Study of Nitric Oxide production by murine peritoneal macrophages induced by Brucella Lipopolysaccharide

Brueclla is a gram negative bacteria that causes Brucellosis. Lipopolysaccharide (LPS) ", the pathogenic agent of Brucella is composed of O-chain, core oligosaccharide and lipid A. in addition, the structural and biological properties of different LPS extracted from different strains are not identical. The first defense system against LPS is nonspecific immunity that causes macrophage activation. Activated macrophages produce oxygen and nitrogen radicals that enhance the protection against intracellular pathogens.In this experiment LPS was extracted by hot phenol- water procedure and the effect of various LPSs on nitric oxide prodution by peritoneal mouse macrophages was examined.Our results demonstrated that the effect of LPS on nitric oxide production is concentration-dependent we observed the maximum response in concentration of 10-20 microgram per milliliter. Also our results demonstrate that LPS extracted from vaccine Brucella abortus (S 19) had a highe effect on nitric oxide production than the LPS from other strain

"EFFECT OF CIMETIDINE AND RANITIDINE ON LIPID PROFILE AND LIPID PEROXIDATION IN γ-IRRADIATED MICE"

Elevated amounts of free radicals due to ionizing radiation have damaging effects on the body. H2-receptor antagonists have potential oxygen radical scavenging properties. We tried to determine the effects of two H2-receptor antagonists (cimetidine and ranitidine) on lipid peroxidation (LPO) and lipid profile (LP) in plasma and liver of γ-irradiated (1Gy/day for 3 days) BALB/c mice. The control group of mice were fed with normal food and drinks but the experiment group of mice were fed control diet and drinking water, containing cimetidine or ranitidine (1mg/lit). After 3 days of supplementation, the animals were subjected to sublethal γ-radiation, which caused a significant increase in cholesterol level in experimental group (100% increase in comparison with the control group), but the amount of phospholipids did not change. The ratio of cholesterol to phospholipid showed a slight increase. Also γ-irradiation caused a significant increase in lipid fluorescence (11-48%), conjugated dienes (33-81%) in liver and increase in malondialdehyde (19-300%) in serum of mice who had received 1.09-3.1 Gy for 1-3 days. Cimetidine or ranitidine supplementation was able to restore the changes of LPO and LP in mice (1 Gy-radiated for 3 days). It is therefore concluded that the mice treated with cimetidine or ranitidine were able to tolerate biomembrane damages provoked by sublethal γ-radiation. This supports the hypothesis that cimetidine or ranitidine may afford an efficient protection against ionizing radiation or diseases that are characterized by in vivo free radical-mediated oxidative stress mechanisms