The circadian clock is responsible for regulating several crucial physiological processes and its disruption can be linked to several diseases, including cardiovascular disorders, diabetes and cancer. In a first approach, the effects of Jetlag on cellular metabolism were addressed using zebrafish fibroblast cells, as these cells are directly light responsive and can be entrained to artificial light dark cycles. Since the circadian rhythm is known to be bidirectionally intertwined with the hypoxic signalling pathway, we set out to investigate the effects of chronodisruption on the master regulator of cellular oxygen metabolism, Hypoxia Inducible Factor-1 and on oxidized peroxiredoxins (Prxox), which represent conserved markers of circadian rhythms across all domains of life. We found that Hif-1 oscillations demonstrated a circadian pattern under control conditions, as reported by others previously, and that disruption of the light/dark settings in form of an applied Jetlag schedule altered the expression levels of Hif-1 protein. Furthermore, Jetlag also led to increased levels of oxidized peroxiredoxins, altering phase as well as period of the circadian oscillation of Prxox. Circadian oscillations of cytosolic hydrogen peroxide, in contrast, showed a clear circadian rhythm under control conditions, which remained completely unaffected by the corrupted lighting conditions. In addition, we found that also basal oxygen consumption and extracellular acidification rate did not alter upon Jetlag conditions. Hence, the present masters thesis addresses for the first time the impact of chronodisruption on hypoxic signalling and selected markers of the cellular redox system by using the directly light responsive zebrafish cells, providing thus a first glance of the impact of Jetlag at the cellular level.