Analyses of stress responses and thier adaptation mechanisms of the body in special references to formation and removal systems of reactive oxigen species.

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We firstly investigated the effects of exercise as a model of stress research, and demonstrated that exercise-induced neutrophil priming was attributed to the increased plasma concentrations of growth hormones, interleukins 6 and 8, and that although neutrophil priming was associated with muscle damage, these stress responses were acclimated by repetition or exercise. Furthermore, we demonstrated that neutrophil activation marker (myeloperoxidase and lactoferrin) increased in plasma and urine after marathon race and also revealed that phagocyte-priming substances such as growth hormone, prolactin, chemokines, colony-stimulating factors rose in plasma and urine. On the other hand, it was demonstrated that immunosuppressive substances such as cortisol and interleukin 10 also rose and antioxidant activity was increased in plasma after marathon race. Among the substances investigated, vitamin C was demonstrated to rise after the race, and this might work as an adaptation mechanisms against oxidative stress. In addition, although we investigated the effects of surgical operation as a model of stress, it was demonstrated that such an extreme stress inhibited neutrophil activity in spite of marked increases in circulating cytokines. Considered together, althogh neutrophils and monocytes are prone to release reactive oxygen species and proteolytic enzymes on exposure to stress because of the increased concentrations of several bioactive substances and consequently inflammation are induced, adaptation mechanisms such as mobilization of antioxidants exist . These findings suggest that supplementation of antioxidants such as vitamin C inhibit pathogenesis due to oxidative stress.