Group Brenneisen

Reactive oxygen species in health and disease

Our group aims to throw a light on the effect of mitochondria- or other endogenous/ exogenous sources- derived reactive oxygen species (ROS, prooxidants) in physiological and pathophysiological processes of the cell, especially skin cells. An imbalance between prooxidants versus antioxidants towards higher concentrations of ROS, called oxidative stress, has been implicated in molecular mechanisms which result in cellular aging and in several pathological states, such as neurodegenerative diseases and carcinogenesis. Large efforts from a variety of research groups including ours are made both to clarify and to better understand the ROS dependent signal cascades and to identify signaling components which are redox-modulated. Aging and carcinogenesis share common features, however, they reveal unique molecular characteristics which finally determine the fate of the cell. For example, as invasion and metastatic spread of tumor cells continue to be the greatest barrier to cure cancer, the understanding of the ROS dependent cellular interaction between tumor cells and its surrounding stroma could assist in the development of novel therapeutic strategies to combat metastatic spread more efficiently in the future (Download PDF).

In that context, antioxidants and/or polymer-coated nanoparticles (<100 nm) (Fig. 1) seem to be a promising tool in prevention of tumor invasion and of (photo)aging processes. The potential role of cerium oxide nanoparticles (nanoceria, CNP) and others in modulation of the physiological and pathophysiological redox signaling will be studied in our research group (Fig. 2) by cell biological, biochemical and molecular biological techniques, using (3 dimensional) in-vitro and in-vivo models (Download PDF).

Fig. 1: Green fluorescence of FITC-labeled cerium oxide nanoparticles (Nanoceria) localized in tumor cells

Fig. 2: Proposed scheme of the dual effect of Nanoceria on tumor and healthy cells

  • bitte hier klicken um diese Seite zu druckenSeite drucken
  • Zuletzt aktualisiert am 17.09.2015
  • URL zur aktuellen Seite: http//