Abstract
•Unequal distribution of molecular O2 can lead to low-O2 stress/hypoxia in plants.•Low-O2 stress can provoke multiple negative effects on plant growth and development.•ROS and NO are important signaling molecules generated in hypoxia stress.•Plants can sense low-O2 stress through N-end rule pathway.•Survival of plants under hypoxia depends on homeostatic balance between ROS and NO.
Molecular oxygen (O2) is a basic requirement of life for many organisms, including plants. As a terminal electron acceptor, during mitochondrial respiration, O2 governs both the energy status and numerous aspects of cellular metabolism by influencing adenosine triphosphate (ATP) synthesis. Although O2 is essential, no active mechanism has been found in plants that can provide uniform O2 within the tissues of various plant organs, including roots and tubers, as well as germinating seeds. As a result, plants cells and tissues can face low-oxygen stress (LOS)/hypoxia under certain environmental conditions. Environmental events such as flooding/water logging can create LOS or absence of O2, and a high rate of cellular metabolism can also cause the O2 deficit. The absence of O2 as a terminal electron acceptor leads to the generation of excess electrons that can leak from the inner mitochondrial membrane, resulting in the production of reactive oxygen species (ROS). With respect to physiological signaling, ROS and nitric oxide (NO) have shown to have a dual behaviour, depending upon the cellular concentrations and/or time of exposure. Both ROS and NO can act as signaling molecules, and depending on their endogenous levels they can activate various downstream signaling pathways or can cause an oxidative burst, leading to cell damage. In addition, previous studies have shown that ROS and NO, when being present at high levels, can react with each other to produce various other forms of ROS and reactive nitrogen species (RNS). The present review focuses on different aspects of LOS and how plants sense decreases in cellular O2 concentrations. The roles played by ROS and NO in relation to maintaining redox homeostasis during impairment of energy metabolism are critically discussed.