Iron, ferritin and proteins of the methionine-centered redox cycle in young and old rat hearts

被引:22
作者
Bulvik, Baruch [2 ]
Grinberg, Leonid [2 ]
Eliashar, Ron [3 ]
Berenshtein, Eddy [2 ]
Chevion, Mordechai [1 ,2 ]
机构
[1] Hebrew Univ Jerusalem, Ganz Chair Heart Studies, Dept Cellular Biochem & Human Genet, Fac Med, IL-91120 Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Fac Med Dent, Dept Cellular Biochem & Human Genet, IL-91120 Jerusalem, Israel
[3] Hadassah Hebrew Univ Hosp, Dept Otolaryngol Head & Neck Surg, Jerusalem, Israel
基金
以色列科学基金会;
关键词
Aging; Ferritin subunits; Methionine sulfoxide reductase; Thioredoxin; Thioredoxin reductase; OXIDATIVE STRESS; SULFOXIDE REDUCTASE; AGED HEART; THIOREDOXIN; PROTECTION; BIOCHEMISTRY; EXPRESSION; RESIDUES; ENZYMES; MUSCLE;
D O I
10.1016/j.mad.2008.10.002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Progressive oxidation of cellular components constitutes a major mechanism of the aging process. An emerging paradigm of redox signaling suggests that low level oxidants activate protective pathways resulting in prolonged cell survival. This report centers on the study of cardiac muscle in young and old rats, including (i) the expression of ferritin (Ft) the major iron storage protein, and (ii) the expression of the major proteins of the methionine-centered redox cycle (MCRC), which controls the cellular methionine redox status. Total amounts of Ft(protein) and its mRNA encoding for Ft L-subunit (Ft-L) were higher in the aged hearts, indicating that the iron-binding capacity of myocardial Ft increased with age. Among the proteins of the MCRC, methionine sulfoxide reductases A and B (MsrA, MsrB) and MsrA mRNA were significantly higher in hearts of old rats with a significant decrease in MsrA activity. The observed up-regulation of the expression of Msr and Ft-L could represent a protective response to the increased oxidative stress in the aging myocardium. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:139 / 144
页数:6
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