PMID- 28642067
OWN - NLM
STAT- MEDLINE
DCOM- 20180412
LR  - 20201209
IS  - 1873-4596 (Electronic)
IS  - 0891-5849 (Linking)
VI  - 110
DP  - 2017 Sep
TI  - Caloric restriction protects livers from ischemia/reperfusion damage by 
      preventing Ca(2+)-induced mitochondrial permeability transition.
PG  - 219-227
LID - S0891-5849(17)30646-9 [pii]
LID - 10.1016/j.freeradbiomed.2017.06.013 [doi]
AB  - Caloric restriction (CR) promotes lifespan extension and protects against many 
      pathological conditions, including ischemia/reperfusion injury to the brain, 
      heart and kidney. In the liver, ischemia/reperfusion damage is related to 
      excessive mitochondrial Ca(2+) accumulation, leading to the mitochondrial 
      permeability transition. Indeed, liver mitochondria isolated from animals 
      maintained on CR for 4 months were protected against permeability transition and 
      capable of taking up Ca(2+) at faster rates and in larger quantities. These 
      changes were not related to modifications in mitochondrial respiratory activity, 
      but rather to a higher proportion of ATP relative to ADP in CR liver 
      mitochondria. Accordingly, both depletion of mitochondrial adenine nucleotides 
      and loading mitochondria with exogenous ATP abolished the differences between CR 
      and ad libitum (AL) fed groups. The prevention against permeability transition 
      promoted by CR strongly protected against in vivo liver damage induced by 
      ischemia/reperfusion. Overall, our results show that CR strongly protects the 
      liver against ischemia/reperfusion and uncover a mechanism for this protection, 
      through a yet undescribed diet-induced change in liver mitochondrial Ca(2+) 
      handling related to elevated intramitochondrial ATP.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Menezes-Filho, Sergio L
AU  - Menezes-Filho SL
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, SP, Brazil. Electronic address: smenezes@iq.usp.br.
FAU - Amigo, Ignacio
AU  - Amigo I
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, SP, Brazil. Electronic address: iamigo@iq.usp.br.
FAU - Prado, Fernanda M
AU  - Prado FM
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, SP, Brazil. Electronic address: fmprado@iq.usp.br.
FAU - Ferreira, Natalie C
AU  - Ferreira NC
AD  - Disciplina de Cirurgia Geral e do Trauma, Laboratorio de Fisiopatologia 
      Cirurgica-LIM-62, Faculdade de Medicina, Universidade de Sao Paulo, SP, Brazil. 
      Electronic address: natalie.chaves@gmail.com.
FAU - Koike, Marcia K
AU  - Koike MK
AD  - Disciplina de Emergencias Clinicas, Laboratorio de Emergencias Clinicas - LIM-51 
      - Faculdade de Medicina - Universidade de Sao Paulo, Brazil. Electronic address: 
      mkoike@usp.br.
FAU - Pinto, Isabella F D
AU  - Pinto IFD
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, SP, Brazil. Electronic address: isabellapinto@usp.br.
FAU - Miyamoto, Sayuri
AU  - Miyamoto S
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, SP, Brazil. Electronic address: miyamoto@iq.usp.br.
FAU - Montero, Edna F S
AU  - Montero EFS
AD  - Disciplina de Cirurgia Geral e do Trauma, Laboratorio de Fisiopatologia 
      Cirurgica-LIM-62, Faculdade de Medicina, Universidade de Sao Paulo, SP, Brazil. 
      Electronic address: efrassonsmontero@usp.br.
FAU - Medeiros, Marisa H G
AU  - Medeiros MHG
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, SP, Brazil. Electronic address: mhgdmede@iq.usp.br.
FAU - Kowaltowski, Alicia J
AU  - Kowaltowski AJ
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, SP, Brazil. Electronic address: alicia@iq.usp.br.
LA  - eng
PT  - Journal Article
DEP - 20170619
PL  - United States
TA  - Free Radic Biol Med
JT  - Free radical biology & medicine
JID - 8709159
RN  - 0 (Mitochondrial Membrane Transport Proteins)
RN  - 0 (Mitochondrial Permeability Transition Pore)
RN  - 0U46U6E8UK (NAD)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Calcium/*metabolism
MH  - *Caloric Restriction
MH  - Hydrogen Peroxide/metabolism
MH  - Liver/*metabolism/pathology
MH  - Male
MH  - Mice
MH  - Mitochondria, Liver/*metabolism
MH  - Mitochondrial Membrane Transport Proteins/*metabolism
MH  - Mitochondrial Permeability Transition Pore
MH  - NAD/metabolism
MH  - Oxygen Consumption/physiology
MH  - Permeability
MH  - Reperfusion Injury/metabolism/pathology/*prevention & control
OTO - NOTNLM
OT  - ATP
OT  - Ca(2+)
OT  - Calorie restriction
OT  - Ischemic protection
OT  - Liver
OT  - Mitochondria
EDAT- 2017/06/24 06:00
MHDA- 2018/04/13 06:00
CRDT- 2017/06/24 06:00
PHST- 2017/02/24 00:00 [received]
PHST- 2017/05/19 00:00 [revised]
PHST- 2017/06/17 00:00 [accepted]
PHST- 2017/06/24 06:00 [pubmed]
PHST- 2018/04/13 06:00 [medline]
PHST- 2017/06/24 06:00 [entrez]
AID - S0891-5849(17)30646-9 [pii]
AID - 10.1016/j.freeradbiomed.2017.06.013 [doi]
PST - ppublish
SO  - Free Radic Biol Med. 2017 Sep;110:219-227. doi: 
      10.1016/j.freeradbiomed.2017.06.013. Epub 2017 Jun 19.