Intertidal invertebrates survive exposures to temperatures as low as -20 degrees C by tolerating the presence of tissue ice. This resistance to freezing is influenced by such factors as the time and temperature of exposure, the rate of cooling during tissue ice formation, the temperature and salinity of the seawater to which the animals have adapted, and the oxygen content of tissues. Freezing injury appears to result primarily from extracellular ice formation, although for certain smaller invertebrates that cool at rates exceeding 0.4 degrees C min-1 during tissue ice formation, intracellular ice formation may be the cause of freezing injury. Extracellular ice formation is a dehydration stress, and injury resulting from extracellular ice appears to involve membrane damage resulting from the loss of a critical amount of cellular water. Physiological mechanisms that lower the temperatures at which extracellular ice causes injury are dependent on factors that either (a) "bind" a certain fraction of intracellular water and thus reduce the amount of water lost during freezing, or (b) increase the resistance of cells to greater quantities of tissue ice. Certain structural components and glycoproteins have been isolated from an intertidal mollusk that can impede or prevent the formation of ice. However, a quantitative relationship between these components and freezing resistance has not been established. The resistance to greater quantities of tissue ice appears to be associated with low levels of tissue oxygen and with anaerobic metabolism. A rise in blood calcium concentration following a shift from aerobic to anaerobic metabolism can account for part of the increased resistance of an intertidal mollusk to greater quantities of tissue ice, while membrane changes and factors that reduce the toxic effects of oxygen may also be involved. The possibility that oxygen is associated with injury resulting from extracellular ice formation in intertidal invertebrates deserves further investigation.