Loss of methionine sulfoxide reductases increases resistance to oxidative stress.
Animals
Catalysis
Methionine
/ analogs & derivatives
Methionine Sulfoxide Reductases
/ genetics
Mice, Transgenic
/ genetics
NF-E2-Related Factor 2
/ genetics
Oxidation-Reduction
/ drug effects
Oxidative Stress
/ genetics
Paraquat
/ pharmacology
Reperfusion Injury
/ drug therapy
Stress, Physiological
/ genetics
Ischemia-reperfusion
Methionine sulfoxide reductases
Methionine-methionine sulfoxide signaling
Oxidative defenses
Oxidative stress
Paraquat
Journal
Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
15
08
2019
revised:
07
10
2019
accepted:
08
10
2019
pubmed:
14
10
2019
medline:
4
9
2020
entrez:
14
10
2019
Statut:
ppublish
Résumé
Oxidation of methionine residues to methionine sulfoxide scavenges reactive species, thus protecting against oxidative stress. Reduction of the sulfoxide back to methionine by methionine sulfoxide reductases creates a cycle with catalytic efficiency. Protection by the methionine sulfoxide reductases is well documented in cultured cells, from microorganisms to mammals. However, knocking out one or two of the 4 mammalian reductases had little effect in mice that were not stressed. We hypothesized that the minimal effect is due to redundancy provided by the 4 reductases. We tested the hypothesis by creating a transgenic mouse line lacking all 4 reductases and predicted that this mouse would be exceptionally sensitive to oxidative stress. The mutant mice were phenotypically normal at birth, exhibited normal post-natal growth, and were fertile. Surprisingly, rather than being more sensitive to oxidative stress, they were more resistant to both cardiac ischemia-reperfusion injury and to parenteral paraquat, a redox-cycling agent. Resistance was not a result of hormetic induction of the antioxidant transcription factor Nrf2 nor activation of Akt. The mechanism of protection may be novel.
Identifiants
pubmed: 31606431
pii: S0891-5849(19)31342-5
doi: 10.1016/j.freeradbiomed.2019.10.006
pmc: PMC6891793
mid: NIHMS1543005
pii:
doi:
Substances chimiques
NF-E2-Related Factor 2
0
Nfe2l2 protein, mouse
0
Methionine
AE28F7PNPL
Methionine Sulfoxide Reductases
EC 1.8.4.-
Paraquat
PLG39H7695
methionine sulfoxide
XN1XVI4B2C
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
374-384Subventions
Organisme : Intramural NIH HHS
ID : Z01 HL000225-31
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA HL000225
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA HL002066
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA HL002066-10
Pays : United States
Informations de copyright
Published by Elsevier Inc.
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