• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.337-345
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• 1995

To evaluate the pathogenicity and immunogenicity of Eimeria tenella to the chicken treated with dexamethasone(DEX) and testosterone propionate (TES), we administered 0.1ml/chicken of dexamethasone and 40mg/chicken of testosterone propionate at 1-, 2-, and 7-days old, respectively. We also immunized with ND oil-emulsion vaccine at 2 weeks old. After that, we immunized and challenged with 100 and $1{\times}10^5$ oocysts/chicken of E tenella at 2 and 4 weeks old, respectively. And then we investigated the HI titers for ND virus, survival rate, body weight gain, lesion score and the weight of the bursa of Fabricius and thymus. The titers for ND virus in the groups treated with TES were higher than those in the groups treated with DEX and CON during 3 to 6 weeks. After challenge, the survival rate of testosterone propionate treated-challenged(TES-CHA) and TES-immunized and challenged(TES-V&C) groups were 61.5 and 83.3% and those of the other groups were all 100%. At 1 week after challenge, the lesion scores of TES-CHA group(4.0) was the highest of all experimental groups. Those of DEX and controlchallenged( CON-CHA) groups were 2.8, and those of all V&C groups were 2.4. During 1 and 2 weeks after immunization, the body weight gains of TES groups were severe low(61.6-82.2g and 189.6-260.4g). During 1 and 2 weeks after challenge, the body weight gains of all CHA groups were lower than those of not challenged groups. But, those of all V AC groups were not different from those of not immunized groups. At 4- and 6-weeks old, the weight of the bursa of Fabricius and thymus in the chicken of all TES groups were lower than those of all control (CON) and DEX groups. Therefore, testosterone propionate acted as immunosuppressive drug. Also, it was thought that the chicken affected a little humoral immunity to E tenella.