Cellular responses to oxidative and osmotic stress.

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‘Cellular responses to oxidative and osmotic stress; sensing, signaling and gene expression’ was the theme of a novel congress held in Egmond aan Zee, The Netherlands, from August 28 to September 1, 1999. The program, attended by 150 participants, included 14 invited lectures by expert scientists studying these types of stress in organisms as diverse as bacteria, yeast, plants, and mammals, as well as 16 selected talks and 90 poster presentations. Oxidative and osmotic stress differ significantly while also displaying overlapping responses. In general, oxidative stress is caused by the intracellular accumulation of reactive oxygen species (ROS) (P. Moradas Ferreira, Porto) or a disturbance of the cellular redox state (J. Teixeira de Mattos, Amsterdam). Hence the oxidative defenses encompass both nonenzymatic (glutathione, thioredoxin) and enzymatic (superoxide dismutase, peroxidases, catalase) detoxification mechanisms which destroy ROS or restore the redox balance. Oxidative stress signals may come from the environment, but can also be generated internally and may cause molecular damage to proteins (P. Moradas Ferreira, Porto), DNA, membranes, etc. Osmotic stress leads to efflux or influx of water from or into the cell: hyperosmotic stress causes shrinking, hypoosmotic stress causes swelling. The cellular responses to this type of stress deal with the activity of water channels (aquaporins) and electrolyte transporters, and the accumulation of osmolytes (I. Booth, Aberdeen; S. Hohmann, Gothenburg) as well as the protection of proteins and subcellular structures. At first glance, therefore, sensing of oxidative stress in principle may include more direct molecular events than sensing of osmotic stress. Focussing on gene expression,