Navegando por Palavras-chave "exercício físico câncer de cólon estresse oxidativo mitocôndria"

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    Respostas oxidativas do cólon e de suas mitocôndrias em resposta ao exercício em camundongos c57bl/6 tratados com 1,2-dimetilhidrazina
    (Universidade Federal de São Paulo (UNIFESP), 2014-09-24) Ribeiro, Rafael Ferreira [UNIFESP]; Nouailhetas, Viviane Louise Andree Nouailhetas [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Introduction: The practice of physical exercise is usually associated with increased quality of life and prevention of chronic degenerative diseases . However, exercise is not always linked with health, it may be related to increased production of free radicals as well. Reactive oxygen species ( ROS ) can directly produce changes in DNA strands , leading to mutagenesis and therefore is considered a significant class of carcinogens , participating in initiation, progression and metastasis of the cancer. Knowing that the intense and exhaustive exercise increases intestinal oxidative stress , whereas the usual moderate exercise reduces stress, we might assume that intense exercise increase the predisposition to develop cancer . On the other hand , some studies indicate a recovery of colon cancer in individuals who do intense physical activity . Objectives: To investigate whether exercise, intense and exhaustive or moderate, induces oxidative stress specifically in the colon of C57Bl / 6 mice and oxidative stress induced by exercise, moderate or intense and exhausting, exert a protective effect for the development of cancer in animals treated with DMH for the development of early lesions of colon cancer. Methods: Male C57BL / 6 strain mice were randomly divided into the following groups : sedentary , treated (CT +) or not with DMH (CT-) , submitted to intense and exhaustive exercise treaty (IEE+) or not with DMH (IEE-) subjected to moderate intensity exercise treaty (MOD+) or not with DMH (MOD-) . For induction of cancer animals were treated with a subcutaneous injection of 1,2- dimethylhydrazine (DMH) (40 mg / kg body weight) for 6 weeks. The EIE protocol consisted of a daily session of treadmill running at 85 % of the maximum speed of each individual animal until its exhaustion for a period of 10 days. Have the MOD protocol consisted of a daily session of treadmill running at 60 % of the maximum speed of each animal for 30 minutes for 10 days. The maximum speed was previously determined by the maximum incremental test (TIM) held before the exercise protocol . Physical performance in response to the training was done by the time of exhaustion and / or alteration of maximum speed in TIM . Changes in the redox state was measured by the amount of lipid peroxidation, protein oxidation ( total colon and their mitochondria ) , citrate synthase (CS) activity and mitochondrial rupture rate . The morphology of the colon was examined in histological cross sections stained with hematoxylin / eosin and methylene blue, in the case of groups CT and CT + reactivity colon was studied by constructing curves not cumulative isometric contractile concentration - responses induced by KCl and carbachol ( CCh ) . Results: There was no change in body weight of the animals and contents of colon protein with treatment with DMH, and no change in physical performance of the animals . Significant increase in protein oxidation colon and their mitochondria by the administration of DMH . Level of lipid peroxidation unaltered by treatment with DMH . Reduction of oxidative damage to tissue proteins and mitochondrial colon with exercise (IEE and MOD) .Levels of oxidative damage in colon proteins only with the execution of IEE in contrast to the MOD. Increasing the CS enzyme activity in isolated mitochondria of colon in the DMH treated animals and animals that underwent MOD, treated or not with DMH, and a reduction in the colon isolated mitochondria of animals treated with DMH and submitted to IEE reaching trigger level similar to that observed for the activity of this enzyme in animals that performed only the IEE. Increase in the amount of ruptured mitochondria in the colon of animals who performed or MOD or IEE, both treated and untreated groups with HMD . Damage to the structure of the mucosa and muscle layers of the colon only in animals subjected to the MOD , with subsequent structural recovery of the muscle layer in animals subjected to the MOD and treated with DMH . Increased reactivity to drug - and electromechanical distal colon by DMH treatment in animals not exercised engagements. Increased reactivity of the proximal colon only the electromechanical coupling by treatment with DMH in the colon distal to more forcefully. Conclusion: Our study suggests a protective effect of exercise is intense and exhaustive or moderate in relation to oxidative damage and mitochondrial activity in the colon of C57Bl / 6 mice subjected to the experimental model of colon cancer induced by DMH . Furthermore, evidence shows that the behavior of the intestine throughout its path does not seem to differ from the mitochondrial oxidative and exercise-induced responses were similar to those as already described in this strain of mice ileum . These findings are interesting in that permit the use as an exercise , non-invasive therapeutic tool to combat the development of intestinal cancer and opens up new opportunities for studies regarding the signaling pathways involved in tumorgênesis process.