Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids

Green, Laura C.; Wagner, David; Glogowski, Joseph A.; Skipper, Paul L.; Wishnok, John S.; Tannenbaum, Steven R.

doi:10.1016/0003-2697(82)90118-x

Cited by 10,825 publications

(5,497 citation statements)

References 11 publications

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“…Gastric nitric oxide levels were measured as total nitrate/nitrite levels with the use of the Griess reagent (Green et al., 1982). Briefly, the stomach homogenate was mixed with Griess reagent and determined at wavelength of 540 nm using a microplate reader (Tecan, Männedorf, Switzerland).…”

Section: Methodsmentioning

confidence: 99%

Protective effects of a triple‐fermented barley extract (FBe) against HCl/EtOH‐induced gastric mucosa damage in mice

Lim¹,

Song

Park

et al. 2018

Food Science & Nutrition

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This study was designed to observe the possible protective effects of a triple‐fermented barley (Hordeum vulgare L.) extract (FBe) obtained by saccharification and using Saccharomyces cerevisiae and Weissella cibaria in alleviating gastric damage induced by a hydrochloric acid (HCl) and ethanol (EtOH) mixture in mice. After oral administration of FBe (300, 200, and 100 mg/kg) followed by 1 hr before and after the single treatment of HCl/EtOH (H/E) mixture, the hemorrhagic lesion scores, histopathology of the stomach, gastric nitrate/nitrite content, lipid peroxidation, and antioxidant defense systems including catalase and superoxide dismutase activities were observed. Following a single oral treatment of H/E‐induced gastric damages as measured by hemorrhagic gross lesions and histopathological gastric, ulcerative lesions were significantly and dose‐dependently (p < 0.01 or p < 0.05) inhibited in mice, when all three different doses of FBe were administered as compared to those in H/E control mice. In particular, FBe also increased gastric nitrate/nitrite content and strengthened the antioxidant defense, with a decrease in the level of gastric lipid peroxidation, but increased the activities of CAT and SOD. Moreover, the effects of FBe are comparable to that of ranitidine, a reference drug. The obtained results suggest that this fermented barley extract prevented mice from H/E‐induced gastric mucosal damages through the suppression of inflammatory responses and oxidative stress‐responsive free radicals. Thus, FBe can be useful to treat patients suffering from gastric mucosal disorders as a potent food supplement, and thereby, it would increase the necessity of application in the food industry.

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Section: Methodsmentioning

confidence: 99%

Protective effects of a triple‐fermented barley extract (FBe) against HCl/EtOH‐induced gastric mucosa damage in mice

Lim¹,

Song

Park

et al. 2018

Food Science & Nutrition

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“…Medium nitrite assay (Green et al, 1982) Sulfanilamide (1% in 3M HCl; w v 71 ) and an equal volume of N-(1-naphthyl) ethylendiammine dihydrochloride (0.02% in water) were added to each sample (including a standard curve). Optical density (OD) was measured by means of a microplate reader (l=545 nm) after 30 min incubation at room temperature.…”

Section: Cell Culturesmentioning

confidence: 99%

Divergent effects of corticotropin releasing hormone on endothelial cell nitric oxide synthase are associated with different expression of CRH type 1 and 2 receptors

Cantarella

Lempereur

Lombardo

et al. 2001

British J Pharmacology

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1 Endothelium is a target for an array of factors involved in in¯ammation. Endothelial cells express receptors for CRH, a neuropeptide produced during in¯ammation. We report both the concentration-dependent inhibitory e ect of CRH upon cytokine-stimulated nitrite release by H5V murine endothelioma cells, and its stimulatory one in HUVEC cells. 2 Western blot analysis showed that CRH inhibits cytokine-stimulated iNOS protein in H5V cells, and, instead, potentiated it in HUVEC cells. 3 H5V cells expressed both CRH receptors (CRH-R1 and R2) mRNAs, whereas HUVEC cells expressed the CRH-R2 mRNA solely. 4 CRH increased medium nitrites and iNOS protein expression in H5V cells pretreated with the selective CRH-R1 antagonist CP 154,526. However, the selective CRH-R2 antagonist anti-Svg-30 failed to produce similar e ects. In fact, anti-Svg-30 inhibited CRH-induced increase of nitrite release and iNOS expression in HUVEC cells. 5 Our results con®rm the activating role of CRH on endothelial cells, although it suggests its possible inhibitory role in the late phase of the in¯ammatory response. NO-mediated e ects of CRH on endothelial cells could be exploited in therapeutic strategies related to in¯ammatory and/or degenerative diseases.

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“…Griess reagent (Green et al, 1982) was used for measurement of NO2-and cadmium filings for conversion of NO3-to NO2-(Davison and Woof, 1978).…”

Section: Measurement Of Capillary Leakage and No Metabolitesmentioning

confidence: 99%

NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, ameliorates interleukin 2-induced capillary leakage and reduces tumour growth in adenocarcinoma-bearing mice

Orucevic

Lala

1996

Br J Cancer

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Summary We tested whether NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, can prevent interleukin 2 (IL-2)-induced capillary leakage in tumour-bearing mice without compromising the therapeutic benefits of IL-2. C3H/HeJ female mice transplanted s.c. with 2.5 x 105 C3-L5 mammary carcinoma cells were treated with: nothing, IL-2 (ten injections of 15 000 Cetus units i.p. every 8 h), L-NAME (0.1, 0.5, or 1 mg ml-1 drinking water), IL-2+L-NAME (0.1 or 0.5 or 1 mg ml-' drinking water).Therapies were given in one round (IL-2, days 10-13; L-NAME, days 9-13) or in two rounds (IL-2, days 10-13 and 20-23; L-NAME, days 9-13 and days 19-23) after tumour transplantation. Capillary leakage was measured from the water contents of the pleural cavities, lungs, spleen and kidneys. Effects of the therapies on the primary tumour size and the number of spontaneous lung metastases were also recorded. NO production was measured as the nitrite+nitrate levels in the serum and in the pleural effusion. After the first round of therapies, addition of L-NAME significantly reduced IL-2-induced pulmonary oedema and water retention in the spleen in a dose-dependent manner. It also significantly reduced the IL-2-induced rise in NO levels in the serum and pleural fluid, but did not affect IL-2-induced pleural effusion or water retention in the kidney. At later stages of tumour growth (day 23), tumours themselves induced significant fluid retention in the lungs and the kidney, which was not aggravated further with the second round of IL-2 therapy. At this time, L-NAME therapy alone ameliorated tumour-induced pulmonary oedema. During both rounds of therapy different doses of L-NAME alone caused a reduction of primary tumour growth as well as spontaneous lung metastases, which improved further with the addition of IL-2. The combination therapy was at least as effective as IL-2 therapy. In summary, L-NAME had anti-tumour effects in vivo, reduced the severity of IL-2-induced capillary leakage in some organs and did not compromise anti-tumour efficacy of IL-2 therapy. Thus, L-NAME could be a valuable adjunct to IL-2-based cancer therapy.Keywords: capillary leak syndrome; interleukin 2 cancer immunotherapy; mammary adenocarcinoma; nitric oxide; NG-nitro-L-arginine methyl ester Interleukin 2 (IL-2) therapy, alone or in combination with ex vivo-generated lymphokine-activated killer (LAK) cells, can cause tumour regression in mice (Rosenberg et al., 1985;Ettinghausen et al., 1988) and in man (Rosenberg, 1989;Fisher et al., 1988; Dutcher et al., 1989;Parkinson et al., 1990). Widespread clinical use of IL-2 has been limited by the low rate of complete remission and by severe toxicity Siegel and Puri, 1991). Capillary leak syndrome is a major side-effect of high-dose IL-2 therapy, characterised by retention of extravascular fluid and hypotension (Siegel and Puri, 1991). It has been observed in humans (Siegel and Puri, 1991; Margolin et al., 1989;Rosenberg et al., 1987) al., 1985) and tumour necrosis factor (TNF)-ca...

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Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids

Cited by 10,825 publications

References 11 publications

Protective effects of a triple‐fermented barley extract (FBe) against HCl/EtOH‐induced gastric mucosa damage in mice

Protective effects of a triple‐fermented barley extract (FBe) against HCl/EtOH‐induced gastric mucosa damage in mice

Divergent effects of corticotropin releasing hormone on endothelial cell nitric oxide synthase are associated with different expression of CRH type 1 and 2 receptors

NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, ameliorates interleukin 2-induced capillary leakage and reduces tumour growth in adenocarcinoma-bearing mice

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