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Titolo:
Antioxidant function of the mitochondrial protein SP-22 in the cardiovascular system
Autore:
Araki, M; Nanri, H; Ejima, K; Murasato, Y; Fujiwara, T; Nakashima, Y; Ikeda, M;
Indirizzi:
Univkuokapat & Environm Hlth, Dept Hlth Dev, Yahatanishi Ku, Kitakyushu, Fu Univ Occupat & Environm Hlth Kitakyushu Fukuoka Japan 807 Kitakyushu, Fu Univ555,upat & Environm Hlth, Dept Internal Med 2, Kitakyushu, Fukuoka 8078 Univ Occupat & Environm Hlth Kitakyushu Fukuoka Japan 8078555 ukuoka 8078 Univ5,ccupat & Environm Hlth, Dept Syst Physiol, Kitakyushu, Fukuoka 807855 Univ Occupat & Environm Hlth Kitakyushu Fukuoka Japan 8078555 uoka 807855 Fukuoka Univ, Sch Med, Dept Biochem, Fukuoka 8140180, Japan Fukuoka Univ Fukuoka Japan 8140180 Dept Biochem, Fukuoka 8140180, Japan
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 4, volume: 274, anno: 1999,
pagine: 2271 - 2278
SICI:
0021-9258(19990122)274:4<2271:AFOTMP>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCARDIAL REPERFUSION INJURY; DEPENDENT PEROXIDE REDUCTASE; SUPEROXIDE-DISMUTASE; OXIDATIVE STRESS; ENDOTHELIAL-CELLS; HYDROGEN-PEROXIDE; FREE-RADICALS; NITRIC-OXIDE; INDUCTION; CATALASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Nanri, H Univ Occupat & Environm Hlth, Dept Hlth Dev, Yahatanishi Ku, 1-1 Iseigaoka, Univ Occupat & Environm Hlth 1-1 Iseigaoka Kitakyushu Fukuoka Japan 807
Citazione:
M. Araki et al., "Antioxidant function of the mitochondrial protein SP-22 in the cardiovascular system", J BIOL CHEM, 274(4), 1999, pp. 2271-2278

Abstract

The mitochondrial protein SP-22 has recently been reported to be a member of the thioredoxin-dependent peroxide reductase family, suggesting that it may be one of the antioxidant systems in mitochondria, which are the major site of reactive oxygen intermediate generation, The aim of this study was to examine whether SP-22 is involved in mitochondrial antioxidant mechanisms and whether its expression is induced by oxidative stresses, particularlythose in mitochondria. The expression of SP-22 protein was enhanced by about 1.5-4.6-fold when bovine aortic endothelial cells (BAEC) were exposed tovarious oxidative stresses, including mitochondrial respiratory inhibitorswhich increased the superoxide generation in BAEC mitochondria. The expression of SP-22 mRNA increased 2.0-3.5-fold with a peak at 3-6 h after exposure to Fe2+/dithiothreitol or a respiratory inhibitor, antimycin A. BAEC with an increased level of SP-22 protein caused by pretreatment with mild oxidative stress became tolerant to subsequent intense oxidative stress. On theother hand, BAEC that had been depleted of SP-22 with an antisense oligodeoxynucleotide against SP-22 mRNA became more labile to oxidative stress than control BAEC. The induction of SP-22 protein by oxidative stress in vivo was demonstrated in an experimental model of myocardial infarction in rat heart. These findings indicate that SP-22 functions as an antioxidant in mitochondria of the cardiovascular system.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 12:47:33