PMID- 26472730
OWN - NLM
STAT- MEDLINE
DCOM- 20161028
LR  - 20181113
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 411
IP  - 1-2
DP  - 2016 Jan
TI  - Effects of mild hyperhomocysteinemia on electron transport chain complexes, 
      oxidative stress, and protein expression in rat cardiac mitochondria.
PG  - 261-70
LID - 10.1007/s11010-015-2588-7 [doi]
AB  - Hyperhomocysteinemia (HHcy) is an independent risk factor of cardiovascular 
      disease, but the mechanisms of tissue injury are poorly understood. In the 
      present study, we investigated the effect of HHcy on rat heart function, 
      activities electron transport chain (ETC) complexes, mitochondrial protein 
      expression, and protein oxidative damage. HHcy was induced by subcutaneous 
      injection of Hcy (0.45 mumol/g of body weight) twice a day for a period of 
      2 weeks. Performance of hearts excised after the Hcy treatment was examined 
      according to the Langendorff method at a constant pressure. Left ventricular 
      developed pressure, as well as maximal rates of contraction (+dP/dt) and 
      relaxation (-dP/dt), was significantly depressed in HHcy rats. HHcy was 
      accompanied by significant inhibition of ETC complexes II-IV, whereas activity of 
      the complex I was unchanged. The decline in ETC activities was not associated 
      with elevated protein oxidative damage, as indicated by unchanged protein 
      carbonyl, thiol, and dityrosine contents. Moreover, the level of protein adducts 
      with 4-hydroxynonenal was decreased in HHcy rats. Additionally, 2D-gel 
      electrophoresis with matrix-assisted laser desorption/ionization time-of-flight 
      mass spectrometry did not show alterations in contents of inhibited ETC 
      complexes. However, mass spectrometry analyses identified 8 proteins whose 
      expression was significantly increased by HHcy. These proteins are known to play 
      important roles in the cellular stress response, bioenergetics, and redox 
      balance. Altogether, the results suggest that oxidative damage and altered 
      protein expression are not possible causes of ETC dysfunction in HHcy rats. 
      Increased expression of the other mitochondrial proteins indicates a protective 
      response to Hcy-induced myocardial injury.
FAU - Timkova, Veronika
AU  - Timkova V
AD  - Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius 
      University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
FAU - Tatarkova, Zuzana
AU  - Tatarkova Z
AD  - Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius 
      University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
FAU - Lehotsky, Jan
AU  - Lehotsky J
AD  - Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius 
      University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
FAU - Racay, Peter
AU  - Racay P
AD  - Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius 
      University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
FAU - Dobrota, Dusan
AU  - Dobrota D
AD  - Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius 
      University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
FAU - Kaplan, Peter
AU  - Kaplan P
AD  - Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius 
      University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic. 
      kaplan@jfmed.uniba.sk.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151015
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0 (Mitochondrial Proteins)
SB  - IM
MH  - Animals
MH  - Electron Transport
MH  - Heart Function Tests
MH  - Hyperhomocysteinemia/*metabolism
MH  - Male
MH  - Mitochondria, Heart/*metabolism
MH  - Mitochondrial Proteins/*metabolism
MH  - *Oxidative Stress
MH  - Rats
MH  - Rats, Wistar
OTO - NOTNLM
OT  - Electron transport chain
OT  - Heart
OT  - Homocysteine
OT  - Mitochondria
OT  - Oxidative stress
OT  - Protein expression
EDAT- 2015/10/17 06:00
MHDA- 2016/11/01 06:00
CRDT- 2015/10/17 06:00
PHST- 2015/07/13 00:00 [received]
PHST- 2015/10/08 00:00 [accepted]
PHST- 2015/10/17 06:00 [entrez]
PHST- 2015/10/17 06:00 [pubmed]
PHST- 2016/11/01 06:00 [medline]
AID - 10.1007/s11010-015-2588-7 [pii]
AID - 10.1007/s11010-015-2588-7 [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2016 Jan;411(1-2):261-70. doi: 10.1007/s11010-015-2588-7. Epub 
      2015 Oct 15.