Lung vitamin E transport processes are affected by both age and environmental oxidants in mice
Creators
- 1. Center for Comparative Respiratory Biology and Medicine, Department of Internal Medicine, University of California Davis, Davis, CA 95616 (United States) and Department of Physiology, University of Siena, Siena via Aldo Moro, 53100 (Italy)
- 2. Center for Comparative Respiratory Biology and Medicine, Department of Internal Medicine, University of California Davis, Davis, CA 95616 (United States)
- 3. Western Regional Research Center, Agricultural Research Service, US Department of Agriculture, Albany, CA 94710 (United States)
- 4. Department of Nutrition, University of California Davis, Davis, CA 95616 (United States)
Description
Despite the physiological importance of alpha-tocopherol (AT), the molecular mechanisms involved in maintaining cellular and tissue tocopherol levels remain to be fully characterized. Scavenger receptor B1 (SRB1), one of a large family of scavenger receptors, has been shown to facilitate AT transfer from HDL to peripheral tissues via apo A-1-mediated processes and to be important in the delivery of AT to the lung cells. In the present studies the effects of age and two environmental oxidants ozone (O3) (0.25 ppm 6 h/day) and cigarette smoke (CS) (60 mg/m3 6 h/day) for 4 days on selected aspects of AT transport in murine lung tissues were assessed. While AT levels were 25% higher (p < 0.05) and 15% lower (p < 0.05) in plasma and lung tissue, respectively, in aged versus young mice, acute environmental exposure to O3 or CS at the doses used had no effect. Gene expression levels, determined by RT-PCR of AT transport protein (ATTP), SRB1, CD36, ATP binding cassette 3 (ABCA3) and ABCA1 and protein levels, determined by Western blots for SRB1, ATTP and ABCA1 were assessed. Aged mouse lung showed a lower levels of ATTP, ABCA3 and SRB1 and a higher level CD36 and ABCA1. Acute exposure to either O3 or CS induced declines in ATTP and SRB1 in both aged and young mice lung. CD36 increased in both young and aged mice lung upon exposure to O3 and CS. These findings suggest that both age and environmental oxidant exposure affect pathways related to lung AT homeostasis and do so in a way that favors declines in lung AT. However, given the approach taken, the effects cannot be traced to changes in these pathways or AT content in any specific lung associated cell type and thus highlight the need for further follow-up studies looking at specific lung associated cell types
Additional details
Identifiers
- DOI
- 10.1016/j.taap.2007.04.010;
- PII
- S0041-008X(07)00192-5;
Publishing Information
- Journal Title
- Toxicology and Applied Pharmacology
- Journal Volume
- 222
- Journal Issue
- 2
- Journal Page Range
- p. 227-234
- ISSN
- 0041-008X
- CODEN
- TXAPA9
INIS
- Country of Publication
- United States
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 39006811
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- ACUTE EXPOSURE; AGING; ATP; ENVIRONMENTAL EXPOSURE; GENES; HOMEOSTASIS; LUNGS; MICE; OXIDIZERS; OZONE; POLYMERASE CHAIN REACTION; RECEPTORS; RESPIRATORY TRACT CELLS; TOBACCO SMOKES; VITAMIN E
- Descriptors DEC
- AEROSOLS; ANIMAL CELLS; ANIMALS; BODY; COLLOIDS; DISPERSIONS; GENE AMPLIFICATION; MAMMALS; MEMBRANE PROTEINS; NUCLEOTIDES; ORGANIC COMPOUNDS; ORGANS; PROTEINS; RESIDUES; RESPIRATORY SYSTEM; RODENTS; SMOKES; SOLS; SOMATIC CELLS; VERTEBRATES; VITAMINS
Optional Information
- Copyright
- Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.