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J Appl Physiol 107: 1532-1538, 2009. First published August 20, 2009; doi:10.1152/japplphysiol.91166.2008
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Vitamin C and E supplementation prevents mitochondrial damage of ileum myocytes caused by intense and exhaustive exercise training

Eloi F. Rosa,1,3 Rafael Ferreira Ribeiro,1 Felipe M. T. Pereira,1 Edna Freymüller,2 Jeannine Aboulafia,1,* and Viviane L. A. Nouailhetas1,*

1Department of Biophysics, ; 2Electron Microscopy Center, Universidade Federal de São Paulo-Campus São Paulo, São Paulo, Brazil, and ; 3Centro Universitário São Camilo, São Paulo, Brazil

Submitted 1 September 2008 ; accepted in final form 17 August 2009

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 Vmax, 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.

C57BL/6 mice; intestine; mitochondria



Address for reprint requests and other correspondence: V. Nouailhetas, Dept. of Biophysics, Universidade Federal de São Paulo-Escola Paulista de Medicina, Rua Botucatu, 862, 7° andar 04023-062 São Paulo, SP, Brazil (e-mail: vivi{at}biofis.epm.br).







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