Literature DB >> 2378748

Effect of fatty acid profiles on the susceptibility of cultured rabbit tracheal epithelial cells to hyperoxic injury.

P A Dennery1, C M Kramer, S E Alpert.   

Abstract

To investigate the role of cellular fatty acid content on the susceptibility of airway epithelial cells to hyperoxic injury, monolayer cultures of rabbit tracheal epithelial (TE) cells were grown to confluence in serum-free media with or without a commercial mixture of cholesterol esters and phospholipid-rich lipoproteins (Excyte III, Miles-Pentex, Kankakee, IL) in conjunction with arachidonic acid complexed to BSA. Monolayer cultures were then exposed to control (5% CO2/air) or hyperoxic atmospheres (95% oxygen/5% CO2) for 2 h using an in vitro system in which cells were maintained at a gas-liquid interface analogous to in vivo conditions. Hyperoxic injury was assessed by cell viability (trypan blue exclusion) and by the generation of lipid peroxides measured as thiobarbituric acid (TBA) reactive substances. Changes in TE cell and cell culture effluent fatty acid content induced by exposure to control or hyperoxic atmospheres were analyzed by gas chromatography. TE cells grown in lipid-unsupplemented media had fatty acid profiles characteristic of essential fatty acid deficiency, whereas the fatty acid content of lipid-supplemented TE cells more closely resembled those of acutely recovered TE cells. Lipid-unsupplemented cells were more susceptible to hyperoxic injury as demonstrated by decreased viability and increased production of TBA-reactive substances compared to cells maintained in lipid-supplemented media. In both lipid-supplemented and unsupplemented cells, hyperoxic exposure was associated with a decreased relative cellular content of the monounsaturated and polyunsaturated fatty acids (PUFA) and an increased content of saturated fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Entities:  

Mesh:

Substances:

Year:  1990        PMID: 2378748     DOI: 10.1165/ajrcmb/3.2.137

Source DB:  PubMed          Journal:  Am J Respir Cell Mol Biol        ISSN: 1044-1549            Impact factor:   6.914


  6 in total

1.  Antenatally administered PPAR-gamma agonist rosiglitazone prevents hyperoxia-induced neonatal rat lung injury.

Authors:  Virender K Rehan; Reiko Sakurai; Julia Corral; Melissa Krebs; Basil Ibe; Kaori Ihida-Stansbury; John S Torday
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2010-08-20       Impact factor: 5.464

2.  Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress.

Authors:  S D Yan; X Chen; A M Schmidt; J Brett; G Godman; Y S Zou; C W Scott; C Caputo; T Frappier; M A Smith
Journal:  Proc Natl Acad Sci U S A       Date:  1994-08-02       Impact factor: 11.205

3.  Advanced glycation end products (AGEs) on the surface of diabetic erythrocytes bind to the vessel wall via a specific receptor inducing oxidant stress in the vasculature: a link between surface-associated AGEs and diabetic complications.

Authors:  J L Wautier; M P Wautier; A M Schmidt; G M Anderson; O Hori; C Zoukourian; L Capron; O Chappey; S D Yan; J Brett
Journal:  Proc Natl Acad Sci U S A       Date:  1994-08-02       Impact factor: 11.205

4.  BCL-2 expression or antioxidants prevent hyperglycemia-induced formation of intracellular advanced glycation endproducts in bovine endothelial cells.

Authors:  I Giardino; D Edelstein; M Brownlee
Journal:  J Clin Invest       Date:  1996-03-15       Impact factor: 14.808

5.  Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice.

Authors:  Abigail L Peterson; Jennifer F Carr; Xiangming Ji; Phyllis A Dennery; Hongwei Yao
Journal:  Metabolites       Date:  2020-08-21

6.  Metabolic dysregulation in bronchopulmonary dysplasia: Implications for identification of biomarkers and therapeutic approaches.

Authors:  Li Yue; Xuexin Lu; Phyllis A Dennery; Hongwei Yao
Journal:  Redox Biol       Date:  2021-08-13       Impact factor: 11.799

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.