Characterization of UPF peptides, members of the glutathione analogues library, on the basis of their effects on oxidative stress-related enzymes

被引:7
作者
Ehrlich, Kersti [1 ]
Ida, Katrin [2 ]
Mahlapuu, Riina [1 ]
Kairane, Ceslava [1 ]
Oit, Ingrid [1 ]
Zilmer, Mihkel [1 ]
Soomets, Ursel [1 ]
机构
[1] Univ Tartu, Dept Biochem, Fac Med, Ctr Excellence Translat Med, EE-50411 Tartu, Estonia
[2] Univ Tartu, Dept Pharm, Fac Med, EE-50411 Tartu, Estonia
关键词
Glutathione; glutathione analogues; glutathione peroxidase; glutathione reductase; MnSOD; NAD(P)H oxidase; oxidative stress; MANGANESE SUPEROXIDE-DISMUTASE; INHIBITS NADPH OXIDASE; CELLULAR GLUTATHIONE; REDUCTASE ACTIVITIES; NAD(P)H OXIDASE; S-THIOLATION; PEROXIDASE; MITOCHONDRIA; ANTIOXIDANTS; NEUTROPHILS;
D O I
10.1080/10715760902918691
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previously the authors have designed and synthesized a library of antioxidative glutathione analogues called UPF peptides which are superior to glutathione in hydroxyl radical elimination. This paper is a follow-up study which investigated the effects of the most promising members of the library (UPF1 and UPF17) on oxidative stress-related enzymes. At concentrations used in vivo experiments neither UPF peptide influenced the activity of glutathione peroxidase (GPx) when purified enzyme or erythrocyte lysate was used. At higher concentrations they inhibited GPx activity. UPF peptides had no effect on glutathione reductase (GR) activity. Also they, as well as glutathione itself, slightly increased MnSOD activity in human brain mitochondria and inhibited oxidative burst caused by neutrophil NAD(P) H oxidase. RT-PCR measurements showed that UPF1 and UPF17 have no effect on GPx and MnSOD expression level in human blood mononuclear cells. The results of this study confirm that investigated UPF peptides do not interfere with the enzymatic mechanisms of antioxidative defence and can be used as themselves or as a lead for the protector molecule design against excessive oxidative stress.
引用
收藏
页码:572 / 580
页数:9
相关论文
共 44 条
[11]   Neurodegenerative diseases and oxidative stress [J].
Emerit, J ;
Edeas, A ;
Bricaire, F .
BIOMEDICINE & PHARMACOTHERAPY, 2004, 58 (01) :39-46
[12]   Cell signalling and the glutathione redox system [J].
Filomeni, G ;
Rotilio, G ;
Ciriolo, MR .
BIOCHEMICAL PHARMACOLOGY, 2002, 64 (5-6) :1057-1064
[13]  
Franco R., 2007, Archives of Physiology and Biochemistry, V113, P234, DOI 10.1080/13813450701661198
[14]   Oxidative stress induced in pathologies:: the role of antioxidants [J].
Gaté, L ;
Paul, J ;
Ba, GN ;
Tew, KD ;
Tapiero, H .
BIOMEDICINE & PHARMACOTHERAPY, 1999, 53 (04) :169-180
[15]   GLUTATHIONE-PEROXIDASE AND GLUTATHIONE-REDUCTASE ACTIVITIES TOWARDS GLUTATHIONE-DERIVED ANTIOXIDANTS [J].
GAULLIER, JM ;
LAFONTANT, P ;
VALLA, A ;
BAZIN, M ;
GIRAUD, M ;
SANTUS, R .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 203 (03) :1668-1674
[16]  
Giorgio M, 2007, NAT REV MOL CELL BIO, V8, p722A
[17]   NAD(P)H oxidase - Role in cardiovascular biology and disease [J].
Griendling, KK ;
Sorescu, D ;
Ushio-Fukai, M .
CIRCULATION RESEARCH, 2000, 86 (05) :494-501
[18]   Biologic and pharmacologic regulation of mammalian glutathione synthesis [J].
Griffith, OW .
FREE RADICAL BIOLOGY AND MEDICINE, 1999, 27 (9-10) :922-935
[19]   PR-39, a proline/arginine-rich antimicrobial peptide, exerts cardioprotective effects in myocardial ischemia-reperfusion [J].
Ikeda, Y ;
Young, LH ;
Scalia, R ;
Ross, CR ;
Lefer, AM .
CARDIOVASCULAR RESEARCH, 2001, 49 (01) :69-77
[20]   Analysis of reactive oxygen species generated by neutrophils using a chemiluminescence probe L-012 [J].
Imada, I ;
Sato, EF ;
Miyamoto, M ;
Ichimori, Y ;
Minamiyama, Y ;
Konaka, R ;
Inoue, M .
ANALYTICAL BIOCHEMISTRY, 1999, 271 (01) :53-58