PMID- 17716000
OWN - NLM
STAT- MEDLINE
DCOM- 20080221
LR  - 20191210
IS  - 1549-1684 (Print)
IS  - 1549-1684 (Linking)
VI  - 10
IP  - 4
DP  - 2007 Dec
TI  - Methionine restriction decreases endogenous oxidative molecular damage and 
      increases mitochondrial biogenesis and uncoupling protein 4 in rat brain.
PG  - 473-84
AB  - Aging plays a central role in the occurrence of neurodegenerative diseases. 
      Caloric restriction (CR) mitigates oxidative stress by decreasing the rate of 
      generation of endogenous damage, a mechanism that can contribute to the slowing 
      of the aging rate induced by this intervention. Various reports have recently 
      linked methionine to aging, and methionine restriction (MetR) without energy 
      restriction also increases life span. We have thus hypothesized that MetR can be 
      responsible, at least in part, for the decrease in endogenous oxidative damage in 
      CR. In this investigation we subjected male rats to exactly the same dietary 
      protocol of MetR that is known to increase their life span. We have found that 
      MetR: (1) decreases the mitochondrial complex I content and activity, as well as 
      complex III content, while the complex II and IV, the mitochondrial flavoprotein 
      apoptosis-inducing factor (AIF) and ATP content are unchanged; (2) increases the 
      mitochondrial biogenesis factor PGC-1alpha; (3) increases the resistance of brain 
      to metabolic and oxidative stress by increasing mitochondrial uncoupling protein 
      4 uncoupling protein 4 (UCP4); and (4) decreases mitochondrial oxidative DNA 
      damage and all five different markers of protein oxidation measured and lowers 
      membrane unsaturation in rat brain. No changes were detected for protein amino 
      acid composition. These beneficial MetR-induced changes likely derived from 
      metabolic reprogramming at the cellular and tissue level can play a key role in 
      the protection against aging-associated neurodegenerative disorders.
FAU - Naudi, Alba
AU  - Naudi A
AD  - Department of Experimental Medicine, Faculty of Medicine, University of 
      Lleida-IRBLLEIDA, c/Montserrat Roig 2, Lleida, Spain.
FAU - Caro, Pilar
AU  - Caro P
FAU - Jove, Mariona
AU  - Jove M
FAU - Gomez, Jose
AU  - Gomez J
FAU - Boada, Jordi
AU  - Boada J
FAU - Ayala, Victoria
AU  - Ayala V
FAU - Portero-Otin, Manuel
AU  - Portero-Otin M
FAU - Barja, Gustavo
AU  - Barja G
FAU - Pamplona, Reinald
AU  - Pamplona R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Rejuvenation Res
JT  - Rejuvenation research
JID - 101213381
RN  - 0 (Ion Channels)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Mitochondrial Uncoupling Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
RN  - 0 (Ppargc1a protein, rat)
RN  - 0 (RNA-Binding Proteins)
RN  - 0 (Slc25a27 protein, rat)
RN  - 0 (Transcription Factors)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - AE28F7PNPL (Methionine)
RN  - EC 7.1.1.2 (Electron Transport Complex I)
SB  - IM
MH  - Adenosine Triphosphate/analysis
MH  - Animals
MH  - Brain/*metabolism
MH  - Caloric Restriction
MH  - Diet, Protein-Restricted
MH  - Electron Transport Complex I/analysis
MH  - Ion Channels/*analysis
MH  - Male
MH  - Methionine/*administration & dosage/physiology
MH  - Mitochondrial Proteins/analysis/*metabolism
MH  - Mitochondrial Uncoupling Proteins
MH  - Nerve Tissue Proteins/metabolism
MH  - Oxidation-Reduction
MH  - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
MH  - RNA-Binding Proteins/*analysis
MH  - Rats
MH  - Rats, Wistar
MH  - Transcription Factors/*analysis
EDAT- 2007/08/25 09:00
MHDA- 2008/02/22 09:00
CRDT- 2007/08/25 09:00
PHST- 2007/08/25 09:00 [pubmed]
PHST- 2008/02/22 09:00 [medline]
PHST- 2007/08/25 09:00 [entrez]
AID - 10.1089/rej.2007.0538 [doi]
PST - ppublish
SO  - Rejuvenation Res. 2007 Dec;10(4):473-84. doi: 10.1089/rej.2007.0538.