Nitric oxide and membrane lipid peroxidation in photosynthetic and non-photosynthetic organisms after oxidative stress exposure

Abstract

Oxidative damage to lipids was characterized in terms of the nature of the oxidant, the type of lipid, and the severity of the oxidation (Simontacchi et al., 2011). Even though malondialdehyde detection with the thiobarbituric acid reactive substances test (TBARS) is the most currently used assay for the determination of lipid oxidation, it is unspecific since the reaction can be reproduced by other biological compounds (Simontacchi et al., 2011). On the other hand, electron paramagnetic resonance (EPR) spectroscopy showed the capacity of detecting the presence of the lipid radicals (LR•) formed during peroxidation, by yielding unique and stable products with spin traps (Malanga and Puntarulo, 2012). Nitric oxide (NO) is recognized both, as a signaling molecule that regulates many enzyme activities, but as a toxic agent as well. It has been found that NO is able to protect animal and plant cell types from oxidative damage resulting from superoxide (O− 2 ), hydrogen peroxide (H2O2) and alkyl peroxides by acting as a terminator of free radical chain reactions (Wink et al., 1995, 1996; Yalowich et al., 1999; Beligni and Lamattina, 2002; Sharpe et al., 2003). Reactive oxygen species (ROS) and reactive nitrogen species (RNS) interact through the reaction of O− 2 with NO, to generate peroxynitrite (ONOO−) at a rate close to diffusion. ONOO− acts as both, a nitrating agent and a powerful oxidant capable of modifying proteins (formation of nitrotyrosine), lipids (lipid oxidation, lipid nitration), and nucleic acids (DNA oxidation and DNA nitration) (Gisone et al., 2004). The purpose of this commentary is to point out that NO complex interactions with other cellular components lead to a wide range of effects depending on the biological system under study and the oxidative stress condition.