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

分析身体的应激反应及其适应机制，特别参考活性氧的形成和去除系统。

基本信息

批准号：
10307009
负责人：
SUGAWARA Kazuo
金额：
$ 16.38万
依托单位：
Hirosaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (A).
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 2000
项目状态：
已结题

项目摘要

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.

我们首先研究了运动作为压力研究模型的影响，并证明运动引起的中性粒细胞启动归因于生长激素、白细胞介素6和8的血浆浓度增加，尽管中性粒细胞启动与肌肉损伤有关，但这些应激反应可以通过重复或运动来适应。此外，我们还发现马拉松比赛后血浆和尿液中的中性粒细胞激活标记物（髓过氧化物酶和乳铁蛋白）增加，血浆和尿液中吞噬细胞启动物质如生长激素、催乳素、趋化因子、集落刺激因子也增加。另一方面，马拉松比赛后，血浆中皮质醇、白细胞介素10等免疫抑制物质也上升，抗氧化活性也增加。在研究的物质中，维生素 C 被证明在比赛后有所增加，这可能是对抗氧化应激的适应机制。此外，虽然我们研究了外科手术作为压力模型的影响，但结果表明，尽管循环细胞因子显着增加，但这种极端压力会抑制中性粒细胞活性。综合考虑，尽管中性粒细胞和单核细胞在受到应激时容易释放活性氧和蛋白水解酶，因为几种生物活性物质浓度增加，从而诱发炎症，但仍存在诸如动员抗氧化剂等适应机制。这些发现表明，补充维生素 C 等抗氧化剂可以抑制氧化应激引起的发病机制。