Ascitis linfocitaria con niveles elevados de adenosina deaminasa secundaria a infección por Chlamydia trachomatis / Lymphocytic ascites with high adenosine deaminase levels secondary to Chlamydia trachomatis infection

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Influence of genetic variations in the SOD1 gene on the development of ascites and spontaneous bacterial peritonitis in decompensated liver cirrhosis.

BACKGROUND: The balance between generation and elimination of reactive oxygen species by superoxide dismutase (SOD) is crucially involved in the pathophysiology of liver cirrhosis. Reactive oxygen species damage cells and induce inflammation/fibrosis, but also play a critical role in immune defense from pathogens. As both processes are involved in the development of liver cirrhosis and its complications, genetic variation of the SOD1 gene was investigated. PATIENTS AND METHODS: Two SOD1 single nucleotide polymorphisms (rs1041740 and rs3844942) were analyzed in 49 cirrhotic patients undergoing liver transplantation. In addition, 344 cirrhotic patients with ascites were analyzed in a cohort of 521 individuals in terms of the relationship of these polymorphisms with spontaneous bacterial peritonitis (SBP). RESULTS: Although rs3844942 showed no associations with complications of cirrhosis, we observed a significant association between rs1041740 and the presence of ascites and SBP in the discovery cohort of patients with cirrhosis. Importantly, the association with SBP was not confirmed in the validation cohort of patients with ascites. By contrast, a trend toward lower SBP rates was observed in carriers of rs1041740. In this cohort, rs1041740 was not associated with survival. CONCLUSION: These data suggest a complex role of SOD1 in different processes leading to complications of liver cirrhosis. rs1041740 might be associated with the development of ascites and possibly plays a role in SBP once ascites has developed.

Triple-drug therapy to prevent pancreatic fistula after pancreatectomy in a rat model.

BACKGROUND: Pancreatic fistula (PF) is one of post-operative complications in pancreatic surgery, but there is no consensus about the optimal treatment for PF. Our group has established a rat model of PF, and we conducted the present investigation to determine the efficacy of the triple-drug therapy (somatostatin analogue, gabexate mesilate, and imipenem/cilastatin) against PF using our rat model. METHODS: In the PF rat model, the triple-drug therapy was administered to the treated (T) group (n = 4), and we compared the results with those of a control (C) group (n = 4). The rats were sacrificed on postoperative day 3 (POD 3) and the levels of amylase and lipase in serum and ascites were measured. The intra-abdominal adhesion was scored. Each pancreas was evaluated pathologically, and inflammation was scored. RESULTS: The ascitic amylase levels on POD 3 were 1982 (1738-2249) IU/L in the C group and significantly lower at 136 (101-198) IU/L in the T group (p = 0.02). The ascitic lipase levels on POD 3 were 406 (265-478) U/L in the C group and significantly lower at 13 (7-17) U/L in the T group (p = 0.02). The intra-abdominal adhesion score on POD 3 was 2 (1-2) in the C group and significantly lower at 0 (0-1) in the T group (p = 0.02). The histological evaluation showed that the average of pancreatic inflammatory score was 8.5 (8-9) in the C group and significantly milder at 5 (5-7) in the T group (p = 0.01). CONCLUSION: Our findings suggest that the triple-drug therapy could be useful as a treatment for PF in clinical settings.

Contribution of the Kallikrein/Kinin System to the Mediation of ConA-Induced Inflammatory Ascites.

Intraperitoneal administration of concanavalin A (ConA, 25 mg/kg b.w.), a cell-binding plant lectin was used for inducing inflammatory ascites, and potential inhibitors were tested in 1 h and 2.5 h experiments, i.e. still before the major influx of leucocytes. At the end of the experiment the peritoneal fluid was collected and measured. The ConA-induced ascites was significantly (p<0.01) and dose-dependently inhibited by icatibant (HOE-140), a synthetic polypeptide antagonist of bradykinin receptors. Aprotinin, a kallikrein inhibitor protein also had significant (p<0.01), but less marked inhibitory effect. L-NAME, an inhibitor of NO synthesis, and atropine methylnitrate, an anticholinergic compound, were ineffective. It is concluded, that the kallikrein/kinin system contributes to the mediation of the ConA-induced ascites by increasing subperitoneal vascular permeability, independent of the eventual vasodilation produced by NO. It is known, that membrane glycoproteins are aggregated by the tetravalent ConA and the resulting distortion of membrane structure may explain the activation of the labile prekallikrein. Complete inhibition of the ConA-induced ascites could not be achieved by aprotinin or icatibant, which indicates the involvement of additional mediators.

Angiotensin receptor blocker–induced visceral angioedema

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Analysis of cases with tuberculous peritonitis: a single-center experience.

BACKGROUND/AIMS: Tuberculous peritonitis (TP) is a rare form of tuberculosis and is caused by peritoneal involvement with Mycobacterium tuberculosis. A distinctive correlation exists between socioeconomic state and disease prevalence. We aimed to evaluate the clinical, laboratory, and radiological findings of patients with TP. MATERIALS AND METHODS: We conducted a retrospective study in patients with peritoneal tuberculosis from January 2004 to October 2008 at Yuzuncu Yil University Medical School Education and Research Hospital. During this time, the data of 21 patients (17 females) with TP were reviewed. RESULTS: Fever, abdominal pain, and anorexia were the most common symptoms. An analysis of ascites showed lymphocyte predominance and low albumin gradient in all patients. Patients with TP had a median ascites adenosine deaminase (ADA) level of 139 U/L (range, 25 to 303U/L). Peritoneal involvement (wet peritonitis) was seen in all the cases. Following 6-month administration of combined anti-TBC treatment, mean serum CA-125 levels were within the normal range among patients who had previously higher serum CA-125 level. Mortality rate in the total cases was 4.6%. CONCLUSION: Peritoneal tuberculosis should be considered in the differential diagnosis of exudative ascites in eastern Turkey. A high level of suspicion is required, especially in high-risk populations living in rural areas. ADA seems to be a sufficient, safe, and inexpensive method to perform the diagnosis of peritoneal tuberculosis. Serum CA-125 levels may play a key role to support the diagnosis as well as disease management of TP.

Expression and significance of cyclooxygenase-2 mRNA in benign and malignant ascites.

AIM: To investigate the mRNA expression of cyclooxygensae-2 (COX-2) in benign and malignant ascites, and to explore the difference in COX-2 mRNA expression among different diseases. METHODS: A total of 36 samples were collected from the Fifth Affiliated Hospital of Sun Yat-Sen University and divided into two experimental groups: benign ascites (n = 21) and malignant ascites (n = 15). Benign ascites included cirrhotic ascites (n = 10) and tuberculous ascites (n = 5). Malignant ascites included oophoroma (n = 7), cancer of colon (n = 5), cancer of the liver (n = 6), gastric cancer (n = 2), and bladder carcinoma (n = 1). The mRNA expression of COX-2 in ascites was examined with reverse transcriptase polymerase chain reaction (RT-PCR) technology, and the positive rate of COX-2 mRNA was compared between different diseases. RESULTS: The positive rate of COX-2 mRNA in malignant ascites was 42.9% (9/21), which was significantly higher than in benign ascites, 6.7% (1/15), difference being significant between these two groups (χ(2) = 4.051, P = 0.044). The proportion of the positive rate in the malignant ascites was as follows: ovarian cancers 57.1% (4/7), colon cancer 40.0% (2/5), liver cancer 33.3% (2/6), gastric cancer 50.0% (1/2), and bladder cancer 0.00% (0/1). However, there was no significant difference in COX-2 mRNA expression among various tumors with malignant ascites (χ(2) = 1.614, P = 0.806). Among the benign ascites, COX-2 mRNA levels were different between the tuberculous ascites (0/5) and cirrhotic ascites (1/10), but there was no significant difference (P = 1.000). CONCLUSION: COX-2 mRNA, detected by RT-PCR, is useful in the differential diagnosis of benign and malignant ascites, which also has potential value in the clinical diagnosis of tumors.

Severe liver cirrhosis markedly reduces AhR-mediated induction of cytochrome P450 in rats by decreasing the transcription of target genes.

Although the induction of cytochrome P450 (CYP) has long been investigated in patients with cirrhosis, the question whether liver dysfunction impairs the response to CYP inducers still remains unresolved. Moreover, the mechanism underlying the possible effect of cirrhosis on induction has not been investigated. Since ethical constraints do not permit methodologically rigorous studies in humans, this question was addressed by investigating the effect of the prototypical inducer benzo[a]pyrene (BP) on CYP1A1 and CYP1A2 in cirrhotic rats stratified according to the severity of liver dysfunction. We simultaneously assessed mRNA level, protein expression and enzymatic activity of the CYP1A enzymes, as well as mRNA and protein expressions of the aryl hydrocarbon receptor (AhR), which mediates the BP effect. Basal mRNA and protein expressions of CYP1A1 were virtually absent in both healthy and cirrhotic rats. On the contrary, CYP1A2 mRNA, protein and enzyme activity were constitutively present in healthy rats and decreased significantly as liver function worsened. BP treatment markedly increased the concentrations of mRNA and immunodetectable protein, and the enzymatic activities of both CYP1A enzymes to similar levels in healthy and non-ascitic cirrhotic rats. Induced mRNA levels, protein expressions and enzymatic activities of both CYPs were much lower in ascitic rats and were proportionally reduced. Both constitutive and induced protein expressions of AhR were significantly lower in ascitic than in healthy rats. These results indicate that the inducibility of CYP1A enzymes is well preserved in compensated cirrhosis, whereas it is markedly reduced when liver dysfunction becomes severe. Induction appears to be impaired at the transcriptional level, due to the reduced expression of AhR, which controls the transcription of CYP1A genes.

Paclitaxel resistance and multicellular spheroid formation are induced by kallikrein-related peptidase 4 in serous ovarian cancer cells in an ascites mimicking microenvironment.

High tumor kallikrein-related-peptidase 4 (KLK4) levels are associated with a poor outcome for women with serous epithelial ovarian cancer (EOC), for which peritoneal dissemination and chemoresistance are key events. To determine the role of KLK4 in these events, we examined KLK4-transfected SKOV-3 and endogenous KLK4 expressing OVCA432 cells in 3-dimensional (3D) suspension culture to mimic the ascites microenvironment. KLK4-SKOV-3 cells formed multicellular aggregates (MCAs) as seen in ascites, as did SKOV-3 cells treated with active KLK4. MCA formation was reduced by treatment with a KLK4 blocking antibody or the selective active site KLK4 sunflower trypsin inhibitor (SFTI-FCQR). KLK4-MCAs formed larger cancer cell foci in mesothelial cell monolayers than those formed by vector and native SKOV-3 cells, suggesting KLK4-MCAs are highly invasive in the peritoneal microenvironment. A high level of KLK4 is expressed by ascitic EOC cells compared to matched primary tumor cells, further supporting its role in the ascitic microenvironment. Interestingly, KLK4 transfected SKOV-3 cells expressed high levels of the KLK4 substrate, urokinase plasminogen activator (uPA), particularly in 3D-suspension, and high levels of both KLK4 and uPA were observed in patient cells taken from ascites. Importantly, the KLK4-MCAs were paclitaxel resistant which was reversed by SFTI-FCQR and to a lesser degree by the general serine protease inhibitor, Aprotinin, suggesting that in addition to uPA, other as yet unidentified substrates of KLK4 must be involved. Nonetheless, these data suggest that KLK4 inhibition, in conjunction with paclitaxel, may improve the outcome for women with serous epithelial ovarian cancer and high KLK4 levels in their tumors.

Heme oxygenase 1-generated carbon monoxide and biliverdin attenuate the course of experimental necrotizing pancreatitis.

OBJECTIVE: The cytoprotective enzyme heme oxygenase 1 (HO-1) is highly up-regulated in acute pancreatitis (AP). In this study, we tested its metabolites as potential therapeutic agents for AP in rats. METHODS: Acute necrotizing pancreatitis was induced by retrograde intraductal injection of sodium taurocholate in rats. Biliverdin hydrochloride (BV HCl) (50 µmol/kg subcutaneously), the carbon monoxide, donor methylene chloride (MC) (500 mg/kg orally), or iron-chelating desferrioxamine (DFO) (125 mg/kg subcutaneously) were administered in a therapeutic manner starting with the first dose 4 hours after taurocholate injection to mimic the effects of HO-1 metabolites. RESULTS: Administration of BV HCl, MC, or DFO showed significant reduction of inflammatory activity in comparison to controls leading to lower myeloperoxidase activity in the pancreas, less edema, lower ascites volumes, and preservation of tissue integrity (P < 0.05). Administration of either BV HCl or MC markedly increased 5-day survival rate (70% and 75% vs 40%; P < 0.05), whereas DFO had no significant effect on survival (60%). When given in therapeutic manner, all 3 substances led to diminished nuclear factor κB activity in the pancreas (P < 0.05). CONCLUSIONS: Therapeutic use of BV HCl and MC led to marked reduction of mortality in experimental pancreatitis. Thus, HO-1 metabolites may present a novel therapeutic approach in AP treatment.

Development of a novel rat model with pancreatic fistula and the prevention of this complication using tissue-engineered myoblast sheets.

BACKGROUND: Pancreatic fistula (PF) is one of the most important complications of pancreatic surgery. The aims of this study were to establish a PF model in rats and to investigate the efficacy of our new method for preventing PF, which utilizes myoblast sheets made using tissue engineering techniques. METHODS: To establish a PF model, the rats underwent transection of each of four pancreatic ducts: the gastric, duodenal, common, and splenic ducts, respectively. Their ascitic amylase and lipase levels were then measured. To investigate the efficacy of myoblast sheets at preventing PF, a myoblast sheet was attached to the pancreatic stump in the PF models. The levels of amylase and lipase in both serum and ascites were then measured, and surgical specimens were investigated pathologically. RESULTS: The new PF model established by transecting the splenic duct in rats may prove very useful. There were no significant differences in serum amylase and lipase levels between the myoblast sheet (+) group and the sheet (-) group. However, there were significant differences in ascitic amylase and lipase levels between the two groups (p < 0.05). Among the pathological findings, the number of inflammatory cells in the myoblast sheet group was smaller than that in the control group. In addition, the presence of the myoblast sheets on the surface of the pancreatic stump was confirmed by immunofluorescence staining. CONCLUSION: Our data demonstrate the efficacy of the new rat model of PF presented herein, and that it might be possible to prevent PF using myoblast sheets.

Diagnosis of spontaneous and secondary bacterial peritonitis in patients with hepatic cirrhosis and ascites.

Spontaneous bacterial peritonitis (SBP) is an infection that is not caused by intra-abdominal source requiring surgery. Nowadays SBP is the main cause of death in patients with cirrhosis. Treatment is carried out with third generation cephalosporins and albumin infusions. The aim of the study is to identify patients with SBP and to be distinguished from the cases with secondary bacterial peritonitis (SecBP) in patients with cirrhosis and ascites. We studied 167 patients with cirrhosis and ascites and SBP was observed in 25 of them, while SecBP--in 22. The diagnosis of SBP is set in neutrophilic leukocytes in ascites > or = 250 cells/mm3 as bacterial cultures are positive in only 16% of them. Completely asymptomatic course had 16% of patients with SBP. Diagnosis of SecBP (according to Runyon's criteria) is based on increased total protein in ascitic fluid > 10 g/l (in 63.7% of patients > 30 g/l), elevated lactate dehydrogenase in ascites (LDH is > 240 U/l in all patients) and glucose < 2,7 mmol/l (only 4.5% of cases with secondary bacterial peritonitis). In support of SecBP are the polymicrobial flora, the isolation of anaerobes, enterococci, fungi, and the very high number of neutrophilic leukocytes in the peritoneal effusion and the refractoriness from conservative treatment. The examination of ascites with Multistix is more informative in secondary than in spontaneous bacterial peritonitis. In suspected secondary bacterial peritonitis CT is indicated.

Rapid diagnosis of spontaneous bacterial peritonitis using leukocyte esterase reagent strips in emergency department: uri-quick clini-10SG® vs. Multistix 10SG®.

BACKGROUND AND AIM: Bacterial peritonitis (SBP) is the most frequent infection in patients with cirrhosis causing significant mortality. Delay in SBP diagnosis is a serious problem. The aim of this study was to evaluate the diagnostic yield of Uri-Quick Clini-10SG® vs. Multistix 10SG® reagent strips in an Emergency Department. MATERIAL AND METHODS: A prospective study of consecutive patients with ascites and paracentesis attending to Emergency Department from March 2005 to February 2007 was made. SBP was defined by ≥ 250 neutrophiles /mm³. The ascites obtained at bedside was immediately tested in a dry test tube with both the Uri-Quick Clini 10SG® and MultistixSG10®. The Uri-Quick Clini 10SG® and Multistix SG10®. Strips were considered positive at grade ≥ 3 (≥ 125 leukocytes/mL). RESULTS: A total of 223 ascitic fluid samples were obtained. There were 49 episodes of SBP. Median age was 54 (range 18-87 year) years; 62.3% were female. The sensitivity, specificity, PPV, NPV, and 95% CI for Uri-Quick Clini 10SG® were 79.6 (64-87), 98.2 (94-99), 90.5 (78-96) and 93.9 (89-96), respectively. For MultistixSG10® the values were 77.5 (64-88), 97.7 (93-98), 90 (77.9-96.2), and 94 (89.4-96.6), respectively. CONCLUSION: The use of reagent strip is useful for SBP diagnosis in an emergency setting. The high PPV allow start antibiotic treatment. In areas without the resources to perform conventional ascites fluid analyses, these strips could be presently used.

Inhibition of glutathione synthesis eliminates the adaptive response of ascitic hepatoma 22 cells to nedaplatin that targets thioredoxin reductase.

Thioredoxin reductase (TrxR) is a target for cancer therapy and the anticancer mechanism of cisplatin involves TrxR inhibition. We hypothesize that the anticancer drug nedaplatin (NDP), an analogue of cisplatin and a second-generation platinum complex, also targets TrxR. Furthermore, we investigate whether the therapeutic efficacy of NDP can be enhanced by simultaneous modulation of 1) TrxR, via NDP, and 2) glutathione (GSH), via the GSH synthesis inhibitor buthionine sulfoximine (BSO). Mice bearing ascitic hepatoma 22 (H22) cells were treated with NDP alone or NDP plus BSO. TrxR activity of H22 cells was inhibited by NDP in a dose-dependent manner. A high correlation between the inhibition of TrxR activity at 6h and the inhibition of ascitic fluid volume at 72h was established (r=0.978, p<0.01). As an adaptive response, the viable ascitic cancer cells after NDP treatment displayed an enlarged cell phenotype, assembled with several-fold more antioxidant enzymes and GSH-predominant non-protein free thiols. This adaptive response was largely eliminated when BSO was co-administered with NDP, leading to the decimation of the H22 cell population without enhancing renal toxicity, since at this dose, NDP did not inhibit renal TrxR activity. In conclusion, the pharmacological effect of NDP involves TrxR inhibition, and the adaptive response of NDP-treated ascitic H22 cells can be efficiently counteracted by BSO. Simultaneous modulation of TrxR and GSH on ascitic H22 cells using NDP plus BSO greatly enhances therapeutic efficacy as compared with the single modulation of TrxR using NDP alone.

MGST1 expression in serous ovarian carcinoma differs at various anatomic sites, but is unrelated to chemoresistance or survival.

OBJECTIVE: To investigate the expression of MGST1 in primary tumors, solid metastases and metastatic effusions in advanced-stage serous ovarian carcinoma (OC) and analyze the association with clinicopathologic parameters, including chemotherapy resistance and survival. METHODS: MGST1 mRNA expression was investigated in 178 tumors (88 effusions, 38 primary carcinomas, 52 solid metastases) from 144 patients using real-time quantitative PCR (qRT-PCR). Forty-two of the 88 effusions were additionally analyzed for MGST1 protein expression by Western blotting. RESULTS: mRNA expression of MGST1 was higher in primary carcinomas and solid metastases compared to effusions (p=0.008 and p=0.012, respectively). In patient-matched samples, mRNA expression of MGST1 was higher in solid metastases compared to effusions (p=0.023), and a trend for higher MGST1 levels in solid metastases compared to primary tumors was observed (p=0.06). Biopsies from primary carcinomas obtained from patients with >200 ml ascites at diagnosis had higher mRNA expression of MGST1 compared to samples from patients with <200 ml ascites (p=0.037). MGST1 mRNA expression was not associated with age, histological grade, tumor stage, residual disease volume, response to chemotherapy, chemotherapy resistance or survival. Western blot analysis of patient-matched effusions showed high concordance between MGST1 protein and mRNA levels measured by qRT-PCR (p<0.001). CONCLUSIONS: The present study documents frequent MGST1 mRNA and protein expression in OC. The data suggest increased activity of oxidative response pathways, reflected by higher mRNA expression, in solid OC tumors compared to metastatic effusions. Additionally, a tumor microenvironment consisting of ascites may induce antioxidant activity.

Effect of malignant ascites on antioxidative potency of two tumoral cells-induced bone metastases: Walker 256/B and MatLyLu.

This study was undertaken to estimate antioxidative status of two malignant-mammary gland carcinoma (Walker 256/B) and malignant-prostate carcinoma cells (MatLyLu) disseminated in ascitic fluids. Malignant carcinoma cells (10(7) cells) were twice serially intraperitoneal injected in male Wistar rats to develop ascites. After 7 days, ascitic fluids were collected, and cells in suspension were usable for biological assays. Cellular lipid peroxidation was assessed by measuring thiobarbituric acid reactive substances (TBARS) levels. Some antioxidant parameters: superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were also assessed. Comparisons with control baseline (cells maintained in normal culture medium) were analyzed. TBARS levels were found to be significantly decreased in both ascitic cancer cells compared to the baseline except for in the ascite I of MatLyLu cells. On the other hand, SOD and CAT activities were found to be statistically increased in the two malignant ascitic passages. GSH-Px levels were elevated in the first and in the second ascitic passages (p<0.05 and p<0.01, respectively). Our results suggest that malignant ascites are associated not only with reduced levels of TBARS but also with increased antioxidant parameters, indicating the increasing antioxidant potency of two cancer cells during malignancies process.

Immune clearance gastric carcinoma cells in ascites by activating caspase-9-induced apoptosis.

Floating gastric adenocarcinoma cells in ascitic fluid are the main cause of peritoneal dissemination. Activation of apoptosis is an important mechanism by which tumor cells are eliminated by the immune surveillance system. Hence, we examined caspase-9 expression and the apoptosis in gastric adenocarcinoma cells in ascitic fluid using immunohistochemistry, real-time polymerase chain reaction and in situ cell death detection kits, flow cytometry. The results revealed strong expression of caspase-9 in 58.49% (31/53) malignant cells and a relatively weak expression of caspase-9 in 41.51% (22/53) malignant cells. The proportion of apoptotic cells in 31 malignant cases with strong caspase-9 expression (35.14 ± 3.42)% was significantly higher than that in 22 malignant cases with relatively weak caspase-9 expression (17.29 ± 7.62)% or in mesothelial cells (10.76 ± 4.21%; p < 0.05). Kaplan-Meier survival curves demonstrated that the patients with low caspase-9 expression showed significantly shorter survival (p < 0.05) than those with high caspase-9 expression. These findings suggest that immune clearance gastric carcinoma cells in ascites activated by caspase-9 helped to improve the prognosis of patients with gastric cancer.

Increased calcium deposits and decreased Ca2+ -ATPase in erythrocytes of ascitic broiler chickens.

The decrease of erythrocyte deformability may be one of the predisposing factors for pulmonary hypertension and ascites in broiler chickens. In mammals, the cytoplasmic calcium is a major regulator of erythrocyte deformability. In this study, the erythrocyte deformability was measured, and the precise locations of Ca2+ and Ca2+ -ATPase in the erythrocytes were investigated in chickens with ascites syndrome induced by low ambient temperature. The results showed that ascitic broilers had higher filtration index of erythrocyte compared with control groups, indicating a decrease in erythrocyte deformability in ascitic broilers. The more calcium deposits were observed in the erythrocytes of ascitic broilers compared with those of the age-matched control birds. The Ca2+ -ATPase reactive grains were significantly decreased on the erythrocyte membranes of ascitic broilers. Our data suggest that accumulation of intracellular calcium and inhibition of Ca2+ -ATPase might be important factors for the reduced deformability of the erythrocytes of ascitic broilers.

Antitumor activity of silver nanoparticles in Dalton's lymphoma ascites tumor model.

Nanomedicine concerns the use of precision-engineered nanomaterials to develop novel therapeutic and diagnostic modalities for human use. The present study demonstrates the efficacy of biologically synthesized silver nanoparticles (AgNPs) as an antitumor agent using Dalton's lymphoma ascites (DLA) cell lines in vitro and in vivo. The AgNPs showed dose- dependent cytotoxicity against DLA cells through activation of the caspase 3 enzyme, leading to induction of apoptosis which was further confirmed through resulting nuclear fragmentation. Acute toxicity, ie, convulsions, hyperactivity and chronic toxicity such as increased body weight and abnormal hematologic parameters did not occur. AgNPs significantly increased the survival time in the tumor mouse model by about 50% in comparison with tumor controls. AgNPs also decreased the volume of ascitic fluid in tumor-bearing mice by 65%, thereby returning body weight to normal. Elevated white blood cell and platelet counts in ascitic fluid from the tumor-bearing mice were brought to near-normal range. Histopathologic analysis of ascitic fluid showed a reduction in DLA cell count in tumor-bearing mice treated with AgNPs. These findings confirm the antitumor properties of AgNPs, and suggest that they may be a cost-effective alternative in the treatment of cancer and angiogenesis-related disorders.