Inducible nitric oxide synthase mediates cytokine release: The time course in conscious and septic rats

Lin, Nien Tsung; Yang, Fwu Lin; Lee, Ru Ping; Peng, Tai Chu; Chen, Hsing I.

doi:10.1016/j.lfs.2005.05.091

Cited by 39 publications

(31 citation statements)

References 30 publications

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“…Similarly, several studies showed that NO production increased by activation of inducible nitric oxide synthase (iNOS) mRNA expression in spleen Data are shown as mean ± S.D. a P \ 0.05 compared to control group, b P \ 0.05 compared to endotoxemia group, c P \ 0.05 compared to taurine group 3-NT: 3-nitrotyrosine, NOx: Reactive nitrogen oxide species and other principal organs after LPS administration [2,5,31]. We also measured 3-NT levels in spleen tissues by HPLC method to investigate the ONOO --mediated damage mechanism after endotoxin administration at 6 th h, and determined that 3-NT levels increased during endotoxemia.…”

Section: Discussionmentioning

confidence: 93%

“…The reaction product, ONOO -, is a powerful oxidant and cytotoxic species [8]. ONOO -is known to be capable of leading to nitration of tyrosine residues, and nitrotyrosine is a specific biomarker of ONOO -generation [2,5,33]. Bian and Murad [1] investigated that the distrubution of nitrotyrosine in spleen, lung and liver, all of which are rich in macrophages and endothelial cells in LPS-treated rats, and they showed that the density of some nitrated proteins was significantly enhanced after LPS treatment by immunublotting and immunohistochemical methods.…”

Section: Discussionmentioning

confidence: 99%

“…The main cellular targets for LPS are endothelial cells lining the vasculature and macrophages which found on high concentrations in the spleen [2,3]. Macrophages and endothelial cells are two major biological sources of nitric oxide (NO).…”

Section: Introductionmentioning

confidence: 99%

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Effects of Taurine on Nitric Oxide and 3-Nitrotyrosine Levels in Spleen During Endotoxemia

et al. 2011

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Taurine (2-aminoethanesulfonic acid) is a free sulfur-containing β-amino acid which has antioxidant, antiinflammatory and detoxificant properties. In the present study, the role of endotoxemia on peroxynitrite formation via 3-nitrotyrosine (3-NT) detection, and the possible antioxidant effect of taurine in lipopolysaccharide (LPS)-treated guinea pigs were aimed. 40 adult male guinea pigs were divided into four groups; control, endotoxemia, taurine and taurine+endotoxemia. Animals were administered taurine (300 mg/kg), LPS (4 mg/kg) or taurine plus LPS intraperitoneally. After 6 h of incubation, when highest blood levels of taurine and endotoxin were attained, the animals were sacrificed and spleen samples were collected. The amounts of 3-nitrotyrosine and taurine were measured by HPLC, and reactive nitrogen oxide species (NOx) which are stable end products of nitric oxide was measured spectrophotometrically in spleen tissues. LPS administration significantly decreased the concentration of taurine whilst increased levels of 3-NT and NOx compared with control group. It was determined that taurine treatment decreased the levels of 3-nitrotyrosine and NOx in taurine+endotoxemia group. The group in which taurine was administered alone, contradiction to well-known antioxidant effect, taurine caused elevated concentration of 3-NT and NOx. This data suggest that taurine protects spleen against oxidative damage in endotoxemic conditions. However, the effect of taurine is different when it is administered alone. In conclusion, taurine may act as an antioxidant during endotoxemia, and as a prooxidant in healthy subjects at this dose.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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Effects of Taurine on Nitric Oxide and 3-Nitrotyrosine Levels in Spleen During Endotoxemia

et al. 2011

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“…Scanning densitometry was performed with an image scan and analysis system (Alpha-Innotech Corp., San Leandro, CA, USA). The current authors followed procedures described previously [18] and the manufacturer's direction.…”

Section: Atp Contentmentioning

confidence: 99%

Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Su¹,

Liu²,

Kao³

et al. 2007

European Respiratory Journal

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Poly (ADP-ribose) synthase or polymerase (PARS and PARP, respectively) is a cytotoxic enzyme which causes cellular damage. Nicotinamide, a compound of vitamin B complex, has been reported to exert an inhibitory effect on PARS or PARP. The present study tests the effects of nicotinamide on acute lung injury and associated alterations following ischaemia/reperfusion (I/R) of the isolated perfused rat's lung.I/R increased the lung weight (LW) to body weight ratio, LW gain, protein and dye tracer leakage, pulmonary arterial pressure and capillary permeability. The insult also increased nitrate/ nitrite, methyl guanidine, tumour necrosis factor-a and interleukin-1b in lung perfusate, while it decreased adenosine triphosphate content with an increase in PARP activity in lung tissue.Most of the I/R-induced changes were abrogated by post-treatment (30 min after I/R) with nicotinamide (100 mg?kg -1 body weight). However, the increase in pulmonary arterial pressure was enhanced by nicotinamide post-treatment. Following I/R, the inducible nitric oxide synthase (iNOS) mRNA expression was enhanced. Nicotinamide reduced the iNOS expression. The results suggest that nicotinamide exerted a protective effect on the acute lung injury caused by ischaemia/reperfusion. The mechanisms may be mediated through the inhibition on the poly (adenosine diphosphate-ribose) polymerase activity, inducible nitric oxide synthase expression and the subsequent suppression of nitric oxide, free radicals and pro-inflammatory cytokines with restoration of adenosine triphosphate.

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“…The recruitment of iNOS-producing neutrophils further enhanced the oxidative stress in the lung. The activated iNOS also enhanced the release of proinflammatory cytokines [19]. The interaction of cytotoxic mediators may create a vicious cycle in the inflammatory process.…”

Section: Discussionmentioning

confidence: 98%

The involvement of nitric oxide, nitric oxide synthase, neutrophil elastase, myeloperoxidase and proinflammatory cytokines in the acute lung injury caused by phorbol myristate acetate

et al. 2008

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Phorbol myristate acetate (PMA) causes acute lung injury (ALI). The present study was designed to elucidate the role of nitric oxide (NO), inducible NO synthase (iNOS), neutrophil elastase (NE) and other mediators in the ALI caused by PMA. In isolated rat's lungs, PMA at various doses (1, 2 and 4 mug/g lung weight) was added into the lung perfusate. Vehicle group received dimethyl sulfoxide (the solvent for PMA) 100 mug/g. We measured the lung weight changes, pulmonary arterial pressure, capillary filtration coefficient, exhaled NO, protein concentration in bronchoalveolar lavage (PCBAL) and Evan blue dye leakage. Nitrate/nitrite, methyl guanidine, proinflammatory cytokines, NE and myeloperoxidase (MPO) in lung perfusate were determined. Histopathological examination was performed. We detected the iNOS mRNA expression in lung tissue. PMA caused dose-dependent increases in variables for lung changes, and nitrate/nitrite, methyl guanidine, proinflammatory cytokines, NE and MPO in lung perfusate. The pathology was characterized by alveolar hemorrhagic edema with inflammatory cell infiltration. Scanning electron microscopy revealed endothelial damage. PMA upregulated the expression of iNOS mRNA. Our results suggest that neutrophil activation by PMA causes release of NE, upregulation of iNOS and a series of inflammatory responses leading to endothelial damage and ALI.

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Inducible nitric oxide synthase mediates cytokine release: The time course in conscious and septic rats

Cited by 39 publications

References 30 publications

Effects of Taurine on Nitric Oxide and 3-Nitrotyrosine Levels in Spleen During Endotoxemia

Effects of Taurine on Nitric Oxide and 3-Nitrotyrosine Levels in Spleen During Endotoxemia

Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

The involvement of nitric oxide, nitric oxide synthase, neutrophil elastase, myeloperoxidase and proinflammatory cytokines in the acute lung injury caused by phorbol myristate acetate

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