Redox homeostasis and antioxidant signaling: a metabolic interface between stress perception and physiological responses.

TLDR: Growing evidence suggests a model for redox homeostasis in which the reactive oxygen species (ROS)–antioxidant interaction acts as a metabolic interface for signals derived from metabolism and from the environment.

Abstract: Low molecular weight antioxidants, such as ascorbate, glutathione, and tocopherol, are information-rich redox buffers that interact with numerous cellular components. In addition to crucial roles in defense and as enzyme cofactors, cellular antioxidants influence plant growth and development by modulating processes from mitosis and cell elongation to senescence and death (De Pinto and De Gara, 2004; Potters et al., 2004; Tokunaga et al., 2005). Most importantly, antioxidants provide essential information on cellular redox state, and they influence gene expression associated with biotic and abiotic stress responses to maximize defense. Growing evidence suggests a model for redox homeostasis in which the reactive oxygen species (ROS)–antioxidant interaction acts as a metabolic interface for signals derived from metabolism and from the environment. This interface modulates the appropriate induction of acclimation processes or, alternatively, execution of cell death programs.