Neculicioiu Vlad Sever, Colosi Ioana Alina, Costache Carmen, Toc Dan Alexandru, Sevastre-Berghian Alexandra, Colosi Horațiu Alexandru, Clichici Simona
Department of Microbiology, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400349 Cluj-Napoca, Romania.
Department of Physiology, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400006 Cluj-Napoca, Romania.
Antioxidants (Basel). 2023 Aug 11;12(8):1600. doi: 10.3390/antiox12081600.
Sleep deprivation is highly prevalent in the modern world, possibly reaching epidemic proportions. While multiple theories regarding the roles of sleep exist (inactivity, energy conservation, restoration, brain plasticity and antioxidant), multiple unknowns still remain regarding the proposed antioxidant roles of sleep. The existing experimental evidence is often contradicting, with studies pointing both toward and against the presence of oxidative stress after sleep deprivation. The main goals of this review were to analyze the existing experimental data regarding the relationship between sleep deprivation and oxidative stress, to attempt to further clarify multiple aspects surrounding this relationship and to identify current knowledge gaps. Systematic searches were conducted in three major online databases for experimental studies performed on rat models with oxidative stress measurements, published between 2015 and 2022. A total of 54 studies were included in the review. Most results seem to point to changes in oxidative stress parameters after sleep deprivation, further suggesting an antioxidant role of sleep. Alterations in these parameters were observed in both paradoxical and total sleep deprivation protocols and in multiple rat strains. Furthermore, the effects of sleep deprivation seem to extend beyond the central nervous system, affecting multiple other body sites in the periphery. Sleep recovery seems to be characterized by an increased variability, with the presence of both normalizations in some parameters and long-lasting changes after sleep deprivation. Surprisingly, most studies revealed the presence of a stress response following sleep deprivation. However, the origin and the impact of the stress response during sleep deprivation remain somewhat unclear. While a definitive exclusion of the influence of the sleep deprivation protocol on the stress response is not possible, the available data seem to suggest that the observed stress response may be determined by sleep deprivation itself as opposed to the experimental conditions. Due to this fact, the observed oxidative changes could be attributed directly to sleep deprivation.
睡眠剥夺在现代社会中极为普遍，甚至可能已达到流行程度。尽管关于睡眠的作用存在多种理论（不活动、能量守恒、恢复、大脑可塑性和抗氧化），但关于睡眠所提出的抗氧化作用仍存在诸多未知之处。现有的实验证据往往相互矛盾，一些研究表明睡眠剥夺后存在氧化应激，而另一些研究则持反对意见。本综述的主要目的是分析关于睡眠剥夺与氧化应激之间关系的现有实验数据，试图进一步阐明围绕这种关系的多个方面，并确定当前的知识空白。我们在三个主要在线数据库中进行了系统检索，以查找2015年至2022年间对具有氧化应激测量的大鼠模型进行的实验研究。本综述共纳入了54项研究。大多数结果似乎表明睡眠剥夺后氧化应激参数发生了变化，这进一步表明睡眠具有抗氧化作用。在反常睡眠剥夺和完全睡眠剥夺方案中以及在多个大鼠品系中均观察到了这些参数的改变。此外，睡眠剥夺的影响似乎超出了中枢神经系统，还会影响外周的多个其他身体部位。睡眠恢复的特征似乎是变异性增加，一些参数会恢复正常，而另一些参数在睡眠剥夺后会出现持久变化。令人惊讶的是，大多数研究表明睡眠剥夺后会出现应激反应。然而，睡眠剥夺期间应激反应的起源和影响仍有些不清楚。虽然不可能完全排除睡眠剥夺方案对应激反应的影响，但现有数据似乎表明观察到的应激反应可能是由睡眠剥夺本身决定的，而不是实验条件。基于这一事实，观察到的氧化变化可能直接归因于睡眠剥夺。
