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Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia
Joint Authors
Rogers, Lynette K.
Tipple, Trent E.
Dunigan-Russell, Katelyn
Li, Rui
Li, Qian
Wall, Stephanie B.
Wood, Rachael
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-01-21
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
Background.
Aurothioglucose- (ATG-) mediated inhibition of thioredoxin reductase-1 (TXNRD1) improves alveolarization in experimental murine bronchopulmonary dysplasia (BPD).
Glutathione (GSH) mediates susceptibility to neonatal and adult oxidative lung injury.
We have previously shown that ATG attenuates hyperoxic lung injury and enhances glutathione- (GSH-) dependent antioxidant defenses in adult mice.
Hypothesis.
The present studies evaluated the effects of TXNRD1 inhibition on GSH-dependent antioxidant defenses in newborn mice in vivo and lung epithelia in vitro.
Methods.
Newborn mice received intraperitoneal ATG or saline prior to room air or 85% hyperoxia exposure.
Glutamate-cysteine ligase (GCL) catalytic (Gclc) and modifier (Gclm) mRNA levels, total GSH levels, total GSH peroxidase (GPx) activity, and Gpx2 expression were determined in lung homogenates.
In vitro, murine transformed club cells (mtCCs) were treated with the TXNRD1 inhibitor auranofin (AFN) or vehicle in the presence or absence of the GCL inhibitor buthionine sulfoximine (BSO).
Results.
In vivo, ATG enhanced hyperoxia-induced increases in Gclc mRNA levels, total GSH contents, and GPx activity.
In vitro, AFN increased Gclm mRNA levels, intracellular and extracellular GSH levels, and GPx activity.
BSO prevented AFN-induced increases in GSH levels.
Conclusions.
Our data are consistent with a model in which TXNRD1 inhibition augments hyperoxia-induced GSH-dependent antioxidant responses in neonatal mice.
Discrepancies between in vivo and in vitro results highlight the need for methodologies that permit accurate assessments of the GSH system at the single-cell level.
American Psychological Association (APA)
Wall, Stephanie B.& Wood, Rachael& Dunigan-Russell, Katelyn& Li, Qian& Li, Rui& Rogers, Lynette K.…[et al.]. 2019. Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1205366
Modern Language Association (MLA)
Wall, Stephanie B.…[et al.]. Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-10.
https://search.emarefa.net/detail/BIM-1205366
American Medical Association (AMA)
Wall, Stephanie B.& Wood, Rachael& Dunigan-Russell, Katelyn& Li, Qian& Li, Rui& Rogers, Lynette K.…[et al.]. Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1205366
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205366