The Granular Type II Pneumonocyte and Lung Antioxidant Defense

Editorials1 March 1974The Granular Type II Pneumonocyte and Lung Antioxidant DefenseCARROLL E. CROSS, M.D.CARROLL E. CROSS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-80-3-409 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTwo cell types predominate in mammalian alveolar epithelium: [1] Type I cells (membranous pneumonocytes), which have a small, nucleated cell body with attenuated peripheral cytoplasm containing a relative paucity of intracytoplasmic organelles, and which cover most of the alveolar surface; and [2] Type II cells (granular pneumonocytes), which are nearly cuboidal with abundant cytoplasmic organelles, including moderate amounts of endoplasmic reticulum, ribosomes, and lamellar inclusions, and which cover areas of the alveolar surface not lined by type I cells. The lamellar inclusions of the type II cells represent sites of synthesis of pulmonary surfactant, the phospholipid-rich substance primarily responsible for...References1. PATTLE R: Surface lining of lung alveoli. Physiol Rev 45:48-79, 1965 CrossrefMedlineGoogle Scholar2. SPENCER H: Pathology of the Lung (Excluding Pulmonary Tuberculosis). Second edition. Oxford, Pergamon Press Inc., 1968 Google Scholar3. KAPANCIWEIBELKAPLAN YEH: Pathogenesis and reversibility of the pulmonary lesions of oxygen toxicity in monkeys. II. Ultrastructural and morphometric studies. Lab Invest 20:101-118, 1969 MedlineGoogle Scholar4. BOWDENADAMSON DI: Reparative changes following pulmonary cell injury. Ultrastructural, cytodynamic and surfactant studies after oxygen exposure. Arch Pathol 92:279-283, 1971 MedlineGoogle Scholar5. ADAMSONBOWDEN ID: The type II cells as progenitor of alveolar epithelial regeneration. A cytodynamic study in mice after exposure to oxygen. 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Author, Article, and Disclosure InformationAffiliations: University of California School of Medicine Davis, California PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByThe alveolar type II epithelial cell: A multifunctional pneumocyteAcute Lung Injury and Positive End Expiratory PressureAlcohol and the Respiratory TractPostnatal tolerance to NO2 toxicityAge-Related Differences in GSH-Shuttle Enzymes in NO 2 – or O 3 –Exposed Rat LungsCorrelation between Morphological and Biochemical Alterations in the Rat Lung Exposed to Nitrogen DioxidePathogenesis of nitrogen dioxide‐induced respiratory lesions in reference to respiratory clearance of inhaled participatesThe covalent binding of 3-methylindole metabolites to bovine tissueNormobaric Oxygen Toxicity of the LungOrigin and Significance of Intranuclear Tubular Inclusions in Type II Pulmonary Alveolar Epithelial Cells of Patients with Bleomycin and Busulfan ToxicityOzone Sensitivity in Aging WI-38 Cells based on Acid Phosphatase ContentBiochemical and morphologic investigation of the influence of chlorphentermine and subsequent withdrawal on newborn rat lungStimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxideA comparative ultrastructural and biochemical study between the effects of chlorphentermine and phentermine on rat lungAlcohol and the lungPrimary Pulmonary Responses to Toxic AgentsBiochemical Effect of Ozone Exposure in Rats Exposed to Cigarette SmokeRole of metabolic activation in the pathogenesis of chemically induced pulmonary disease: mechanism of action of the lung-toxic furan, 4-ipomeanol.Proliferation of type II alveolar cells: A review of common responses in toxic lung injuryBiochemical parameters of BHT-induced cell growth in mouse lungLung growth in mice after a single dose of butylated hydroxytoluenePulmonary surfactant: A surface chemistry viewpoint 1 March 1974Volume 80, Issue 3Page: 409-411KeywordsCytoplasmEpitheliumHealth services researchLungsPneumoniaPrevention, policy, and public healthPulmonary diseasesRibosomes Issue Published: 1 March 1974 PDF DownloadLoading ...