Cited by 167Cell Adhesion Molecules ResearchVitamin C and Antioxidants ResearchAntioxidant Activity and Oxidative Stress

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

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Lehr, H A, Frei, B, Arfors, K E·1994·Proceedings of the National Academy of Sciences

Abstract

A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro- and macrovascular endothelium. A previous study, using a skinfold chamber model for intravital fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro- and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 +/- 11.0 vs. 149.6 +/- 38.7 leukocytes per mm2, P < 0.01; arterioles, 8.5 +/- 4.2 vs. 54.3 +/- 21.6 leukocytes per mm2, P < 0.01; aortas, 0.8 +/- 0.4 vs. 12.4 +/- 5.6 leukocytes per mm2, P < 0.01; means +/- SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CS-induced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 +/- 22.2 microM, n = 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.

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Crossref · 10.1073/pnas.91.16.7688

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Authors
Lehr, H. A., Frei, B., & Arfors, K. E.
Affiliations
Institut für Chirurgische Forschung (DE)
Venue
Proceedings of the National Academy of Sciences
Published
1994-08-02
Volume
91
Issue
16
Pages
7688-7692
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2052075519
Cited by
167
References
42
Citations by year
2026: 1 · 2025: 1 · 2024: 5 · 2023: 2 · 2022: 1 · 2020: 5 · 2019: 2 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 7 · 2013: 3 · 2012: 3
FWCI
3.88
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (7r29hl049954-05)
  • National Heart, Lung, and Blood Institute (HL49954)
Topics
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Health Sciences › Nursing › Nutrition and Dietetics › Vitamin C and Antioxidants Research
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
vitamin C, cigarette smoke, leukocyte adhesion, leukocyte aggregation, platelet aggregation, endothelium, atherosclerosis, emphysema, antioxidants, vitamin E, probucol, intravital microscopy, hamster model, cardiovascular disease, lung disease
MeSH terms
Animals, Aorta, Ascorbic Acid, Cell Adhesion, Cell Aggregation, Endothelium, Vascular, Cricetinae, Leukocytes, Mesocricetus, Microcirculation, Microscopy, Electron, Scanning, Microscopy, Fluorescence, Probucol, Staining and Labeling, Superoxides, Vitamin E, Smoke Inhalation Injury, Reactive Oxygen Species

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