In vivo inhibition of inducible nitric oxide and evaluation of the brain tissue damage induced by Toxocara canis larvae in experimentally infected mice

Nitric oxide (NO) is known to be produced by macrophages, endothelial cells and neurons and synthesized by an enzyme called nitric oxide synthase (NOS). Various effector mechanisms and infections can affect the NO production. Excessive amount of NO will lead to biochemical reactions, which cause toxic effects. In this study the role of NO has been evaluated in larval toxocarosis, which is a systemic parasite infection caused by T. canis larvae. Infection was established in the Balb/c mice with or without inducible NOS (iNOS) inhibition and the effects of infection and NOS inhibition were observed according to the results of SOD and LPx measurements in brain tissue and NADPH-diaphorase (NADP-d) histochemistry. Results of NADPH-d histochemistry indicate that iNOS inhibition has protective effect on the brains of infected mice and that larval T. canis infection could be related to oxidative stress, and NO production and iNOS inhibition can protect the tissue from damage in this infection

Alterations in superoxide dismutase activities, lipid peroxidation and glutathione levels in thinner inhaled rat lungs: Relationship between histopathological properties

Paint thinner has widespread use in industry. The use of thinner among children as a narcotic agent has become a social and health problem. There is some evidence that organic solvents may express their toxicity by the way of reactive oxygen species (ROS) induced cell damage. ROS has been shown to induce lipid peroxidation in biological membranes. This study examined peroxidative and histopathological changes in the rat lung, during 5 weeks of thinner inhalation. Significant increases were found in lipid peroxidation (MDA + 4-DHA) levels related to the duration of inhalation. As opposed to increases in the lipid peroxidation levels, significant decreases in superoxide dismutase activities and glutathione levels were observed from the third inhalation week to the end of the fifth week. At the beginning of the inhalation slight inflammatory changes, intraalveolar and interstitial extravasation and oedema in lung parenchyma were noted. As the inhalation period extended, chronic inflammatory changes, alveolar epithelial proliferation, collapse, emphysematous changes and interstitial fibrosis in lung were detected. (C) 1998 The Italian Pharmacological Society

Effects of iloprost on lipid peroxidation parameters in cerebral hypoperfusion model induced by right common carotid artery occlusion

Our aim was to study effects of iloprost on lipid peroxidation parameters in cerebral hypoperfusion model induced by right common carotid artery occlusion. The rats were divided into 4 weight-matched groups. Sham-operated group (S) (n=10); Hypoperfused (H) (n=10); Early iloprost administered after hypoperfusion (HE) (n= 10); Late iloprost administered after hypoperfusion (HQ (n=10). Plasma MDA levels of H, HE and HL groups were significantly higher than S group (respectively p<0.001. p<0.05. p<0.001). Values of intraerythrocytic Cu-Zn SOD activity of H. HE and HL groups were significantly higher than those of S group (p<0.001). The right hemisphere tissue MDA levels of S group were highest (P<0.05). HE group right hemisphere Cu-Zn SOD activity was higher than other groups, on the other hand HL group right hemisphere Cu-Zn SOD activity significantly lower than other groups (p<0.001). Our findings revealed that the early iloprost treatment might be protected the brain tissue from oxidative damage

The role of nitric oxide in pediatric patients with portal hypertension

The hyperdynamic circulation of cirrhosis and portal hypertension has been postulated to be due to the vasodilatory effects of nitric oxide. However, there have been conflicting results in adults and no studies in children. We aimed to measure the nitric oxide level in serum of pediatric patients with portal hypertension with and without cirrhosis, in order to assess its role in the development of hemodynamic changes. We measured nitric oxide levels in 41 pediatric patients (21 patients with intrahepatic portal hypertension and 20 with extrahepatic portal hypertension). The mean age of the study population was 11.2 +/- 4.6 years; 53 per cent were female. Twenty healthy children were included as a control group. Nitric oxide levels were measured by Boehringer-Mannheim colorimetric assay and the statistical significance was calculated by Kruskal-Wallis one-way ANOVA. Significantly higher nitric oxide levels were found in patients independent of the type of portal hypertension compared with the control group (29.4 +/- 6 in patients with intrahepatic portal hypertension, 29.5 +/- 5.8 in patients with extrahepatic portal hypertension, and 23.6 +/- 6.5 in the control group; p < 0.007). These data showed a difference between the groups and suggest that nitric oxide, predominantly independent of cirrhosis, plays a primary role in the pathogenesis of portal hypertension