Abiotic stress is the primary cause of crop loss worldwide, reducing average yields for most major crop plants by more than 50%. Plants as sessile organisms are constantly exposed to changes in environmental conditions. When these changes are rapid and extreme, plants generally perceive them as stresses. However stresses are not necessarily a problem for plants because they have evolved effective mechanisms to avoid or reduce the possible damages. The response to changes in environment can be rapid, depending on the type of stress and can involve either adaptation mechanisms, which allow them to survive the adverse conditions, or specific growth habitus to avoid stress conditions. In fact, plants can perceive abiotic stresses and elicit appropriate responses with altered metabolism, growth and development. The regulatory circuits include stress sensors, signalling pathways comprising a network of protein-protein interactions, transcription factors and promoters, and finally the output proteins or metabolites (table 1). A number of abiotic stresses such as extreme temperatures, high light intensity, osmotic stresses, heavy metals and a number of herbicides and toxins lead to over production of reactive oxygen species (ROS) including H2O2 causing extensive cellular damage and inhibition of photosynthesis. Normally, ROS are rapidly removed by antioxidative mechanisms, but this removal can be impaired by stresses themselves (Allan & Fluhr, 2007), causing a rise in their intracellular concentration and an increase of the damage. To prevent or repair these damages, plant cells use a complex defence system, involving a number of antioxidative stress-related defence genes that, in turn, induce changes in the biochemical plant machinery. Studies have shown that ROS probably require additional molecules to transduce and amplify defence signals. ROS production and anti-oxidant processes, all act in a synergistic, additive or antagonistic way, related to the control of oxidative stress. Responses to stress are not linear pathways, but are complex integrated circuits involving multiple pathways and in specific cellular compartments, tissues, and the interaction of additional cofactors and/or signalling molecules to coordinate a specified response to a given stimulus (Dombrowski, 2009). Onset of a stress triggers some (mostly unknown) initial sensors, which then activate cytoplasmic Ca2+ and protein signalling pathways, leading to stress-responsive gene expression and physiological changes (Bressan et al., 1998;