Patterns of peroxidative ethane emission from submerged rice seedlings indicate that damage from reactive oxygen species takes place during submergence and is not necessarily a post-anoxic phenomenon

Abstract

Using ethane as a marker for peroxidative damage to membranes by reactive oxygen species (ROS) we examined the injury of rice seedlings during submergence in the dark. It is often expressed that membrane injury from ROS is a post-submergence phenomenon occurring when oxygen is re-introduced after submergence-induced anoxia. We found that ethane production, from rice seedlings submerged for 24-72 h, was stimulated to 4-37 nl gFW(-1), indicating underwater membrane peroxidation. When examined a week later the seedlings were damaged or had died. On de-submergence in air, ethane production rates rose sharply, but fell back to less than 0.1 nl gFW(-1) h(-1) after 2 h. We compared submergence-susceptible and submergence-tolerant cultivars, submergence starting in the morning (more damage) and in the afternoon (less damage) and investigated different submergence durations. The seedlings showed extensive fatality whenever total ethane emission exceeded about 15 nl gFW(-1). Smaller amounts of ethane emission were linked to less extensive injury to leaves. Partial oxygen shortage (O(2) levels <1%) imposed for 2 h in gas phase mixtures also stimulated ethane production. In contrast, seedlings under anaerobic gas phase conditions produced no ethane until re-aerated: then a small peak was observed followed by a low, steady ethane production. We conclude that damage during submergence is not associated with extensive anoxia. Instead, injury is linked to membrane peroxidation in seedlings that are partially oxygen deficient while submerged. On return to air, further peroxidation is suppressed within about 2 h indicating effective control of ROS production not evident during submergence itself.

Phytoremediation of Organic Contaminants in Soil and Groundwater

“…It has been shown that tissue damage starts very early (probably within hours) after the onset of stress. [91] Owing to the importance of ROS in plants, a potent antioxidant apparatus has been developed to keep ROS under control which consists of 1) small antioxidant molecules such as the hydrophilic ascorbate, glutathione, or (glycolated) polyphenols, or the lipohilic tocopheros and b-carotene, and 2) antioxidant enzymes like ascorbate peroxidase (APX), glutathione reductase (GR), or SOD (superoxide dismutase). These enzymes mostly consist of an enzyme family and function in close cooperation with each other and the small antioxidant molecules.…”

The Submergence Tolerance Regulator Sub1A Mediates Stress-Responsive Expression of AP2/ERF Transcription Factors

“…The obvious phenotypic difference under desubmergence after prolonged submergence between the tolerant and intolerant cultivars suggests that FR13A maintains a high antioxidant defense system but IR42 does not (Almeida et al, 2003). Despite the importance of protecting antioxidant systems during anoxia, there are few reports that explore the differential expression of enzymes associated with antioxidant defense in submergence-tolerant cultivars (Santosa et al, 2007). In addition, it has been reported that ROS is needed for cell elongation in Arabidopsis (Arabidopsis thaliana; Foreman et al, 2003).…”

Oxidative Stress Components Explored in Anoxic and Hypoxic Global Gene Expression Data

“…The presence of ROS under oxygen deprivation stress is somewhat a paradox and indeed some oxygen is needed for ROS production under oxygen deprivation stress, and hence it is preferable to talk about severe hypoxia in most cases, and of a reoxygenation period when atmospheric oxygen conditions are again introduced (Branco-Price et al 2008). The biochemistry behind ROS production and antioxidative defense as well as the damage produced under oxygen deprivation is well documented (Yan et al 1996;Biemelt et al 1998Biemelt et al , 2000Blokhina et al 2000Blokhina et al , 2001Blokhina et al , 2003Fukao and Bailey-Serres 2004;Santosa et al 2007). The evidence for the regulatory role of ROS under oxygen deprivation in the control of gene expression (Pucciariello et al 2012), the negative feedback regulation of H 2 O 2 levels by Rop-RopGAP4 interaction (Baxter-Burrell et al 2002), and the activation of MAPK kinases in response to mitochondrial ROS resulting in better survival under hypoxia (Chang et al 2012), all point to a complex relationship between hypoxic metabolic rearrangements, ROS levels, and their cellular localization and affect the physiological outcome of oxidative stress.…”