Commentary

Abstract

HIGHLIGHTED TOPICSCommentaryGary C. SieckGary C. Sieck Editor Journal of Applied PhysiologyPublished Online:01 Oct 2002https://doi.org/10.1152/japplphysiol.00674.2002MoreSectionsPDF (20 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat The Highlighted Topics article selected for this issue of the Journal of Applied Physiology, “Lung hypoxia: antioxidant and antiapoptotic effects of liposomal α-tocopherol,” by Minko and colleagues (p. 1550–1560), studies the effects of liposomal α-tocopherol on lung edema clearance. Pulmonary edema is a life-threatening condition caused by cardiovascular pathologies (e.g., myocardial infarct, mitral or aortic valve disease, cardiomyopathy), inhalation of noxious substances, and exposure to high altitude. Despite extensive research during the past 20 yr, effective prevention and therapy for pulmonary edema remains unclear. While investigating the mechanisms of lung injury under different pathological conditions associated with oxygen deficiency, Minko and colleagues found that “classical” lung edema associated with fluid infiltration into alveoli is preceded by transient interstitial edema. The mechanisms involved in this initial stage of pulmonary edema were found to be common to many etiologically different tissue hypoxias (e.g., those related to high altitude, hemorrhage, anemia, severe stress, etc.). Further analysis showed that lipid peroxidation and apoptosis are two main mechanisms responsible for damage to endothelial and interstitial barriers, increasing the permeability of these barriers and, consequently, the incidence of interstitial edema. These authors also found that antiapoptotic and antioxidant defenses are key mechanisms of cellular resistance to lung injury caused by hypoxia. Accordingly, they hypothesized that an increase in cellular defenses may reduce membrane damage and prevent limited interstitial edema from progressing into full alveolar lung edema. Liposomes were utilized to increase the cellular levels of the antioxidant α-tocopherol. Using liposomal α-tocopherol, these investigators pursued three main objectives: 1) to provide for the water solubility of the drug, 2) to increase the antioxidant cellular defense, and 3) to compensate (at least partially) for the alveolar phospholipid deficit caused by hypoxia. The results showed that liposomal α-tocopherol limited lipid peroxidation and apoptosis in lung tissues, reduced lung damage and disturbances in lung biomechanics, increased the efficacy of lung gas exchange, and significantly decreased the mortality of animals from lung edema, thereby supporting their hypothesis. These results indicate that liposomal α-tocopherol may be a useful therapy for the prevention and correction of lung edema.FOOTNOTES10.1152/japplphysiol.00674.2002This article has no references to display. Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationCited ByTumor-specific targeting of an anticancer drug delivery system by LHRH peptide25 August 2005 | Proceedings of the National Academy of Sciences, Vol. 102, No. 36 More from this issue > Volume 93Issue 4October 2002Pages 1549-1549 Copyright & PermissionsCopyright © 2002 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00674.2002History Published online 1 October 2002 Published in print 1 October 2002 Metrics