Table 7.6Studies of oxidative stress in animals exposed to smoke

StudyAnimals (number)Smoke exposureRoute of administrationEffect
Number of cigarettesExposure timeTime between exposure and measurement
Uotila 1982Syrian hamsters (NR)5
1 hours
2 hours
20 hours Measurement during exposureSmoking chamberExperiment 1a—Blood: MUG increased after 20 hours
Experiment 2b—Blood: MUG increased during smoking
Cotgreave et al. 1987Sprague- Dawley rats (NR)81 hour0 hoursNose onlyBAL fluid: intracellular GSH decreased; free GSH decreased; extracellular GSH decreased
Blood: GSH showed no significant change; cysteine increased
Lung tissue: cysteine showed no significant change
Bilimoria and Ecobichon 1992Sprague- Dawley rats (8)
Hartley guinea pigs (NR)
40, 120, and 240 puffsNR0, 3, and 6 hoursNose onlyLung homogenate: GSH decreased at 0 hours in rats but only at high exposures in guinea pigs; levels returned to preexposure within 3 hours
Ascorbic acid: no reduction in either species
Wright et al. 1999Rats (NR)72 hours24 hoursNose onlyLung homogenate CNOS mRNA and protein showed no significant change; INOS mRNA increased, protein showed no significant change; ENOS mRNA increased, protein showed no significant change
Cavarra et al. 2001bC57BL/6J mice with smoke exposure (35), controls (70)520 minutes0, 20, and 60 minutesSmoking chamberBAL fluid at 0 hours: trolox equivalent antioxidant capacity decreased, levels returned to preexposure within 20 minutes; glutathione disulfide increased; ascorbic acid decreased; protein thiols decreased; neither total glutathione nor vitamin E showed any significant change; 8-epi-PGF increased; prevented in a subgroup of case/controls by pretreatment with N-acetylcysteine
Plasma: 8-epi-PGF increased at 0, 20, and 60 minutes; total cell count, alveolar macrophages, polymorphonuclear neutrophils, and lymphocytes showed no significant change; human secretory leukoprotease inhibitor inactivated
Aoshiba et al. 2003aC57BL/6 mice (6)101 hour1, 3, 16, and 24 hoursSmoking chamberLung tissue: 8-oxo-dG and 4-HNE increased after 1 hour in bronchial epithelial cells and type II alveolar cells; cellularity increased after 1–16 hours
BAL fluid: 8-oxo-dG levels increased after 1 hour; no significant change after 24 hours

Source: Adapted from van der Vaart et al. 2004 with permission from BMJ Publishing Group Ltd., © 2004.

Note: 4-HNE = 4-hydroxy-2-nonenal; 8-epi-PGF2α = 8-epi-prostaglandin F; 8-oxo-dG = 7-hydroxy-8-hydroxy-2′-deoxyguanosine; BAL = bronchoalveolar lavage; CNOS = constitutive nitric oxide synthase; ENOS = endothelial nitric oxide synthese; GSH = reduced glutathione; INOS = inducible nitric oxide synthase; mRNA = messenger RNA; MUG = methylumbelliferyl glucuronide; NR = data not reported.


Lungs were isolated, ventilated with cigarette smoke, and perfused with 4-MUG.


Isolated lungs were simultaneously ventilated with cigarette smoke and perfused with MUG.

From: 7, Pulmonary Diseases

Cover of How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease
How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General.
Centers for Disease Control and Prevention (US); National Center for Chronic Disease Prevention and Health Promotion (US); Office on Smoking and Health (US).

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.