PMID- 10600829
OWN - NLM
STAT- MEDLINE
DCOM- 20000119
LR  - 20180913
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 277
IP  - 6
DP  - 1999 Dec
TI  - Effects of methionine on endogenous antioxidants in the heart.
PG  - H2124-8
LID - 10.1152/ajpheart.1999.277.6.H2124 [doi]
AB  - The deficiency of methionine, an essential amino acid, is associated with 
      cardiovascular lesions. Because different types of cardiac pathologies are caused 
      by a decrease in antioxidants, we examined the effects of methionine on 
      myocardial antioxidant enzymes in hemodynamically assessed rats that were treated 
      with methionine (10 mg/ml) in drinking water for 12, 24, and 48 h. Glutathione 
      peroxidase (GSHPx) activity was significantly increased to 150.5 +/- 12.2 and 
      191.7 +/- 13.7% of the control value at 12 and 24 h, respectively, followed by a 
      decline to 120 +/- 24.6% at 48 h. The mRNA levels of GSHPx at these time points 
      were 151.2 +/- 12.0, 218.7 +/- 35.3, and 173.5 +/- 25.2%, respectively. 
      Superoxide dismutase (SOD) activity was 144.3 +/- 3.7, 114.3 +/- 10.1, and 143.1 
      +/- 11. 2% at 12, 24, and 48 h, respectively. Catalase (Cat) activity was 272.4 
      +/- 5.4, 237.8 +/- 16.6, and 224.1 +/- 17.3% of the control value. The expression 
      of Cat and SOD mRNA was unchanged at 12, 24, and 48 h. The lipid peroxidation was 
      decreased by 24.4 +/- 11.2, 54. 9 +/- 0.1, and 6.4 +/- 2.1% at 12, 24, and 48 h, 
      respectively. Methionine had no effect on the ventricular or aortic pressures, 
      heart rate, and myocardial glutathione levels at any of the time points. The 
      study shows that methionine has a significant effect on the myocardial 
      antioxidant enzyme activities, and only changes in GSHPx enzyme activity 
      correlated with the mRNA changes. These antioxidant changes may have a role in 
      the beneficial effects of methionine in pathological rather than physiological 
      conditions.
FAU - Seneviratne, C K
AU  - Seneviratne CK
AD  - Institute of Cardiovascular Sciences, St. Boniface General Hospital Research 
      Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, 
      Winnipeg, Manitoba, Canada R2H 2A6.
FAU - Li, T
AU  - Li T
FAU - Khaper, N
AU  - Khaper N
FAU - Singal, P K
AU  - Singal PK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Antioxidants)
RN  - 0 (RNA, Messenger)
RN  - AE28F7PNPL (Methionine)
RN  - EC 1.11.1.6 (Catalase)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Antioxidants/*metabolism
MH  - Catalase/genetics/*metabolism
MH  - Gene Expression Regulation, Enzymologic/*drug effects
MH  - Glutathione/metabolism
MH  - Glutathione Peroxidase/genetics/*metabolism
MH  - Heart/*physiology
MH  - Hemodynamics/*physiology
MH  - Male
MH  - Methionine/*pharmacology
MH  - Myocardium/*metabolism
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Superoxide Dismutase/genetics/*metabolism
MH  - Time Factors
MH  - Transcription, Genetic/*drug effects
EDAT- 1999/12/22 00:00
MHDA- 1999/12/22 00:01
CRDT- 1999/12/22 00:00
PHST- 1999/12/22 00:00 [pubmed]
PHST- 1999/12/22 00:01 [medline]
PHST- 1999/12/22 00:00 [entrez]
AID - 10.1152/ajpheart.1999.277.6.H2124 [doi]
PST - ppublish
SO  - Am J Physiol. 1999 Dec;277(6):H2124-8. doi: 10.1152/ajpheart.1999.277.6.H2124.