PMID- 9727550
OWN - NLM
STAT- MEDLINE
DCOM- 19980917
LR  - 20190623
IS  - 0009-7322 (Print)
IS  - 0009-7322 (Linking)
VI  - 98
IP  - 8
DP  - 1998 Aug 25
TI  - Inhibitory effects of antioxidants on neonatal rat cardiac myocyte hypertrophy 
      induced by tumor necrosis factor-alpha and angiotensin II.
PG  - 794-9
AB  - BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) and angiotensin II (Ang II) 
      modulate heart failure in part by provoking the hypertrophic response. Signal 
      transduction pathways of those factors are implicated in reactive oxygen 
      intermediates (ROIs). Therefore, we hypothesized that TNF-alpha and Ang II might 
      cause myocyte hypertrophy via the generation of ROIs. METHODS AND RESULTS: To 
      test the hypothesis, we tested whether TNF-alpha and Ang II could induce the 
      generation of ROIs and whether antioxidants such as butylated hydroxyanisole 
      (BHA), vitamin E, and catalase might inhibit the hypertrophy in cultured neonatal 
      rat cardiac myocytes. ROIs were measured by the ROI-specific probe 
      2',7'-dichlorofluorescin diacetate in cultured cardiac myocytes. We demonstrated 
      that TNF-alpha and Ang II induced the generation of ROIs in a dose-dependent 
      manner. TNF-alpha (10 ng/mL) and Ang II (100 nmol/L) enlarged cardiac myocytes 
      and increased [3H]leucine uptake, and BHA (10 micromol/L) significantly inhibited 
      both effects. Other antioxidants, such as vitamin E (1 microg/mL) and catalase 
      (100 U/mL), also inhibited the enlargement of cardiac myocytes induced by 
      TNF-alpha. CONCLUSIONS: These results indicate that TNF-alpha and Ang II cause 
      hypertrophy in part via the generation of ROIs in cardiac myocytes.
FAU - Nakamura, K
AU  - Nakamura K
AD  - Department of Cardiovascular Medicine, Okayama University Medical School, Japan. 
      cardio@cc.okayama-u.ac.jp
FAU - Fushimi, K
AU  - Fushimi K
FAU - Kouchi, H
AU  - Kouchi H
FAU - Mihara, K
AU  - Mihara K
FAU - Miyazaki, M
AU  - Miyazaki M
FAU - Ohe, T
AU  - Ohe T
FAU - Namba, M
AU  - Namba M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Antioxidants)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 10028-17-8 (Tritium)
RN  - 11128-99-7 (Angiotensin II)
RN  - 1406-18-4 (Vitamin E)
RN  - 25013-16-5 (Butylated Hydroxyanisole)
RN  - EC 1.11.1.6 (Catalase)
RN  - GMW67QNF9C (Leucine)
SB  - IM
MH  - Angiotensin II/*toxicity
MH  - Animals
MH  - Animals, Newborn
MH  - Antioxidants/*therapeutic use
MH  - Butylated Hydroxyanisole/therapeutic use
MH  - Cardiomegaly/chemically induced/*drug therapy
MH  - Catalase/therapeutic use
MH  - Cells, Cultured
MH  - Leucine/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/metabolism
MH  - Recombinant Proteins/toxicity
MH  - Tritium
MH  - Tumor Necrosis Factor-alpha/*toxicity
MH  - Vitamin E/therapeutic use
EDAT- 1998/09/04 00:00
MHDA- 1998/09/04 00:01
CRDT- 1998/09/04 00:00
PHST- 1998/09/04 00:00 [pubmed]
PHST- 1998/09/04 00:01 [medline]
PHST- 1998/09/04 00:00 [entrez]
AID - 10.1161/01.cir.98.8.794 [doi]
PST - ppublish
SO  - Circulation. 1998 Aug 25;98(8):794-9. doi: 10.1161/01.cir.98.8.794.