Diet restriction in mice causes differential tissue responses in total reducing power and antioxidant compounds

Citation
G. Dubnov et al., Diet restriction in mice causes differential tissue responses in total reducing power and antioxidant compounds, EUR J NUTR, 39(1), 2000, pp. 18-30
Citations number
37
Categorie Soggetti
Food Science/Nutrition
Journal title
EUROPEAN JOURNAL OF NUTRITION
ISSN journal
14366207 → ACNP
Volume
39
Issue
1
Year of publication
2000
Pages
18 - 30
Database
ISI
SICI code
1436-6207(200002)39:1<18:DRIMCD>2.0.ZU;2-N
Abstract
Background: Diet restriction (DR) has been shown to extend the life spans o f various laboratory animals, the mechanism may involve a decrease in oxida tive stress. When determining if the total tissue defense has been altered, it is important to observe the overall direct antioxidant capacity, which consists of low molecular weight antioxidants (LMWA) and enzymes. Aim: To determine DR induced changes in total reducing power and overall di rect antioxidant capacity of various mouse tissues. Methods: Young female Sabra mice were fed a 60% food restricted diet for 40 days (DR group). Organs of the DR group and of ad libitum (AL) fed control s were then dissected and examined. A cyclic voltammetry method was used to quantify the total reducing power, which correlates with the overall LMWA activity. Specific LMWA were identified by HPLC-ECD. Superoxide dismutase a ctivity and H2O2 degrading ability were measured in order to include the en zymatic antioxidant component. Results: Short-term DR caused alterations in the total reducing power of va rious mouse tissues, indicating changes in the total scavenging ability of these tissues. Overall direct antioxidant capacity of heart, kidney and mus cle was enhanced; liver and small intestine deteriorated; brain did not dif fer between DR and AL groups; lung and spleen exhibited a mixed response. Conclusions: We have shown for the first time that DR causes changes in the total reducing power of different mouse tissues, thus, affecting the overa ll direct antioxidant capacity. These findings support the suggestion that there may be a biological regulation of the antioxidant system.