Chapter 25 Singlet Oxygen-Induced Oxidative Stress in Plants

Abstract

In the present oxidizing environment, metabolic processes such as photosynthesis and respiration are mostly responsible for the generation of reactive oxygen species (ROS) including singlet oxygen (1O2) in chloroplasts, mitochondria, peroxisomes and other sites of the plant cell. Imbalance between ROS production and their detoxification by enzymatic and non-enzymatic means results in higher net ROS formation and consequent oxidative damage which ultimately causes cell death. 1O2 often acts as a signaling molecule involved in pathogen defense responses such as hypersensitive reactions and systemic acquired resistance, stress hormone production, acclimation and programmed cell death. In plants, 1O2 is mainly produced by the chlorophyll (Chl) and its tetrapyrrole metabolic intermediates in the presence of light via type II photosensitization reactions. Diphenyl ethers cause the accumulation of protoporphyrin IX that generates 1O2 via photosensitization reactions and causes necrotic spots and cell death by destroying the plasma membrane. Similarly, exogenous application of 5-aminolevulinc acid (ALA) results in the accumulation of other Chl biosynthesis intermediates such as protochlorophyllide which generates 1O2 in the light causing cell death. Genetic mutants that are deficient in Chl biosynthetic enzymes or regulatory proteins accumulate excess tetrapyrroles leading to excess 1O2 generation and cell death. Similarly, plants that are genetically deficient in Chl degradation enzymes accumulate excess Chl catabolic products; this generates 1O2, via photosensitization reactions, and causes cell death. As there is no enzymatic means available to detoxify 1O2, it is essential to minimize its production rather than detoxifying it after it is generated. In this article the mechanisms of generation of 1O2, its detoxification, its mode of cellular damage and ways to minimize its destructive potential and programmed cell death are discussed.