Cool season crops face intermittent drought. Exposure to drought and other abiotic stresses is known to increase tolerance of the plants against subsequent exposure to such stresses. Storage of environmental signals is also proposed. Preexposure to a dehydration shock improved adaptive response during subsequent dehydration treatment in a cool season crop chickpea (Cicer arietinum). We have identified 101 dehydration-inducible transcripts of chickpea by repetitive rounds of cDNA subtraction; differential DNA-array hybridization followed by northern-blot analysis and analyzed their responses to exogenous application of abscisic acid (ABA). Steady-state expression levels of the dehydration-induced transcripts were monitored during the recovery period between 2 consecutive dehydration stresses. Seven of them maintained more than 3-fold of expression after 24 h and more than 2-fold of expression level even at 72 h after the removal of stress. Noticeably, all of them were inducible by exogenous ABA treatment. When the seedlings were subjected to recover similarly after an exposure to exogenous ABA, the steady-state abundances of 6 of them followed totally different kinetics returning to basal level expression within 24 h. This observation indicated a correlation between the longer period of abundance of those transcripts in the recovery period and improved adaptation of the plants to subsequent dehydration stress and suggested that both ABA-dependent and -independent mechanisms are involved in the maintenance of the messages from the previous stress experience.Plants are often exposed to various environmental stresses when grown in field and within a physiological tolerance limit. A mild abiotic stress induces an adaptive response in the plant, allowing it to grow with a greater tolerance to the same or different stresses (Siminovitch and Cloutier, 1982;Lang et al., 1994;Mantyla et al., 1995;Knight et al., 1998). Pretreatment with thermal or chemical shock induced a substantial chilling tolerance in germinated cucumber seeds (Jennings and Saltveit, 1994). Wilted excised cabbage leaves recovered turgor in absence of water uptake when allowed to lose water at a slow rate (Levitt, 1986). Plants express a number of genes in response to water deficit. At the cellular level, a part of this response results from cell damage, whereas the others correspond to adaptive processes. Adaptation to water deficit brings about changes in the metabolic processes and perhaps in the structure of the cell that allows the cells to continue metabolism at low water potential (Ingram and Bartels, 1996). Dehydration and other stresses cause rapid elevation in the cytosolic free calcium ion ([Ca 12 ] cyt ) concentration (Knight et al., 1991). As an adaptive response, the subsequent stresses show altered magnitude and kinetics of [Ca 12 ] cyt , depending on the nature and intensity of the previous stress even after a 48-h deacclimation period, indicating existence of a signal storage mechanism. Different stress-exposure alters cytosolic ...

Numerous articles and several reviews have been published on the role of antioxidants, and diet and lifestyle modifications in cancer prevention. However, the potential role of these factors in the management of human cancer have been largely ignored. Extensive in vitro studies and limited in vivo studies have revealed that individual antioxidants such as vitamin A (retinoids), vitamin E (primarily alpha-tocopheryl succinate), vitamin C (primarily sodium ascorbate) and carotenoids (primarily polar carotenoids) induce cell differentiation and growth inhibition to various degrees in rodent and human cancer cells by complex mechanisms. The proposed mechanisms for these effects include inhibition of protein kinase C activity, prostaglandin E1-stimulated adenylate cyclase activity, expression of c-myc, H-ras, and a transcription factor (E2F), and induction of transforming growth factor-beta and p21 genes. Furthermore, antioxidant vitamins individually or in combination enhance the growth-inhibitory effects of x-irradiation, chemotherapeutic agents, hyperthermia, and biological response modifiers on tumor cells, primarily in vitro. These vitamins, individually, also reduce the toxicity of several standard tumor therapeutic agents on normal cells. Low fat and high fiber diets can further enhance the efficacy of standard cancer therapeutic agents; the proposed mechanisms for these effects include the production of increased levels of butyric acid and binding of potential mutagens in the gastrointestinal tract by high fiber and reduced levels of growth promoting agents such as prostaglandins, certain fatty acids and estrogen by low fat. We propose, therefore, a working hypothesis that multiple antioxidant vitamin supplements together with diet and lifestyle modifications may improve the efficacy of standard and experimental cancer therapies.