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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Molecular hydrogen reduces acute exercise-induced inflammatory and oxidative stress status

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Autor(es):
Nogueira, Jonatas E. [1, 2] ; Passaglia, Patricia [3] ; Mota, Clarissa M. D. [3] ; Santos, Bruna M. [3] ; Batalhao, Marcelo E. [4] ; Carnio, Evelin C. [3, 4] ; Branco, Luiz G. S. [5, 3, 2]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Sch Phys Educ & Sports Ribeirao Preto, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Sch Nursing Ribeirao Preto, Dept Gen & Specialized Nursing, Ribeirao Preto, SP - Brazil
[5] Univ Sao Paulo, Dent Sch Ribeirao Preto, Dept Morphol Physiol & Basic Pathol, BR-14040904 Ribeirao Preto, SP - Brazil
Número total de Afiliações: 5
Tipo de documento: Artigo Científico
Fonte: Free Radical Biology and Medicine; v. 129, p. 186-193, DEC 2018.
Citações Web of Science: 6
Resumo

Physical exercise induces inflammatory and oxidative markers production in the skeletal muscle and this process is under the control of both endogenous and exogenous modulators. Recently, molecular hydrogen (H-2) has been described as a therapeutic gas able to reduced oxidative stress in a number of conditions. However, nothing is known about its putative role in the inflammatory and oxidative status during a session of acute physical exercise in sedentary rats. Therefore, we tested the hypothesis that H-2 attenuates both inflammation and oxidative stress induced by acute physical exercise. Rats ran at 80% of their maximum running velocity on a closed treadmill inhaling either the H-2 gas (2% H-2, 21% O-2, balanced with N-2) or the control gas (0% H-2, 21% O-2, balanced with N-2) and were euthanized immediately or 3 h after exercise. We assessed plasma levels of inflammatory cytokines {[}tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta and IL-6] and oxidative markers {[}superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. In addition, we evaluated the phosphorylation status of intracellular signaling proteins {[}glycogen synthase kinase type 3 (GSK3 alpha/beta) and the cAMP responsive element binding protein (CREB)] that modulate several processes in the skeletal muscle during exercise, including changes in exercise-induced reactive oxygen species (ROS) production. As expected, physical exercise increased virtually all the analyzed parameters. In the running rats, H-2 blunted exercise-induced plasma inflammatory cytokines (TNF-alpha and IL-6) surges. Regarding the oxidative stress markers, H-2 caused further increases in exercise-induced SOD activity and attenuated the exercise-induced increases in TBARS 3 h after exercise. Moreover, GSK3 alpha/beta phosphorylation was not affected by exercise or H-2 inhalation. Otherwise, exercise caused an increased CREB phosphorylation which was attenuated by H-2. These data are consistent with the notion that H-2 plays a key role in decreasing exercise-induced inflammation, oxidative stress, and cellular stress. (AU)

Processo FAPESP: 16/17681-9 - Alterações fisiopatológicas durante a inflamação sistêmica
Beneficiário:Luiz Guilherme de Siqueira Branco
Modalidade de apoio: Auxílio à Pesquisa - Temático