Two Faces of Vitamin E in the Lung
Year: 2014
Type: article
Abstract: The hypothesis for tocopherol isoform-dependent effects on asthma prevalence by Cook-Mills and colleagues (1) is derived in part from their important animal work, but also their interpretation of our own work with g-tocopherol (gT) in experimental asthma.Although we have recently demonstrated that gT-enriched supplements can reduce endotoxin-induced neutrophil responses in human lung (2), we think the authors misinterpret our results in experimental asthma models when they conclude that gT was effective against neutrophilic, but not eosinophilic, inflammation.Both our results with antigen-induced asthma and rhinitis in rats (3) and ozone-induced exacerbation of allergic rhinitis (4) demonstrate 70-100% reduction in tissue or lavage eosinophils.We saw no effect of gT on any attendant neutrophil airway inflammation.Our results were also striking for the complete abolition by gT of mucous cell metaplasia in nasal and pulmonary airways, which is a key feature of clinical rhinitis and asthma.Therefore, our results with the allergic brown Norway rats are opposed to the enhanced allergic responses associated with gT, as described in vitro and in BALB/c mice (5, 6).The use of different rodent species (brown Norway rat vs. BALB/c mouse) may contribute to the disparate observations in these animal models.Furthermore, we provided gT by oral delivery rather than by the subcutaneous route in mice, which would bypass liver metabolism.This is an important distinction considering that the antiinflammatory metabolites of gT are known to be more potent than those of its precursor in inhibiting COX-2-and 5-LOXmediated eicosanoids (7,8).Epidemiologic data suggesting positive correlations between plasma gT levels and diseases including lung disease are intriguing.However, there are many interpretations that can be made from these associations.One is, as the authors suggest, that gT promotes lung and inflammatory disease.A second is that these diseases result in an increase of gT as a response to ongoing disease.A third is that gT may be a co-nutrient with other agents that promote disease.Indeed, many plant oils that are commonly used in the United States but not Europe (such as corn oil and soybean oil) not only contain high levels gT but are also high in polyunsaturated fatty acids and n-6 fatty acids, which are known to contribute oxidative stress and promote inflammation.Thus, the apparent effect of gT may be a result of the polyunsaturated fatty acids and n-6 fatty acids contained in these oils.Interestingly, safflower and olive oils, which contain relatively
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2017707590