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Embryos are extremely sensitive to all environmental factors at the so-called 'critical stages' of normal development. Under an influence of various adverse factors, the maximal levels of mortality concurs with the critical stages. In our experiments with the embryos of the common toad, the stages of early neurula and tail bud were characterized as the critical once. However, once the threshold values of several adverse factors were exceeded, the stages of mid-blastula and mid-gastrula became the critical stages. If the oxygen concentration, density of embryos or toxicant concentration surpassed their threshold values, embryonic development has been arrested at the mid-blastula or mid-gastrula stages. The pattern of this reaction depended on the particular factor. In the case of high density and hypoxic conditions, development proceeded normally until the mid-gastrula stage, then stopped and embryos underwent mass mortality. Under the high copper concentrations (10, 25 and 50 mg / L) the development was slowed down at the blastula stage and arrested at the mid-gastrula stage. Developmental arrest can last for several days (up to 86h, i.e 81% of normal development, which lasts about 100h). If existing conditions were left as is, almost all embryos died (about 90%), but small fraction of embryos survived and reached the stage of hatching. The most interesting finding is that if conditions were sharply improved, the long-term developmental arrest has been cancelled. The embryos survived and managed to reach the hatchling stage much faster than in the course of normal development. We suppose that the developmental arrest occurring at one of the critical stages can be viewed as an adaptation allowing the embryos to survive: embryos are able not to proceed to the next developmental stage (e.g. formation of neural plate) waiting for ceasing of the adverse environmental influence.