Nasal Secretion of the Ozone Scavenger Uric Acid

Peden, David B.; Swiersz, Melanie; Ohkubo, Kimihiro; Hahn, Barbara; Emery, Brian E.; Kaliner, Michael

doi:10.1164/ajrccm/148.2.455

Cited by 59 publications

(45 citation statements)

References 20 publications

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“…In support of this, increases in UA levels were found to correlate well with lactoferrin [29], a protein predominately derived from mucosal gland secretions. De novo synthesis of UA within the nasal epithelium seems an unlikely source, as the concentration and activity of xanthine dehydrogenase within the nasal epithelium are low [29]. Also, the time course of repletion is incompatible with such an explanation.…”

Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

“…PEDEN et al [29] demonstrated that NL fluid UA concentrations are increased following cholinergic stimulation of the airways, suggesting that glandular secretion may be important. In support of this, increases in UA levels were found to correlate well with lactoferrin [29], a protein predominately derived from mucosal gland secretions. De novo synthesis of UA within the nasal epithelium seems an unlikely source, as the concentration and activity of xanthine dehydrogenase within the nasal epithelium are low [29].…”

Section: Discussionmentioning

confidence: 99%

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Ozone-induced lung function decrements do not correlate with early airway inflammatory or antioxidant responses

Blomberg¹,

Mudway²,

Nordenhäll³

et al. 1999

Eur Respir J

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To obtain information on the real-time events occurring within human respiratory tract lining fluids (RTLFs) during ozone exposure, sequential nasal lavage was performed on 13 human volunteers exposed on separate occasions to 0.2 parts per million O 3 and filtered air (2-h exposures, with intermittent exercise).Nasal lavage was performed and blood samples obtained at four time points throughout each exposure: pre-exposure (Pre-E), 1 h into exposure (1h-E), immediately postexposure (0h-PE) and 1 h post-exposure (1h-PE). Endobronchial mucosal biopsies were obtained at 1.5 h-post exposure (1.5 h-PE).Nasal RTLF neutrophilia was not apparent during, or 1.5 h after, O 3 exposure. Furthermore, activation of the pre-existing neutrophil population did not occur. Airway permeability was not altered by this O 3 exposure regimen. Sequential lavage resulted in significant washout of RTLF ascorbic acid, reduced glutathione, extracellular superoxide dismutase and myeloperoxidase at 1h-E, 0h-PE and 1.5h-PE relative to baseline Pre-E values. In contrast, RTLF uric acid (UA), total protein and albumin concentrations did not display washout kinetics. Of the antioxidants examined, only UA was clearly depleted by O 3 , concentrations, falling by 6.22 mmol . L -1 at 1h-E, compared with 1.61 mmol . L -1 (p<0.01) during control air exposure. The establishment of a new pseudo-steady-state concentration of RTLF UA (70% of Pre-E values) during the second hour of O 3 exposure was coincident with a small but significant increase in plasma UA concentration (19.27 (O 3 ) versus 1.95 mmol . L -1 (air), p<0.05).These data demonstrate that inhalation of 0.2 parts per million O 3 results in the depletion of nasal respiratory tract lining fluid uric acid and that this regional loss of uric acid leads to a small increase in plasma uric acid concentration. Whilst the reaction of uric acid with inspired O 3 may confer protection locally, the role of upper airway uric acid as a sink for inhaled O 3 is not supported by these findings.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Ozone-induced lung function decrements do not correlate with early airway inflammatory or antioxidant responses

Blomberg¹,

Mudway²,

Nordenhäll³

et al. 1999

Eur Respir J

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“…Several investigators including the present authors suspect that the majority of RTLF uric acid is derived from the circulation in much the same way as vitamin C. However, this cannot be the only source of uric acid in the upper airways, especially the nasal cavity, where RTLF has much higher uric acid concentrations than in the lower airways [23]. De novo synthesis of uric acid within the nasal epithelium seems an unlikely source, as the concentration and activity of xanthine dehydrogenase within the nasal epithelium is low [26]. It is likely that high concentrations of uric acid in the upper airways are achieved through active secretion of uric acid from cells lining the respiratory tract.…”

Section: The Respiratory Tract Lining Fluid Antioxidant Poolmentioning

confidence: 99%

“…RTLF is a two layer structure, comprising a lower aqueous Sol phase and an upper mucus, Gel phase. PEDEN et al [26] have demonstrated that in the nasal cavity, RTLF Sol phase uric acid concentration is increased following cholinergic stimulation of the airways. Furthermore, they demonstrated that the increase in uric acid correlated positively with lactoferrin concentration, but not with albumin.…”

Section: The Respiratory Tract Lining Fluid Antioxidant Poolmentioning

confidence: 99%

Air pollution and the elderly: oxidant/antioxidant issues worth consideration

Kelly¹,

Dunster²,

Mudway³

2003

European Respiratory Journal

105

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The elderly are frequently classified as being particularly susceptible to air pollution. The basis of this increased sensitivity is not known but it is likely that it is linked to age-related impaired function of the lung. However, given this uncertainty and increased impact of air pollution of this section of the community there is a need to explore the mechanisms involved.Gaseous air pollutants such as ozone and nitrogen dioxide, or many of the components adsorbed onto the surface of respirable particles, are either powerful oxidants or capable of generating free radicals. If unabated, oxidants can cause injury to the delicate cells that line the respiratory tract. Small molecular weight antioxidant defences present in respiratory tract lining fluid (RTLF) represent the first line of defence against a range of oxidants that enter the lung. The quantity and quality of the RTLF airways antioxidant network are, therefore, likely to be important determinants of the impact of the oxidant challenge on the underlying respiratory epithelium.As yet, comprehensive information on the distribution and variability of respiratory tract lining fluid antioxidant defences is only available in young, mainly healthy volunteers. Studies undertaken in patients with a range of respiratory diseases suggest that marked changes in the distribution of respiratory tract lining fluid antioxidants can occur. Information is not currently available on the impact of ageing on the respiratory tract lining fluid antioxidant defence network. As several respiratory tract lining fluid antioxidants are of dietary origin, the elderly, who often have different dietary patterns to younger individuals, may have decreased availability of important antioxidants. Given these possibilities, a better understanding of respiratory tract lining fluid antioxidant defences in the aged lung is warranted.

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