Chronic exposure to water-pipe smoke induces alveolar enlargement, DNA damage and impairment of lung function

Abderrahim Nemmar, Suhail Al-Salam, Priya Yuvaraju, Sumaya Beegam, Javed Yasin, Badreldin H. Ali

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Background/Aim: Epidemiological evidence indicates that water-pipe smoking (WPS) adversely affects the respiratory system. However, the mechanisms underlying its effects are not well understood. Recent experimental studies reported the occurrence of lung inflammation and oxidative stress following acute and subacute exposure to WPS. Here, we wanted to verify the extent of inflammation and oxidative stress in mice chronically-exposed to WPS and to evaluate, for the first time, its effect on alveolar injury and DNA damage and their association with impairment of lung function. Methods: Mice were nose-only exposed to mainstream WPS (30 min/day; 5 days/week for 6 consecutive months). Control mice were exposed using the same protocol to atmospheric air only. At the end of the exposure period, several respiratory parameters were assessed. Results: In bronchoalveolar lavage fluid, WPS increased neutrophil and lymphocyte numbers, lactate dehydrogenase, myeloperoxidase and matrix metallopeptidase 9 activities, as well as several proinflammatory cytokines. In lung tissue, lipid peroxidation, reactive oxygen species, superoxide dismutase activity and reduced glutathione were all increased by WPS exposure. Along with oxidative stress, WPS exposure significantly increased lung DNA damage index. Histologically the lungs of WPS-exposed mice had foci of mixed inflammatory cells infiltration in the interalveolar interstitium which consisted of neutrophils, lymphocytes and macrophages. Interestingly, we found dilated alveolar spaces and alveolar ducts with damaged interalveolar septae, and impairment of lung function following WPS exposure. Conclusion: We show the persistence of lung inflammation and oxidative stress in mice chronically-exposed to WPS and demonstrate, for the first time, the occurrence of DNA damage and enlargement of alveolar spaces and ducts associated with impairment of lung function. Our findings provide novel mechanistic elucidation for the long-term effects of WPS on the respiratory system.

Original languageEnglish
Pages (from-to)982-992
Number of pages11
JournalCellular Physiology and Biochemistry
Volume38
Issue number3
DOIs
Publication statusPublished - Mar 1 2016

Fingerprint

Smoke
DNA Damage
Smoking
Lung
Water
Oxidative Stress
Respiratory System
Pneumonia
Neutrophils
Bronchoalveolar Lavage Fluid
Lymphocyte Count
Metalloproteases
L-Lactate Dehydrogenase
Nose
Lipid Peroxidation
Peroxidase
Superoxide Dismutase
Glutathione
Reactive Oxygen Species
Macrophages

Keywords

  • Alveolar injury
  • Chronic exposure
  • DNA damage
  • Inflammation
  • Lung function
  • Nose-only exposure
  • Oxidative stress
  • Water-pipe smoking

ASJC Scopus subject areas

  • Physiology

Cite this

Chronic exposure to water-pipe smoke induces alveolar enlargement, DNA damage and impairment of lung function. / Nemmar, Abderrahim; Al-Salam, Suhail; Yuvaraju, Priya; Beegam, Sumaya; Yasin, Javed; Ali, Badreldin H.

In: Cellular Physiology and Biochemistry, Vol. 38, No. 3, 01.03.2016, p. 982-992.

Research output: Contribution to journalArticle

Nemmar, Abderrahim ; Al-Salam, Suhail ; Yuvaraju, Priya ; Beegam, Sumaya ; Yasin, Javed ; Ali, Badreldin H. / Chronic exposure to water-pipe smoke induces alveolar enlargement, DNA damage and impairment of lung function. In: Cellular Physiology and Biochemistry. 2016 ; Vol. 38, No. 3. pp. 982-992.
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AB - Background/Aim: Epidemiological evidence indicates that water-pipe smoking (WPS) adversely affects the respiratory system. However, the mechanisms underlying its effects are not well understood. Recent experimental studies reported the occurrence of lung inflammation and oxidative stress following acute and subacute exposure to WPS. Here, we wanted to verify the extent of inflammation and oxidative stress in mice chronically-exposed to WPS and to evaluate, for the first time, its effect on alveolar injury and DNA damage and their association with impairment of lung function. Methods: Mice were nose-only exposed to mainstream WPS (30 min/day; 5 days/week for 6 consecutive months). Control mice were exposed using the same protocol to atmospheric air only. At the end of the exposure period, several respiratory parameters were assessed. Results: In bronchoalveolar lavage fluid, WPS increased neutrophil and lymphocyte numbers, lactate dehydrogenase, myeloperoxidase and matrix metallopeptidase 9 activities, as well as several proinflammatory cytokines. In lung tissue, lipid peroxidation, reactive oxygen species, superoxide dismutase activity and reduced glutathione were all increased by WPS exposure. Along with oxidative stress, WPS exposure significantly increased lung DNA damage index. Histologically the lungs of WPS-exposed mice had foci of mixed inflammatory cells infiltration in the interalveolar interstitium which consisted of neutrophils, lymphocytes and macrophages. Interestingly, we found dilated alveolar spaces and alveolar ducts with damaged interalveolar septae, and impairment of lung function following WPS exposure. Conclusion: We show the persistence of lung inflammation and oxidative stress in mice chronically-exposed to WPS and demonstrate, for the first time, the occurrence of DNA damage and enlargement of alveolar spaces and ducts associated with impairment of lung function. Our findings provide novel mechanistic elucidation for the long-term effects of WPS on the respiratory system.

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KW - Oxidative stress

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