PMID- 28840535
OWN - NLM
STAT- MEDLINE
DCOM- 20190204
LR  - 20190215
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 55
IP  - 6
DP  - 2018 Jun
TI  - Chronic Exposure to beta-Alanine Generates Oxidative Stress and Alters Energy 
      Metabolism in Cerebral Cortex and Cerebellum of Wistar Rats.
PG  - 5101-5110
LID - 10.1007/s12035-017-0711-3 [doi]
AB  - beta-Alanine occurs naturally in the human central nervous system and performs 
      different functions. It can act as either a neurotransmitter or a neuromodulator, 
      depletion of taurine levels and competitive antagonist of gamma-aminobutyric acid 
      (GABA). The beta-amino acid accumulation exerts an important biological function as 
      delay in brain development, oxidative stress and disturbances in energy 
      metabolism, characterized as an inborn error of metabolism classified as 
      beta-alaninemia. We evaluated the effects of the chronic administration of beta-alanine 
      on some parameters of oxidative stress and enzymes of energy metabolism in 
      cerebral cortex and cerebellum of 21-day-old Wistar rats. The animals received 
      peritoneal injections of beta-alanine (300 mg/kg of body weight), and the controls 
      received the same volume (10 mul/g of body weight) of saline solution (NaCl 0.9%), 
      twice a day at 12-h interval, from the 7th to the 21st postpartum day. We 
      observed that beta-amino acid was able to increase the levels of reactive oxygen 
      species (ROS) in the two tissues; however, only in cerebral cortex total content 
      of sulfhydryl was increased. ROS are possibly acting on antioxidant enzymes 
      glutathione peroxidase (GPx) (cerebral cortex and cerebellum) and superoxide 
      dismutase (SOD) (cerebellum) inhibiting their activities. We also evaluated the 
      activities of enzymes of the phosphoryl transfer network, where we observed an 
      increase in hexokinase and cytosolic creatine kinase (Cy-CK) activities; however, 
      it decreased glyceraldehyde 3-phosphate dehydrogenase (GAPDH), pyruvate kinase 
      (PK) and lactate dehydrogenase (LDH) activities, in both tissues. Besides, the 
      beta-alanine administration increased the activities of complex II, complex IV and 
      succinate dehydrogenase (SDH). Those results suggest that the chronic 
      administration of beta-alanine causes cellular oxidative damage, significantly 
      changing the energy metabolism.
FAU - Gemelli, Tanise
AU  - Gemelli T
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil.
FAU - de Andrade, Rodrigo Binkowski
AU  - de Andrade RB
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil.
FAU - Rojas, Denise Bertin
AU  - Rojas DB
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil.
FAU - Zanatta, Angela
AU  - Zanatta A
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil.
FAU - Schirmbeck, Gabriel Henrique
AU  - Schirmbeck GH
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil.
FAU - Funchal, Claudia
AU  - Funchal C
AD  - Centro Universitario Metodista IPA, Rua Cel. Joaquim Pedro Salgado, 80, Porto 
      Alegre, RS, CEP 90420-060, Brazil.
FAU - Wajner, Moacir
AU  - Wajner M
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil.
FAU - Dutra-Filho, Carlos Severo
AU  - Dutra-Filho CS
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil.
FAU - Wannmacher, Clovis Milton Duval
AU  - Wannmacher CMD
AD  - Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Instituto 
      de Ciencias Basicas da Saude, Rua Ramiro Barcelos 2600, Porto Alegre, RS, CEP 
      90035-003, Brazil. clovisdw@ufrgs.br.
LA  - eng
GR  - 306928/2014-0/Conselho Nacional de Desenvolvimento Cientifico e Tecnologico 
      (CNPq)-Brazil/
PT  - Journal Article
DEP - 20170824
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (Electron Transport Chain Complex Proteins)
RN  - 11P2JDE17B (beta-Alanine)
SB  - IM
MH  - Animals
MH  - Cerebellum/*pathology
MH  - Cerebral Cortex/*pathology
MH  - Electron Transport Chain Complex Proteins/metabolism
MH  - Energy Metabolism/*drug effects
MH  - Oxidative Stress/*drug effects
MH  - Rats, Wistar
MH  - beta-Alanine/administration & dosage/*toxicity
OTO - NOTNLM
OT  - Energy metabolism
OT  - Mitochondrial respiratory chain
OT  - Oxidative stress
OT  - beta-alanine
OT  - beta-alaninemia
EDAT- 2017/08/26 06:00
MHDA- 2019/02/05 06:00
CRDT- 2017/08/26 06:00
PHST- 2017/02/15 00:00 [received]
PHST- 2017/08/07 00:00 [accepted]
PHST- 2017/08/26 06:00 [pubmed]
PHST- 2019/02/05 06:00 [medline]
PHST- 2017/08/26 06:00 [entrez]
AID - 10.1007/s12035-017-0711-3 [pii]
AID - 10.1007/s12035-017-0711-3 [doi]
PST - ppublish
SO  - Mol Neurobiol. 2018 Jun;55(6):5101-5110. doi: 10.1007/s12035-017-0711-3. Epub 
      2017 Aug 24.