Stimulation of Erythrocyte Membrane Blebbing by Naproxen Sodium.
calcium
cell size
eryptosis
oxidative stress
Journal
Dose-response : a publication of International Hormesis Society
ISSN: 1559-3258
Titre abrégé: Dose Response
Pays: United States
ID NLM: 101308899
Informations de publication
Date de publication:
Historique:
received:
28
07
2019
revised:
24
10
2019
accepted:
10
12
2019
entrez:
28
1
2020
pubmed:
28
1
2020
medline:
28
1
2020
Statut:
epublish
Résumé
Naproxen sodium is a nonsteroidal anti-inflammatory drug (NSAID) having antipyretic and analgesic properties, mainly used for the treatment of rheumatoid arthritis and osteoarthritis. Eryptosis is an alternative term used for suicidal erythrocyte death. In the current study, eryptotic effect of naproxen sodium characterized by membrane blebbing was investigated in erythrocytes after 48 hours of treatment with different concentrations (1-25 µM). The experimental work related to investigation of eryptosis was done by cell size measurement and confirmation of calcium role in the induction of membrane blebbing. As a possible mechanism of eryptosis, oxidative stress induced by naproxen sodium was determined by catalase, glutathione peroxidase, and superoxide dismutase activities. Similarly, hemolytic effect of naproxen sodium was also determined by hemolysis measurement. Results of our study illustrated that the therapeutic doses (10-25 µM) of naproxen sodium induce oxidative stress, confirmed by significant decrease in superoxide dismutase, catalase, and glutathione peroxidase activities that lead to the triggering of cell death by eryptosis and hemolysis.
Identifiants
pubmed: 31983907
doi: 10.1177/1559325819899259
pii: 10.1177_1559325819899259
pmc: PMC6961146
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1559325819899259Informations de copyright
© The Author(s) 2020.
Déclaration de conflit d'intérêts
Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Références
J Biol Regul Homeost Agents. 2016 Jul-Sep;30(3):785-788
pubmed: 27655498
J Appl Toxicol. 2001 Jan-Feb;21(1):69-73
pubmed: 11180282
Res Vet Sci. 2014 Feb;96(1):147-52
pubmed: 24388762
Cell Death Differ. 2001 Dec;8(12):1197-206
pubmed: 11753567
Dose Response. 2019 Aug 11;17(3):1559325819869076
pubmed: 31447619
Toxins (Basel). 2013 Apr 19;5(4):703-16
pubmed: 23604064
J Pharmacol Exp Ther. 2007 Aug;322(2):453-60
pubmed: 17473175
Physiol Res. 2015;64(6):891-6
pubmed: 26047376
Chemosphere. 2017 Dec;188:414-423
pubmed: 28898774
Cureus. 2019 Apr 18;11(4):e4493
pubmed: 31259111
Eur J Pharmacol. 2017 Jun 15;805:51-57
pubmed: 28315341
Ecotoxicol Environ Saf. 2018 Jun 7;161:270-280
pubmed: 29886314
Cell Physiol Biochem. 2018;50(6):2283-2295
pubmed: 30423572
Cell Physiol Biochem. 2013;32(6):1600-9
pubmed: 24335345
Toxins (Basel). 2015 Apr 23;7(5):1396-410
pubmed: 25915718
Basic Clin Pharmacol Toxicol. 2014 Nov;115(5):396-402
pubmed: 24717091
Int J Biochem Cell Biol. 2012 Aug;44(8):1236-43
pubmed: 22561748
J Biol Regul Homeost Agents. 2017 Apr-Jun;31(2):419-424
pubmed: 28685547
Toxins (Basel). 2014 May 13;6(5):1559-74
pubmed: 24828755
Mol Nutr Food Res. 2009 Apr;53(4):431-40
pubmed: 19065580
Biophys J. 2008 Mar 1;94(5):1836-53
pubmed: 17921219
Cell Death Differ. 2003 Feb;10(2):249-56
pubmed: 12700653
Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1183-92
pubmed: 16910766
J Physiol. 2002 Mar 15;539(Pt 3):847-55
pubmed: 11897854
Cell Physiol Biochem. 2012;30(3):512-22
pubmed: 22814298
Blood Transfus. 2017 May;15(3):218-221
pubmed: 28518048