Abstract
Summary Light at Night (LAN) and light interference (LI) are part of modern life, which disrupt the natural light/dark cycle, causing alteration at physiological and molecular levels, partly by suppressing melatonin (MLT) secretion at night. Heat shock proteins (HSP) are activated by various stressors. We assessed HSP70 changes and gene expression in brain tissue (BT) and hepatic tissue (HT) of Golden spiny mice (Acomys russatus), acclimated to LI for 2(sLI), 7 (mLI) and 21(lLI) nights. The effect of MLT treatment on LI-mice was also assessed. HSP70 levels increased in BT and HT after sLI, while after mLI and lLI, HSP70 decreased to basic levels. Changes in HSP70 levels as a response to MLT occurred after sLI only in the HT. However, hsp70 expression following sLI increased in BT, but not in HT. MLT treatment and sLI caused decrease in hsp70 levels in BT and increase in hsp70 in HT. sLI-acclimation elicited stress response in A. russatus as expressed by increased HSP70 levels and gene expression. Longer acclimation decreases protein and gene expression to their basic levels. We conclude, that for BT and HT of A. russatus LI is a short-termed stressor, our results also revealed that A. russatus can acclimate to LI, possibly because of its circadian system plasticity, which allows it to behave both as a nocturnal and as a diurnal rodent. To the best of our knowledge, this is the first study showing the effect of LI as a stressor on the cellular level, by activating HSP70.