Document Detail

Vitamin C and E supplementation prevents mitochondrial damage of ileum myocytes caused by intense and exhaustive exercise training.
MedLine Citation:
PMID:  19696358     Owner:  NLM     Status:  MEDLINE    
Intense and exhaustive exercise (IEE) is associated with oxidative stress in skeletal muscle, and we recently reported that intestine is sensitive to IEE. In the present study, we investigated the possible relationship between the effects of IEE on morphology and oxidative markers in the ileum and isolated mitochondria. C57BL/6 mice were ascribed either to a control group comprising two subgroups, one sedentary and another exercised for 10 days (E10), or to a corresponding supplemented control group again comprising two subgroups, one sedentary and another exercised for 10 days (E10-V). The IEE program consisted of a single daily treadmill running session at 85% of V(max), until animal exhaustion. Vitamins C (10 mg/kg) and E (10 mg/kg) were concurrently intraperitoneally administered 2 h before the exercise sessions. IEE was shown to cause 1) impairment of ileum internal membrane mitochondria verified by ultramicrography analysis; 2) increase in ileum carbonyl content (117%) and reduction in antioxidant capacity (36%); 3) increase in mitochondria carbonyl content (38%), increase in the percentage of ruptured mitochondria (25.3%), increase in superoxide dismutase activity (186%), and reduction in citrate synthase activity (40.4%) compared with control animals. Observations in the vitamin-supplemented exercised animals (E10-V) were 1) healthy appearance of myocyte mitochondria; 2) decrease in ileum carbonyl content (66%) and increase in antioxidant capacity (53%); 3) decrease in mitochondria carbonyl content (43%), decrease in the percentage of ruptured mitochondria (30%), slight increase in superoxide dismutase activity (7%), and significant increase in citrate synthase activity (121%) compared with E10 animals. Therefore, the present results strongly corroborate the hypothesis that IEE leads to marked disturbances in intestinal mitochondria, mainly in redox status, and affects whole intestinal redox status.
Eloi F Rosa; Rafael Ferreira Ribeiro; Felipe M T Pereira; Edna Freymüller; Jeannine Aboulafia; Viviane L A Nouailhetas
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-08-20
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  107     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-11-05     Completed Date:  2010-01-13     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1532-8     Citation Subset:  IM    
Dept. of Biophysics, Universidade Federal de São Paulo-Campus São Paulo, São Paulo, Brazil.
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MeSH Terms
Administration, Oral
Ascorbic Acid / administration & dosage*
Cells, Cultured
Dietary Supplements
Mice, Inbred C57BL
Mice, Inbred Strains
Mitochondria / physiology*
Muscle Fibers, Skeletal / cytology*,  drug effects,  physiology*
Physical Endurance / drug effects,  physiology*
Physical Exertion / drug effects,  physiology*
Vitamin E / administration & dosage*
Reg. No./Substance:
1406-18-4/Vitamin E; 50-81-7/Ascorbic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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