Estimation of nasal epithelial lining fluid using urea as a marker

Kaulbach, Helen C.; White, Martha V.; Igarashi, Yasushi; Hahn, Barbara; Kaliner, Michael

doi:10.1016/0091-6749(93)90125-y

Cited by 70 publications

(48 citation statements)

References 29 publications

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“…Nasal application of decongestants results in the development of a concentration gradient. Assuming a total nasal epithelial lining fluid volume of 800 l/nostril (Kaulbach et al, 1993), oxymetazoline used in its current product concentration of 1.6 mM (nose sprays for adults and school children) at a dosage volume of 45 l/puff will be diluted to form a concentration gradient that refers to levels of the active substance used in our experiments (estimated mean value Ϸ 0.1 mM). Therefore, the obtained results are of relevance in situ.…”

Section: Discussionmentioning

confidence: 99%

Oxymetazoline Inhibits Proinflammatory Reactions: Effect on Arachidonic Acid-Derived Metabolites

Beck‐Speier¹,

Dayal²,

Karg³

et al. 2005

J Pharmacol Exp Ther

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The nasal decongestant oxymetazoline effectively reduces rhinitis symptoms. We hypothesized that oxymetazoline affects arachidonic acid-derived metabolites concerning inflammatory and oxidative stress-dependent reactions. The ability of oxymetazoline to model pro-and anti-inflammatory and oxidative stress responses was evaluated in cell-free systems, including 5-lipoxygenase (5-LO) as proinflammatory, 15-lipoxygenase (15-LO) as anti-inflammatory enzymes, and oxidation of methionine by agglomerates of ultrafine carbon particles (UCPs), indicating oxidative stress. In a cellular approach using canine alveolar macrophages (AMs), the impact of oxymetazoline on phospholipase A 2 (PLA 2 ) activity, respiratory burst and synthesis of prostaglandin E 2 (PGE 2 ), 15(S)-hydroxy-eicosatetraenoic acid (15-HETE), leukotriene B 4 (LTB 4 ), and 8-isoprostane was measured in the absence and presence of UCP or opsonized zymosan as particulate stimulants. In cell-free systems, oxymetazoline (0.4 -1 mM) inhibited 5-LO but not 15-LO activity and did not alter UCP-induced oxidation of methionine. In AMs, oxymetazoline induced PLA 2 activity and 15-HETE at 1 mM, enhanced PGE 2 at 0.1 mM, strongly inhibited LTB 4 and respiratory burst at 0.4/0.1 mM (p Ͻ 0.05), but did not affect 8-isoprostane formation. In contrast, oxymetazoline did not alter UCP-induced PLA 2 activity and PGE 2 and 15-HETE formation in AMs but inhibited UCP-induced LTB 4 formation and respiratory burst at 0.1 mM and 8-isoprostane formation at 0.001 mM (p Ͻ 0.05). In opsonized zymosanstimulated AMs, oxymetazoline inhibited LTB 4 formation and respiratory burst at 0.1 mM (p Ͻ 0.05). In conclusion, in canine AMs, oxymetazoline suppressed proinflammatory reactions including 5-LO activity, LTB 4 formation, and respiratory burst and prevented particle-induced oxidative stress, whereas PLA 2 activity and synthesis of immune-modulating PGE 2 and 15-HETE were not affected.

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Section: Discussionmentioning

confidence: 99%

Oxymetazoline Inhibits Proinflammatory Reactions: Effect on Arachidonic Acid-Derived Metabolites

Beck‐Speier¹,

Dayal²,

Karg³

et al. 2005

J Pharmacol Exp Ther

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“…Collection of nasal RTLFs by instillation of 5 ml saline into one nostril for 10 sec has thus been estimated to result in approximately 10-fold dilution of nasal RTLFs (158). This implies that local antioxidant concentrations, as estimated from reported nasal lavage levels listed in Table 3 (152,165,166).…”

Section: Respiratory Tract Lining Fluidsmentioning

confidence: 99%

“…As in other extracellular fluids (152)(153), the antioxidants in RTLFs are variable in nature ( (156)(157)(158). RTLF dilution by commonly performed lavage procedures has been estimated to be about 100-fold, and lower RTLF (ELF) concentrations of GSH have been reported to be in the range of 100 to 500 pM (135,144,159).…”

Section: Respiratory Tract Lining Fluidsmentioning

confidence: 99%

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Oxidative stress and antioxidants at biosurfaces: plants, skin, and respiratory tract surfaces.

Cross

Vliet

Louie

et al. 1998

Environ Health Perspect

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Atmospheric pollutants represent an important source of oxidative and nitrosative stress to both terrestrial plants and to animals. The exposed biosurfaces of plants and animals are directly exposed to these pollutant stresses. Not surprisingly, living organisms have developed complex integrated extracellular and intracellular defense systems against stresses related to reactive oxygen and nitrogen species (ROS, RNS), including 03 and NO2. Plant and animal epithelial surfaces and respiratory tract surfaces contain antioxidants that would be expected to provide defense against environmental stress caused by ambient ROS and RNS, thus ameliorating their injurious effects on more delicate underlying cellular constituents. Parallelisms among these surfaces with regard to their antioxidant constituents and environmental oxidants are presented. The reactive substances at these biosurfaces not only represent an important protective system against oxidizing environments, but products of their reactions with ROS/RNS may also serve as biomarkers of environmental oxidative stress. Moreover, the reaction products may also induce injury to underlying cells or cause cell activation, resulting in production of proinflammatory substances including cytokines. In this review we discuss antioxidant defense systems against environmental toxins in plant cell wall/apoplastic fluids, dead keratinized cells/interstitial fluids of stratum corneum (the outermost skin layer), and mucus/respiratory tract lining fluids.-Environ Health Perspect 1 06(Suppl 5): 1241-1251 (1998 The aim of this review is to highlight certain parallels between the antioxidant mechanisms responsible for protecting diverse environmentally exposed biosurfaces. Although there are numerous other environmental oxidants that contribute to surface oxidative stress (e.g., oxides of nitrogen, cigarette smoke, radiation), our focus will be on 03 as a representative environmental oxidant and on the antioxidants with which it can be expected to react at plant, skin, and respiratory tract surfaces. Although in most circumstances the oxidant can be expected to be neutralized, products of reactions with constituents of the extracellular fluids, e.g., cytotoxic aldehydes produced by reactions of 03 with extracellular lipids (12-14), may be largely responsible for cell or tissue injury by environmental toxins. Structural ConsiderationsThe similarities of the interfaces between the environment and plant and animal tissues are simplistically depicted in Figure 1. In plants, uptake of environmental toxins can be expected to occur mainly at the cell wall surface and, via the stomata, within the extracellular apoplastic fluids (15-17). The skin and the respiratory tract are the animal organs most direcdy exposed to oxidant air pollutants. Although numerous studies have documented the effects of oxidants on lungs, and have to some extent directed attention to the importance of the respiratory tract lining fluids (RTLFs) (18)(19)(20)(21)(22), only a few studies have described possible oxi...

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“…Albumin, creatinine and urea were quantified by the Beckman Synchron CX5 Delta Clinical System (Beckman Coulter Inc., Fullerton, CA, USA). Concentrations of biomarkers in NALF were adjusted for the variable dilution of the recovered epithelial lining fluid, either by calculating the absolute amount of recovered protein or by adjusting the concentration in NALF with the plasma/NALF concentration ratio of urea [21,22]. These adjustments were made for each nostril separately and then the mean value was calculated and used for the statistical analyses.…”

Section: Examination Of Study Participantsmentioning

confidence: 99%

Biomarkers of early respiratory effects in smoking adolescents

Miert¹,

Sardella²,

Bernard³

2011

Eur Respir J

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Noninvasive biomarkers can be used to evaluate airways damage caused by tobacco smoke, but studies so far have only involved adult smokers. In this study, we evaluated whether such biomarkers can detect early respiratory effects in adolescents passively or actively exposed to tobacco smoke.In a cross-sectional study of 845 adolescents (mean age 16 yrs), we measured exhaled nitric oxide (NO) and various epithelial markers in nasal lavage fluid (NALF) and serum, including Clara cell protein (CC16) and surfactant protein (SP)-D. Information about smoking habits and potential confounders was collected by questionnaire. Four groups of equal size (n536), of nonsmokers, passive smokers, light smokers (,5 cigarettes?day -1 , median 0.08 pack-yrs) and heavy smokers (o5 cigarettes?day -1 , median 0.35 pack-yrs), were matched using an automated procedure. The levels of exhaled NO and of CC16 in NALF were significantly decreased in the group of heavy smokers. A trend towards lower levels of CC16 in NALF was observed in passive smokers. There were no significant changes in serum CC16 and SP-D, which suggests that the deep lung epithelium had not yet been affected by smoking.In conclusion, tobacco smoke can cause early changes in the airways of adolescents with a cumulative smoking history of ,1 pack-yr.

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Estimation of nasal epithelial lining fluid using urea as a marker

Cited by 70 publications

References 29 publications

Oxymetazoline Inhibits Proinflammatory Reactions: Effect on Arachidonic Acid-Derived Metabolites

Oxymetazoline Inhibits Proinflammatory Reactions: Effect on Arachidonic Acid-Derived Metabolites

Oxidative stress and antioxidants at biosurfaces: plants, skin, and respiratory tract surfaces.

Biomarkers of early respiratory effects in smoking adolescents

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