Transient changes in inflammatory and oxidative stress markers with total sleep deprivation

Sleep deprivation (SD) is known to modulate inflammatory and oxidative stress markers. How these markers change over the SD period have seldom been studied in healthy young adults. Seventeen healthy young adults with a mean age of 19.8 ± 1.0 years underwent an experimental protocol consisting of 36 h of total SD. We tested whether the stress response was towards adaptation or a worsening of the response. We analysed blood for gene expression levels of interleukins (IL-1β, IL-6, IL-33), tumour necrosis factor-α (TNF-α), glutathione (GSH), heat-shock protein 70 (HSP70), and a member of the signal transducers and activators of transcription (STAT3) family with quantitative real-time polymerase chain reaction (qRT-PCR). We also measured plasma levels of cortisol and malondialdehyde (MDA) with a spectrophotometer. All measurements were made at baseline and at the 24th and 36th hour of the study. IL-1β, IL-6, and GSH gene expression levels were up-regulated at the 24th hour and down-regulated at the 36th hour (p < 0.05 for all). IL-33 gene expression levels showed no change at the 24th hour and down-regulation at the 36th hour. TNF-α gene expression levels were down-regulated at the 24th hour and up-regulated at the 36th hour. Cortisol levels showed a gradual increase at all the measurement points (p < 0.05 for all). HSP70, MDA, and STAT3 had no significant changes. The present study demonstrated that the hyperactivation of the hypothalamic–pituitary–adrenal (HPA) and sympathetic-adrenal-medullary (SAM) axes shown by the up-regulation of genes seen after a sleepless night is a normal response to acute stress, and by increasing the time spent sleepless, the HPA and SAM axes may return to their normal functioning levels.