Fucoid algae live in the intertidal region where they experience daily fluctuations in light and external osmotic environment. High light, especially in combination with ultraviolet (UV) radiation and hyper-osmotic stress affected the cellular physiology of Fucus embryos. Two photoinhibition responses were recognised. Firstly, a rapid decline of the photosystem II (PSII) efficiency, linked with the operation of the xanthophyl cycle, followed by a slower decline correlated with reactive oxygen species (ROS) production. As a result of enhanced ROS production, a slower repair of the PSII efficiency was observed, particularly with increased UV-B doses. Development of the embryos was transiently affected by UV-B. The cellular signal transduction pathway during hyper-osmotic stress was investigated. ROS production in response to hyperosmotic stress comprised two distinct components. The first ROS component coincided closely with the origin of a Ca2+ wave in the peripheral cytosol at the growing cell apex, had an extracellular origin, and was necessary for the Ca2+ wave. Patch clamp experiments showed that a non-selective cation channel was stimulated by H2O2, and may underlie the initial cytosolic Ca2+ elevation. The spatio-temporal pattern of the Ca2+ wave was thus determined by peripheral ROS production. The second, later ROS component localised to the mitochondria and was a direct consequence of the Ca2+ wave. The first, but not the second component was required for short-term adaptation to osmotic stress, probably through the activity of cell wall bromoperoxidases. Mitogen-activated protein kinases may be involved in the hyper-osmotic stress response downstream or independently of the mitochondrial ROS production.