Role of prostaglandin H synthase in activation of acrylonitrile to cyanide

The present study aimed at investigating the in-vitro oxidation of acrylonitrile [ACN] to cyanide [CN] by prostaglandin H synthase [PHS]. Detection of CN is considered a marker for free radical intermediates involved in ACN-induced toxicity. First, most favorable circumstances for ACN oxidation were characterized: pH [4.5], temperature [37 degree C] and time of incubation [60 min.]. In addition, the concentrations of ACN, PHS and H2O2 in incubation mixtures were assessed for further reaction characterization. The reaction maximum velocity [Vmax] was calculated to be 582.75 pmol CN/mL/min and the Michaelis-Menten constant [Km] was 149.25 µmol ACN. Adding PHS inhibitors; resveratrol, quercetin, indomethacin or troloc-C to the reaction mixtures significantly reduced the rate of ACN oxidation. In conclusion, the present study demonstrates the ability of PHS to oxidize ACN to CN and provides a clue for the explanation of ACN target toxicity

Hepatotoxicity and oxidative stress induced byNaja haje crude venom

Background Snake venoms are synthesized and stored in venom glands. Most venoms are complex mixtures of several proteins, peptides, enzymes, toxins and non-protein components. In the present study, we investigated the oxidative stress and apoptosis in rat liver cells provoked by Naja haje crude injection (LD50) after four hours.Methods Wistar rats were randomly divided into two groups, the control group was intraperitoneally injected with saline solution while LD50-dose envenomed group was intraperitoneally injected with venom at a dose of 0.025 μg/kg of body weight. Animals were killed four hours after the injection. Lipid peroxidation, nitric oxide and glutathione levels were measured as oxidative markers in serum and liver homogenate. In addition, liver function parameters and activities of antioxidant enzymes were determined.ResultsN. haje crude venom (0.025 μg/kg of body weight) enhanced lipid peroxidation and nitric oxide production in both serum and liver with concomitant reduction in glutathione, catalase, glutathione reductase and glutathione-S-transferase activities. Superoxide dismutase and glutathione peroxidase activities were significantly increased in liver of envenomed rats. These findings were associated with apoptosis induction in the liver. In addition, N. haje crude venom caused hepatic injury as indicated by histopathological changes in the liver tissue with an elevation in total bilirubin, serum alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transpeptidase, and alkaline phosphatase.Conclusions Based on the present results, it can hypothesized that N. haje crude venom is a potent inducer of toxin-mediated hepatotoxicity associated with apoptosis in the liver.(AU)

Hepatotoxicity and oxidative stress induced by Naja haje crude venom

Snake venoms are synthesized and stored in venom glands. Most venoms are complex mixtures of several proteins, peptides, enzymes, toxins and non-protein components. In the present study, we investigated the oxidative stress and apoptosis in rat liver cells provoked by Naja haje crude injection (LD50) after four hours. Wistar rats were randomly divided into two groups, the control group was intraperitoneally injected with saline solution while LD50-dose envenomed group was intraperitoneally injected with venom at a dose of 0.025 μg/kg of body weight. Animals were killed four hours after the injection. Lipid peroxidation, nitric oxide and glutathione levels were measured as oxidative markers in serum and liver homogenate. In addition, liver function parameters and activities of antioxidant enzymes were determined.

C - reactive protein levels in cerebral infaarctioninpatients on hemodialysis

Serum C-reactive protein [CRP] concentration issensitive marker of underlying systemic inflammation. Patientsunder continuous hemodialysis have an activated inflammatoryresponse, evidenced by increased serum CRP levels especiallyin patients with cerebral stroke. The study was performed toevaluate serum levels of CRP as inflammatory markers inpatients with stroke under continuous hemodialysis. The study was included 33 patients with chronicrenal failure under continuous hemodialysis divided into twogroups. Group I included 23 patients with acute stroke. Group II [control group] included 10 patients without stroke. All patientswere subjected to complete history and clinical examinationwith special emphasis to history of co-morbid conditions,hypertension, diabetes mellitus and cardiovascular disease.Serum creatinine, urea, CBC, albumin, lipid profile, calcium,fasting and post prandial blood sugar, sodium, potassium, serumuric acid, phosphorus, C-reactive protein and other investigationwere evaluated. In addition axial CT or MRI was performed atadmission and after 72 hours. The following parameterswere significantly higher in groupe I when compared to group II;ages [t=3.5. p< 0.01], CRP [t=7.1, p<0.001], serum creatinine [tett, p<0.0] and blood urea [t=4.3, p<0.01], while serumlevels of Hb% and serum calcium were significantly lower ingroup I when compared to group II [t=3.1, p<0.01 and t=2.2,p<0.05 respectively]. On the hand no significant differences inthe other studied parameters between two groups. Serum levelsof CRP were positively correlated with INR [r=520, p<0.05] and negatively correlated with serum calcium [r=0.580, p<0.05] and serum albumin [r=-540, p<0.05]. On the other hand nosignificant correlations were found between CRP and otherstudied parameters. According to ROC curve between group Iand II in CRP the cutoff were greater than 12 with sensitivity,specificity, Positive Perdictive Value and Negative PredictiveValue were 100% by accuracy 100%. Elevatedserum CRP could be a predictor of cerebrovascular stroke indialysis patients. Therefore, regular determination of serumCRP may be helpful to detect early signs of tissue damage andasymptomatic inflammation in these patients