associated with Macrovipera lebetina obtusa and Montivipera raddei venom intoxication and condition of biomembranes

Studies on the interaction of snake venom and organized lipid interfaces have been conducted using a variety of systems, including BLMs, SUVs and GUVs. The present study was undertaken to elucidate how the plastic properties (namely, its microviscosity, thickness, permeability) of model membranes from native lipids of different tissues of rats change in the course of Macrovipera lebetina obtusa (MLO), Montivipera raddei (MR) and Naja kaouthia (NK) venoms processing. The presence of viper venom in organism leads to increasing of the electrical resistance of BLMs from liver and muscle lipids approximately on a sequence, while the BLMs from brain lipids have not shown noticeable differences of plastic properties compared to the control. Giant unilamellar vesicles (GUVs) with a mean diameter of 30μm have a minimum curvature and mimic cell membranes in this respect. Snake venom was added to the sample chamber before the vesicles were formed. The membrane fluorescence probes, ANS and pyrene, were used to assess the state of the membrane and specifically mark the phospholipid domains. Fluorescent spectra were acquired on a Varian fluorometer instrument. ANS and pyrene allow us to quantify the fluidity changes in the membrane by measuring of the fluorescence intensity. The presence of viper venom in GUVs media reveals a noticeable decreasing of membrane fluidity compared to the control, while the binding of fluorophores with GUVs modified by venom leads to the appearance of channel activity. These studies also emphasize the importance of a membrane surface curvature for its interaction with enzymatic components of venom.

Antimicrobial Profile of Selected Snake Venoms and Their Associated Enzymatic Activities

Aims: To investigate the antiviral and antibacterial profile of several crude snake venoms and to assess some of their enzymatic activities. Methodology: The antiviral activities of Naja haje, Bitis arietans, Naja nigricollis and Echis carinatus snake venoms were investigated against Herpes simplex virus type1, Rift valley fever virus and Vesicular stomatitis virus using the end point of cytopathic effect method. Antibacterial activities of Bitis arietans, Cerastes cerastes, Echis carinatus, Vipera lebetina, Naja naja, Pseudechis australis, Naja nigricollis and Naja haje venoms were examined against Staphylococcus aureus, Escherichia coli, Salmonella typhimurium and Pseudomonas aeruginosa using disc diffusion method. Microdilution method was used to determine the venom's minimum inhibitory concentration. L-amino acid oxidase and phospholipase A2 activities of crude venoms were evaluated using enzymatic assays. Results: Naja nigricollis, Bitis arietans and Echis carinatus snake venoms exhibited significant antiviral activities against all test viruses, except for N. haje treated cells. The mean depletion of viral infectivity titer of venom pretreated cells was higher than its depletion post viral infection for all three venoms showing antiviral activities. Naja nigricollis exhibited the highest antiviral activity against test viruses and recorded a mean depletion of viral infectivity titer in venom pretreated cells of 3.8 log (10) / ml , 3.2 log (10) / ml and 2.5 Research Article British Microbiology Research Journal, 2(4): 251-263, 2012 252 log (10) / ml for HSV-1, RVFV and VSV, respectively. Pseudechis australis, followed by Naja naja and Naja nigricollis venoms, showed the highest inhibitory activity against test bacteria with inhibition zones ranging from 11-17 mm, 8-14 mm and 8-13 mm, respectively. Minimum inhibitory concentrations of test venoms against different bacterial strains ranged from 156 μg / ml to 1.25 mg / ml. Maximum Lamino oxidase activity was detected in Naja naja, Cerastes cerastes and Pseudechis australis. The highest Phospholipase A2 activity was identified in Bitis arietans, Pseudechis australis, Naja naja and Naja nigricollis. Conclusion: It can be concluded that snake venoms or their bioactive derivatives can be promising therapeutic agents against some microbial infections. Further investigations will be carried out for purification and more characterization of the biologically active components in snake venoms.

Incidence of Snake Bites in Kashan, Iran During an Eight Year Period (2004-2011)

Background:Snake bites are one of the significant health problems in the tropical and subtropical regions. Snake bite is a common medical emergency in Iran, and the epidemiological features and management of such cases vary from region to region.Objectives:This present research study was conducted to obtain new information about the epidemiology of snake bites in the region of Kashan, located in the central part of Iran.Patients and Methods:This research was a descriptive retrospective study. Data from 2004 to 2011 of snakebite cases were collected from case reports. Information included; age and sex of the victim, district, month of incident, mortality, and time of bite.Results:The results of this study showed that the majority of snake bite patients were male (96%). The age distribution of patients indicated that the greatest rate of snake bites occurred among the 15-24 year old group. Data collected in this study revealed that the highest incidence of snake bite cases took place in summer (60%) and the lowest number occurred in winter, with no snake bite cases being recorded. The peak number of snakebite cases was seen during June-September.Conclusions:It was concluded that snake bite cases in Kashan are similar to other areas in Iran from an epidemiological point of view, including; age distribution rates, gender and site of the bites. The existence of Macrov ipera lebetina, a dangerous venomous snake, can cause a range of clinical effects among residents in central parts of Iran, such as Kashan area.

Determination of in vivo toxicity and in vitro cytotoxicity of venom from the Cypriot blunt-nosed viper Macrovipera lebetina lebetina and antivenom production

The venomous Levantine viper, Macrovipera lebetina lebetina is endemic to Cyprus. The objective of this study was to investigate in vitro cytotoxicity, in vivo lethality, and antivenom production followed by a re-immunization schedule in mice against Macrovipera lebetina lebetina venom. The LD50 value was estimated as 7.58 mg/kg within 24 hours by different venom doses administrated intraperitoneally in mice. Freund's complete and incomplete adjuvants were used for first and second immunization of mice in antivenom production. A cell-based assay was performed to determine the effects of Macrovipera lebetina lebetina venom and antivenom neutralizing potency on L929 cell viability. The snake venom toxicity and cytotoxicity were examined and comparison of results showed good correlation, the LD50 value was tenfold higher than the IC50 value. The IC50 value was 0.62 ± 0.18 mL after 48 hours treatment while the calculated value was 1.62 ± 0.25 mL for the culture media totally refreshed after two hours treatment with venom. The in vitro efficacy of antivenom against Macrovipera lebetina lebetina venom was found to be low. This is the first report that describes the in vivo and in vitro toxic effects of Macrovipera lebetina lebetina venom and antivenom production against this species.

Electroporation and electropermeabilization of lipid bilayer membranes in the course of snakes’ venom intoxication

The present study was undertaken to elucidate how the plastic properties of model membranes from native lipids of different tissues of rats change in the course of Macrovipera lebetina obtuse (MLO), Montivipera raddei (MR) and Naja kaouthia (NK) venoms processing. The presence of viper venom in organism lead to increasing of the electrical resistance of BLMs from liver and muscle lipids approximately on a sequence, while the BLMs from brain lipids has not shown a noticeable differences of plastic properties compare the control. The same concentration of cobra venom leads to decreasing of electrical resistance of BLMs from 1011 Ohm till 108 Ohm. The low concentration of venom leads to appearance of channel activity. Especially it is noticeable in liver lipids in media of bivalen ions.

Snake venom toxin from Vipera lebetina turanica sensitizes cancer cells to TRAIL through ROS- and JNK-mediated upregulation of death receptors and downregulation of survival proteins

Snake venom toxin from Vipera lebetina turanica sensitizes cancer cells to TRAIL through ROS- and JNK-mediated upregulation of death receptors and downregulation of survival proteins

Cerastes cerastes and Vipera lebetina Snake Venoms Apoptotic – Stimulating Activity to Human Breast Cancer Cells and Related Gene Modulation

Apoptosis occurs normally during development and aging as a homeostatic mechanism to maintain cell populations. Dysregulation of apoptosis can disrupt the equilibrium between cell growth and cell death leading to the development of cancer. Thus, the investigation of new biological apoptotic activators could play an important role in cancer therapy. In the present study, Cerastes cerastes and Vipera lebetina snake venoms were evaluated for their ability to activate apoptosis in cancer cells where test venoms exhibited a concentration and time dependent cytotoxic effect on breast cancer (MCF-7) cells. Typical apoptotic morphological features were demonstrated in venom treated cells detected via transmission electron microscope. In addition, flow cytometric analysis showed an increase in the percentage of apoptotic cells post 24 h treatment relative to venom concentrations. At the molecular level, test venoms induced apoptosis were mediated by up regulation of pro-apoptotic genes (p53 & Bax) and down regulation of anti-apoptotic gene (Bcl-2) in MCF-7 cells, indicating that these venoms could serve as apoptotic stimulators, presenting a novel and potential therapeutic strategy for cancer treatment.

Purification and Characterization of a Fibrinolytic Enzyme from Snake Venom of Macrovipera Lebetina Turanica

Purification and Characterization of a Fibrinolytic Enzyme from Snake Venom of Macrovipera Lebetina Turanica