Good stress, bad stress and oxidative stress: insights from anticipatory cortisol reactivity.
Good stress, bad stress and oxidative stress: insights from anticipatory cortisol reactivity.
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DOI：
10.1016/j.psyneuen.2013.02.004
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发表时间：
2013-09
影响因子：
3.7
通讯作者：
Epel, Elissa
中科院分区：
文献类型：
--
作者：
Aschbacher, Kirstin;O'Donovan, Aoife;Wolkowitz, Owen M.;Dhabhar, Firdaus S.;Su, Yali;Epel, Elissa
关键词：
慢性心理应激似乎会加速生物衰老，氧化损伤是这一过程的重要潜在介导者。然而，心理应激促进氧化损伤的机制知之甚少。这项研究调查的理论，皮质醇增加，在一个急性应激事件有可能增强或破坏心理生物学的抗氧化能力，这取决于身体的慢性心理应激的事先暴露。为了实现一系列的慢性压力暴露，48名绝经后妇女被招募的病例对照设计，匹配的妇女照顾配偶痴呆症（慢性压力模型）与年龄相仿的对照妇女的配偶是健康的。参与者完成了一份问卷，评估了前一个月的压力感受，并提供了空腹血液。氧化损伤的3个指标：8-异前列腺素F2α（IsoP）、脂质过氧化、8-羟基鸟苷（8-OxoG）和8-羟基脱氧鸟苷（8-OHdG），分别反映RNA/DNA的氧化损伤。在大约一周内，参与者完成了标准化的急性实验室应激任务，同时测量唾液皮质醇反应。从0到30分钟的增加被定义为“峰值”皮质醇反应性，而从0到15分钟的增加被定义为“预期”皮质醇反应性，表示在准备压力任务时开始的皮质醇反应。处于慢性压力下的女性具有更高的8-oxoG，对RNA的氧化损伤（p<0.01）。一个温和的调解模型进行了测试，其中假设，提高预期皮质醇反应将调解感知压力和氧化应激损伤升高之间的关系，但只有在妇女慢性压力。与该模型一致，自举路径分析发现，通过预期皮质醇反应性，从感知压力到8-OxoG和IsoP（但不是8-OHdG）有显着的间接路径，显示了慢性压力参与者之间的预期关系（p≤.01.）有趣的是，在那些慢性压力暴露较低的人中，中度（与低水平相比）的感知压力与氧化损伤水平的降低有关。因此，这项研究支持了慢性应激暴露通过频繁和持续激活下丘脑-肾上腺-肾上腺轴促进氧化损伤的新模型。这也支持了较少研究的“良性压力”模型，即可管理的生活压力水平可能会增强对氧化损伤的心理生物学弹性。
Chronic psychological stress appears to accelerate biological aging, and oxidative damage is an important potential mediator of this process. However, the mechanisms by which psychological stress promotes oxidative damage are poorly understood. This study investigates the theory that cortisol increases in response to an acutely stressful event have the potential to either enhance or undermine psychobiological resilience to oxidative damage, depending on the body's prior exposure to chronic psychological stress. In order to achieve a range of chronic stress exposure, forty-eight post-menopausal women were recruited in a case-control design that matched women caring for spouses with dementia (a chronic stress model) with similarly aged control women whose spouses were healthy. Participants completed a questionnaire assessing perceived stress over the previous month and provided fasting blood. Three markers of oxidative damage were assessed: 8-iso-prostaglandin F2α (IsoP), lipid peroxidation, 8-hydroxyguanosine (8-OxoG) and 8-hydroxy-2′-deoxyguanosine (8-OHdG), reflecting oxidative damage to RNA/DNA respectively. Within approximately one week, participants completed a standardized acute laboratory stress task while salivary cortisol responses were measured. The increase from 0 to 30 min was defined as “peak” cortisol reactivity, while the increase from 0 to 15 min was defined as “anticipatory” cortisol reactivity, representing a cortisol response that began while preparing for the stress task. Women under chronic stress had higher 8-oxoG, oxidative damage to RNA (p<.01). A moderated mediation model was tested, in which it was hypothesized that heightened anticipatory cortisol reactivity would mediate the relationship between perceived stress and elevated oxidative stress damage, but only among women under chronic stress. Consistent with this model, bootstrapped path analysis found significant indirect paths from perceived stress to 8-OxoG and IsoP (but not 8-OHdG) via anticipatory cortisol reactivity, showing the expected relations among chronically stressed participants (p≤.01.) Intriguingly, among those with low chronic stress exposure, moderate (compared to low) levels of perceived stress were associated with reduced levels of oxidative damage. Hence, this study supports the emerging model that chronic stress exposure promotes oxidative damage through frequent and sustained activation of the Hypothalamic-Pituitary-Adrenal axis. It also supports the less studied model of ‘eustress’ - that manageable levels of life stress may enhance psychobiological resilience to oxidative damage.
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影响因子：
5
作者：
COHEN, S;KAMARCK, T;MERMELSTEIN, R
通讯作者：
MERMELSTEIN, R
DOI：
10.1073/pnas.96.3.1059
发表时间：
1999-02-02
影响因子：
11.1
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15.1
作者：
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Ben-Zvi, Amos
DOI：
10.1016/j.mrfmmm.2008.09.003
发表时间：
2008-12-15
影响因子：
2.3
作者：
Fimognari, Carmela;Sestili, Piero;Hrelia, Patrizia
通讯作者：
Hrelia, Patrizia
DOI：
10.1016/j.bbrc.2003.10.105
发表时间：
2003-11-28
影响因子：
3.1
作者：
Irie, M;Asami, S;Kasai, H
通讯作者：
Kasai, H