Downregulation of cellular metabolism during environmental stress: Mechanisms and implications
Abstract
Survival time of organisms during exposure to environmental stresses that limit energy availability is, in general, directly related to the degree of metabolic depression achieved. The energetic cost savings realized by the organism is a consequence primarily of the ability to depress ion pumping activities of cells, macromolecular synthesis, and macromolecular turnover. Evidence supporting the concept of channel arrest-the reduction in ion leakage across cell membranes during hypometabolic states-has highlighted the energetic benefits of limiting ATP turnover related to cellular ion homeostasis. Depression of protein synthesis results in substantial bioenergetic savings. However, when protein synthesis is arrested, the preservation of macromolecules becomes increasingly important as the duration of quiescence is extended because the cellular capacity for replenishing these components is reduced. It is likely that the rate of macromolecular degradation is a key feature that sets the upper time limit for survival during chronic environmental stress.